Diagnosis:

Upon physical exam the above symptoms are noted, on auscultation inspiratory crackles and wheezing are usually present. Hydration status should be noted, as RSV is a diffuse small airway disease, leading to bronchiolitis.

Non-specific lab tests such as ABGs, CBC, and O2 sat., and age of child help determine candidates for admittance. Secretions can be analyzed using PCR but are expensive, a sophisticated virology lab is required in terms of antigen detection.

Imaging X-Ray is commonly ordered, revealing (nonspecific) hyperinflated lung fields, diffuse interstitial infiltrates, and in more advanced cases focal atelectasis.

DDx: Asthma, bronchitis, adenovirus, pneumonia, metapnuemovirus, influenza.

Treatment:  See part 2 coming soon!

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infection (LRTI) in children in the world¹. Because it’s so common, it’s important for medical students in the hospital to be familiar with the virus, especially in how it presents in the Emergency Department, and how to determine to admit the patient or send them home to rest.

RSV belongs to the Paramyxoviridae family, Pneumovirinae subfamily. It’s a negative sense ssRNA virus (don’t forget virology!). It is spread via direct contact, inhilation, and can last up to 5 hours as a fomite on surfaces. Incidence: The virus is more common in children and most get it by 2-3 years of age, peak incidence is 2-7 months of age. However, anyone can get the virus especially the elderly. At risk are children who attend childcare, children who are not breastfed, living with smokers or being exposed to cigarette smoke, prematurity (<35weeks), and congenital immunodeficiency⁴ .

Epidemiology: It’s well known to be seasonal (late fall, winter, early spring) but varies by region (see chart). 4-5 million children are affected each year and ~125,000 are admitted, although admittance rates are slowly increasing. A retrospective study showed 24% of LRTI hospitalizations among children <5 years of age during the 10 study years, 1997-2006 were due to RSV⁵ .

http://www.cdc.gov/Features/dsRSV/

The x-ray shows lung hyperinflation with a flattened diaphragm and opacification in the right lung apex (red circle) and left lung base (blue circle) from atelectasis. Obviously, the same changes can be seen in the x-ray of a child with acute asthma. This is one reason why children with acute asthma are often misdiagnosed as having pneumonia. http://reference.medscape.com/features/slideshow/pediatric-respiratory

click for larger view

References:

1. Morbidity & Mortality Weekly Report. 2007;56(48):1263-1265.

2. Corneli HM, Zorc JJ, Mahajan P, Majahan P, Shaw KN, Holubkov R. “A multicenter, randomized, controlled trial of dexamethasone for bronchiolitis.” N Engl J Med. Jul 26 2007;357(4):331-9. [Medline].

3. Seo S, Campbell AP, Xie H, Chien JW, Leisenring WM, Englund JA, Boeckh M. “Outcome of Respiratory Syncytial Virus Lower Respiratory Tract Disease in Hematopoietic Cell Transplant Recipients Receiving Aerosolized Ribavirin: Significance of Stem Cell Source and Oxygen Requirement.” Biol Blood Marrow Transplant. 2013 Jan 5. doi:pii: S1083-8791(12)01178-0. 10.1016/j.bbmt.2012.12.019. [Epub ahead of print] PMID: 23298855 (PubMed)

4. http://emedicine.medscape.com/article/971488-overview#showall

5. Stockman LJ, Curns AT, Anderson LJ, Fischer-Langley G. “Respiratory syncytial virus-associated hospitalizations among infants and young children in the United States, 1997-2006.”

Pediatr Infect Dis J. 2012 Jan;31(1):5-9. http://www.ncbi.nlm.nih.gov/pubmed/21817948

Compiled by: Nick Mancuso

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

So you’re the ED doc and they might have a stroke. Qu’est-ce que tu vas faire*!?!

Firstly, a head CT.  This is the first branch of the decision tree.  As previously mentioned, strokes are either hemorrhagic or ischemic, and the management of each is entirely different (ie do they get tPa or not). Without regards to whether to use tPa or not, this will focus on the ischemic subtype.

And within this subtype of ischemic stroke patients who cannot receive tPa, one comes to another branch in the decision tree.  Is the patient in atrial fibrillation (afib)?  Usually this can be evident from physical exam (ie irregularly irregular pulse) and telemetry, but an EKG can be confirmatory.  The management of an ischemic stroke in afib (aka cardioembolic ischemic stroke) differs greatly from one that isn’t (aka noncardioembolic ischemic stroke).  Cardioembolic strokes requires anticoagulants (eg warfarin) while a non-cardioembolic stroke only requires anti-platelets (eg aspirin).  Once again, the following will only focus on non-cardioembolic stroke and choice of anti-platelet.

*That’s French speak for ‘What ya gonna do’

Aspirin is dece*

There is some controversy in the stroke world as to the initial choice of anti-platelet for secondary prophylaxis of non-cardioembolic ischemic strokes.  One thing most everyone can agree on though is the utility of aspirin.  Aspirin within 48 hours has shown to decrease stroke reoccurrence and improve long term outcomes in multiple trials and meta-analyses _1,2,8.

*Dece= decent in Caucasian phrasin’

So what about the other fancy anti-platelets? 

There have been a multitude of trials that one is welcome to read by following the references below but I present my personal summary for secondary prophylaxis based on what I’ve read in the trials:

- Aspirin is more effective than placebo_1,2

-Aggrenox (dipyramidole+aspirin) is better than placebo₃

-Plavix is better than aspirin in composite vascular endpoint (you can decide for yourself whether that’s truly better for stroke or not)₇

-Aggrenox may be better than aspirin_3,5

-Plavix and Aggrenox are equivalent₄

- ASA+ Plavix is equivalent to plavix alone but increases risks of bad side effects (eg bleeding)₆

- Ticlopidine is better than placebo₉

-Ticlopidine may be better than aspirin but with increased costs, lab f/u (i.e. biweekly CBC’s the first 3 months due to risk of neutropenia), and worse side effects may decrease the cost/benefit ratio₁₀

Blah blah too many words—Break it down, C Belch

So a patient comes in with signs of stroke.  Their CT is negative for bleed and they’re outside of the tPa window.  They’re not in afib.  What are you gonna do?  My personal guidelines based on the evidence:

-          Aggrenox or Plavix monotherapy are good initial choices for non-cardioembolic ischemic strokes and better than aspirin alone

-          Do NOT use aspirin + Plavix dual therapy for these types of strokes due to the increased risks of bleeding. Leave that combo for cardiologists.

-          Aspirin and ticlopidine are also good initial choices.  But aspirin may be less effective than Aggrenox or Plavix monotherapy and ticlopidine has a poor side effect profile and increased costs

Public Service announcement:  As always, each patient is different and requires a personalized and evidence based approach to medication choices based on side effect profile and individual patient preference.  I also reference below the American College of Chest physician’s recommendations₁₁ —they set forth their own guidelines based on the evidence which are very similar to what is proposed above.  And if all else fails, ask your friendly neighborhood pharmacist.

Sources:

1. The International Stroke Trial (IST). Lancet. 1997 May 31; 349 (9065): 1569-81
2. Chinese Acute Stroke Trial (CAST). Lancet 1997 Jun 7; 349 (9066): 1641-9
3. European Stroke Prevention Study 2 (ESPS 2).  J Neurol Sci. 1996; 143(1-2): 1-13
4. PRoFESS trial.  NEJM. 2008; 359 (12): 1238-1251
5. European/Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT).  Lancet. 2006; 367 (9534):  1665-1673
6. MATCH trial.  Lancet. 2004. Jul 24-30; 364(9431):  331-7
7. CAPRIE trial.  Lancet.  1996 Nov 16; 348(9038):  1329-39
8. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, MI, and stroke in high risk pts.  (Antithrombotic Trialists’ Collaboration).  BMJ.  2002 Jan 12; 324 (7329):  71-86
9. Canadian American Ticlopidine Study (CATS).  Lancet.  1989 Jun 3; 1(8649):  1215-20
10. A randomized trial comparing ticlopidine HCL w/ asa for prevention of stroke in high risk pts.  (TASS).  NEJM.  1989 Aug 24; 321 (8):  501-7
11. Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence based clinical practice guidelines.  Feb 2012; 141 (2_suppl)

Compiled by: Chris Belcher

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

Note that Tamiflu is now FDA approved for patients age 2-weeks and older (FDA NEWS RELEASE link)

Pregnant women

Oseltamivir is preferred for treatment of pregnant women. Pregnant women are recommended to receive the same antiviral dosing as nonpregnant persons

• Zanamivir might be preferred by some providers because of its limited systemic absorption; however, respiratory complications that might be associated with zanamivir because of its inhaled route of administration need to be considered, especially in women at risk for respiratory problems
• Pregnant women are known to be at higher risk for complications from infection with seasonal influenza viruses and severe disease among pregnant women was reported during past pandemics
• Oseltamivir, zanamivir, rimantadine, and amantadine are “Pregnancy Category C” medications, indicating that data from clinical studies are not adequate to assess the safety of these medications for pregnant women

Persons w/ impaired renal function

Oseltamivir: For patients with creatinine clearance of 10–30 mL per minute, a reduction of the treatment dosage of oseltamivir to 75 mg once daily and in the chemoprophylaxis dosage to 75 mg every other day is recommended

• Serum concentrations of oseltamivir carboxylate, the active metabolite of oseltamivir, increase with declining renal function.

Person w/ Immunosuppression

• oseltamivir was safe and well tolerated when used during the control of an influenza outbreak among hematopoietic stem cell transplant recipients living in a residential facility
• Source: (retrospective study: Vu D, Peck AJ, Nichols WG, et al. Safety and tolerability of oseltamivir prophylaxis in hematopoietic stem cell transplant recipients: a retrospective casecontrol study. Clin Infect Dis 2007;45:187–93.)

SUMMARY FOR TREATMENT RECOMMENDATIONS:

• Clinical trials and observational data show that early antiviral treatment can shorten the duration of fever and illness symptoms, and may reduce the risk of complications from influenza
• Persons at higher risk for influenza complications recommended for antiviral treatment include:
  • children aged younger than 2 years;*
  • adults aged 65 years and older;
  • persons who are morbidly obese (i.e., body-mass index is equal to or greater than 40)
  • persons with immunosuppression, including that caused by medications or by HIV infection;
  • women who are pregnant or postpartum (within 2 weeks after delivery);
  • persons aged younger than 19 years who are receiving long-term aspirin therapy;
  • persons with chronic pulmonary (including asthma), cardiovascular (except hypertension alone), renal, hepatic, hematological (including sickle cell disease), metabolic disorders (including diabetes mellitus), or neurologic and neurodevelopment conditions (including disorders of the brain, spinal cord, peripheral nerve, and muscle such as cerebral palsy, epilepsy [seizure disorders], stroke, intellectual disability [mental retardation], moderate to severe developmental delay, muscular dystrophy, or spinal cord injury);
  • American Indians/Alaska Natives;
  • residents of nursing homes and other chronic-care facilities.
• When indicated, antiviral treatment should be started as soon as possible after illness onset, ideally within 48 hours of symptom onset. However, antiviral treatment might still be beneficial in patients with severe, complicated or progressive illness and in hospitalized patients when started after 48 hours of illness onset, as indicated by observational studies.
• When indicated, antiviral treatment should be started as soon as possible after illness onset, ideally within 48 hours of symptom onset. However, antiviral treatment might still be beneficial in patients with severe, complicated or progressive illness and in hospitalized patients when started after 48 hours of illness onset, as indicated by observational studies.
• Decisions about starting antiviral treatment should not wait for laboratory confirmation of influenza
• The recommended duration of treatment is 5. Longer treatment regimens might be necessary in severely ill hospitalized patients or persons with immunosuppression

SUMMARY FOR CHEMOPROPHYLAXIS

• Antiviral medications are approximately 70% to90% effective in preventing influenza and are useful adjuncts to influenza vaccination (** CDC does not recommend routine use of antiviral meds for chemophrophylaxis to limit possibilities of antiviral resistance)
• An emphasis on close monitoring and early initiation of antiviral treatment is an alternative to chemoprophylaxis after a suspected exposure for some persons.
• To be effective as chemoprophylaxis, an antiviral medication must be taken each day for the duration of potential exposure to a person with influenza and continued for 7 days after the last known exposure.
• Antiviral chemoprophylaxis generally is not recommended if more than 48 hours have elapsed since the last exposure to an infectious person.

SUMMARY OF INFLUENZA VACCINATION

• All persons aged 6 months and older should be vaccinated annually.
• Protection of persons at higher risk for influenza-related complications should continue to be a focus of vaccination efforts.
• When vaccine supply is limited, vaccination efforts should focus on delivering vaccination to persons who:
  • are aged 6 months–4 years (59 months);
  • are aged 50 years and older;
  • have chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, neurologic, hematologic, or metabolic disorders (including diabetes mellitus);
  • are immunosuppressed (including immunosuppression caused by medications or by human immunodeficiency virus);
  • are or will be pregnant during the influenza season;
  • are aged 6 months–18 years and receiving long-term aspirin therapy and who therefore might be at risk for experiencing Reye syndrome after influenza virus infection;
  • are residents of nursing homes and other chronic-care facilities;
  • are American Indians/Alaska Natives;
  • are morbidly obese (body-mass index is 40 or greater);
  • are health-care personnel;
  • are household contacts and caregivers of children aged younger than 5 years and adults aged 50 years and older, with particular emphasis on vaccinating contacts of children aged younger than 6 months; and
  • are household contacts and caregivers of persons with medical conditions that put them at higher risk for severe complications from influenza.

VACCINATION IN PERSONS ALLERGIC TO EGGS

Generally, egg allergic patients can safely receive TIV. Individuals with a history of severe (life threatening) allergy to eating eggs should consult with a specialist with expertise allergy prior to receiving TIV

Updated recommendations based on 2011 morbidity and mortality report from CDC:

Recommendations regarding influenza vaccination for persons who report allergy to eggs — Advisory Committee on Immunization Practices (ACIP), 2011–12 influenza season

1. Persons who have experienced only hives following exposure to egg should receive influenza vaccine with the following additional measures:

a) Because studies published to date involved use of TIV, TIV rather than LAIV should be used.

b) Vaccine should be administered by a health-care provider who is familiar with the potential manifestations of egg allergy.

c) Vaccine recipients should be observed for at least 30 minutes for signs of a reaction following administration of each vaccine dose.

 Other measures, such as dividing and administering the vaccine by a two-step approach and skin testing with vaccine, are not necessary.

2. Persons who report having had reactions to egg involving angioedema, respiratory distress, lightheadedness, or recurrent emesis, or persons who required epinephrine or other emergency medical intervention, particularly those that occurred immediately or within minutes to hours after egg exposure are more likely to have a serious systemic or anaphylactic reaction upon reexposure to egg proteins. Before receipt of vaccine, such persons should be referred to a physician with expertise in the management of allergic conditions for further risk assessment

3. All vaccines should be administered in settings in which personnel and equipment for rapid recognition and treatment of anaphylaxis are available. ACIP recommends that all vaccination providers be familiar with the office emergency plan

4. Some persons who report allergy to egg might not be egg allergic. Those who are able to eat lightly cooked egg (e.g., scrambled eggs) without reaction are unlikely to be allergic. Conversely, egg-allergic persons might tolerate egg in baked products (e.g., bread or cake); tolerance to egg-containing foods does not exclude the possibility of egg allergy (35). Egg allergy can be confirmed by a consistent medical history of adverse reactions to eggs and egg-containing foods, plus skin and/or blood testing for immunoglobulin E antibodies to egg proteins.

5. A previous severe allergic reaction to influenza vaccine, regardless of the component suspected to be responsible for the reaction, is a contraindication to receipt of influenza vaccine.

References:

• http://www.cdc.gov/flu/professionals/

• Antiviral Agents for the Treatment and Chemoprophylaxis of Influenza Recommendations of the Advisory Committee on Immunization Practices (ACIP)

Compiled by: Sakib Motalib

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

The 2012/13 vaccine contains the typical triad against an H1N1, H3N2, and an influenza B variant.

• A/California/7/2009 (H1N1)-like virus
• A/Victoria/361/2011 (H3N2)-like virus
• B/Wisconsin/1/2010-like virus.

Symptoms overlap with many URI’s, however the classics:

Abrupt onset, Chills, Varying fever temps, Myalgias, Frontal/retro-orbital headache, Sore throat, Nausea/Vomiting

Diagnosis

can be difficult because samples are sent to labs and take time to get results. A nasopharyngeal culture is taken. Most diagnosis is done at the bedside based on clinical criteria. Rapid tests are not accurate and results vary. (Check continue reading for more info about diagnostic tests!)

Treatment:

Read part 2!

For some cool data and graphs from the CDC continue reading…

Anyone who has had the news on knows, this year’s flu season is expected to be, and already is, a bad one. Walk into your local Emergency Department and everyone is wearing the iconic mask, sitting in the waiting room because of overcrowding and other illnesses peaking. Here’s a brief summary of this year’s seasonal flu so far:

The vaccine is recommended for everyone over 6 months old, especially children, pregnant women, the elderly, and healthcare workers. Administration is IM, infants and younger children should be vaccinated in the anterolateral thigh, adults and older children, the deltoid is preferred. 6 through 35 months receive 0.25 mL per dose; persons aged ≥36 months receive 0.5 mL per dose. FluMist intranasal is given via a 0.2 mL prefilled intranasal sprayer to those over 2 years old. As of 12/14/12 127 million doses had been distributed. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6132a3.htm#fig1

Characterized cases so far by the CDC include:

H1N1

-100% of 17 H1N1 viruses tested were characterized as A/California/7/2009-like

H3N2

-(99.3%) of the 281 H3N2 influenza viruses tested have been characterized as A/Victoria/361/2011-like

Influenza B

-(68.7%) of the 115 influenza B viruses tested so far this season have been characterized as B/Wisconsin/1/2010-like

-(31.3%) of 115 influenza B viruses tested have been from the B/Victoria lineage of viruses

• Since the start of the season, influenza A (H3N2) viruses have predominated nationally, followed by influenza B viruses, while 2009 H1N1 viruses have been identified rarely. The predominant circulating virus has varied by state and by region. (http://www.cdc.gov/flu/weekly/)

Diagnostic tests for the Flu

From the CDC:

• Rapid Influenza Diagnostic Tests (RIDTs) can be useful to identify influenza virus infection as a cause of respiratory outbreaks in any setting. RIDTs produce very quick results, but the results may not be accurate. Sensitivities of RIDTs are generally 40-70%, but a range of 10-80% has been reported compared to viral culture or reverse transcription polymerase chain reaction (RT-PCR). Specificities of RIDTs are approximately 90-95% (range 85-100%). Thus, false negative results occur more commonly than false positive results. In particular, false negative test results are common during influenza season. Clinicians should realize that a negative RIDT result does NOT exclude a diagnosis of influenza in a patient with suspected influenza.
• Other testing (immunofluorescence, RT-PCR, viral culture) is more accurate, but can take longer. When influenza is suspected and antiviral treatment is indicated, antiviral treatment should begin as soon as possible and should not wait for the results of testing.

To Minimize False RIDT Results

• Collect specimens as early in the illness as possible (ideally less than 4 days from illness onset).
• Follow-up negative results with confirmatory tests (RT-PCR or viral culture) if a laboratory-confirmed influenza diagnosis is desired.

References:

“FDA approves vaccines for the 2012-2013 influenza season”. Press Release. FDA. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm315365.htm

Oseltamivir phosphate package insert http://www.gene.com/download/pdf/tamiflu_prescribing.pdf

“Seasonal Influenza Vaccination Resources for Health Professionals.” web http://www.cdc.gov/flu/professionals/vaccination

Compiled by: Nick Mancuso

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

Here’s an excerpt:

600 people reached the top of Mt. Everest in 2012. This blog got about 3,800 views in 2012. If every person who reached the top of Mt. Everest viewed this blog, it would have taken 6 years to get that many views.

Click here to see the complete report.

1) Ischemic: blood vessel supplying the brain is obstructed by a clot

• Embolism
• Thrombosis 

2) Hemorrhagic: blood vessel bursts, blood leaks throughout brain #1 Risk Factor: High blood Pressure Other Risk Factors:

• Age
• Sex: Male
• Ethnicity: African Americans, Mexican Americans, Hawaiians, Asian Americans
• Smoking
• Fat, cholesterol-rich diet
• Overweight
• Pregnancy
• Birth-control Pills
• Smoking
• Diabetes
• Renal problems
• Atrial Fibrillation

Signs of Stroke

• Sudden, severe headache
• High blood pressure
• Problems with vision, reflexes, walking, movement, speaking, coherence
• Vertigo
• “Bruit” noise when listening to carotid arteries in neck with stethoscope

Treatment Options:

• Ischemic: Blood thinners to reduce clots: warfarin, heparin, Coumadin
• Hemorrhagic: surgery to remove blood in brain, repair damaged blood vessels

Academic life in emergency medicine NIH stroke scale PV card. Great resource:

http://academiclifeinem.blogspot.com/2010/02/paucis-verbis-card-nih-stroke-scale.html

Click continue reading for high yield quickhits on a few specific types of stroke and brain imaging examples

Location of Stroke determines range of symptoms Branches of Internal Carotid Artery

• Middle cerebral artery (MCA):
  • Supplies lateral, frontal, and parietal lobes, anterior and lateral temporal lobes
  • Region supplied by MCA is large (easiest path for embolism)
  • Anterior Cerebral Artery (ACA):
    • Supplies medial frontal and parietal lobes, anterior internal capsule, and basal ganglia

Branches of Basilar Artery

• Posterior Cerebral Artery (PCA):
  • supplies thalamus and brainstem, occipital lobes, posterior and medial temporal lobes
  • Perforating Arteries

Radiology of Stroke: Middle Cerebral Artery

• Cerebral Angiogram: determine which vessels are obstructed or ruptured
• Carotid Duplex Ultrasound: determine if carotid arteries are narrowed
• CT Scan: during stroke
• MRI: during or after stroke
• Echocardiogram: determine atrial fibrillation causing stroke
• Magnetic resonance angiography

—————————————————————————————–

Hypertensive hemorrhage

• HTN is leading cause of spontaneous intraparenchmal hematoma
• Most commonly occur in basal ganglia, thalamus, pons, and cerebellum
  • ** Most common site is putamen. Internal capsule that lies adjacent to putamen and is almost always involved à leading to hemiparesis
  • Pontine hemorrhage = present with deep coma, paraplegia that developed within a few min, pinpoint pupil, no horizontal eye movements
• **Presentation = initially with focal symptoms, rapidly progress to signs of elevated intracranial pressure
  • Unilateral weakness, slurred speech à focal lesion in cerebral cortex
  • Global symptoms = elevated intracranial pressure
  • ** look for associated marked hypertension, rapid progression of symptoms
•  ** noncontrast CT can help distinguish hemorrhagic from ischemic strokes

 Cerebellar hemorrhage

• ** Symptoms = Acute onset occipital headache, repeated vomiting, gait ataxia, vertigo
  • Small hemorrhage may not manifest with any other neurological deficit
  • Large hemorrhage à 6^th nerve paralysis, conjugate deviation, blepharospasm, become stuporous in a few hours
• Cerebral hemorrhage due to excess anticoagulation
  • ** Tx = fresh frozen plasma (FFP) for rapid reversal of anticoagulation
• Tx = immediate evacuation of the hematoma
  • If left untreated, stupor or coma may ensue due to brainstem compression
  • ** Do CT scan without  contrast in all patients with a stroke to distinguish between hemorrhagic or ischemic stroke
    • * If evidence of ischemic stroke à carotid Doppler and TEE to evaluate for possible source of embolism

Thalamic stroke (Dejerine-Roussy syndrome)

• Stroke involving ventral postero-lateral (VPL) nucleus of the thalamus à loss of sensory information from the contralateral side of the body
• Symptoms = contralateral hemianesthesia accompanied by transient hemiparesis, athetosis, or ballistic movements
• ** Look for hemi-sensory loss with severe dysesthesia typical thalamic stroke

Lacunar Stroke

• **Caused by microatheroma and liphyalinosis in small penetrating arteries of the brain
• ** Always suspect lacunar stroke if patient presents with limited neurologic deficit
  • Typical scenarios = pure motor, pure sensor stroke, ataxic hemiparesisi, dysarthria-clumsy hand syndrome
• ** principal cause of lacunar stroke = HTN
• ** Most common site for a lacunar infarct is the posterior internal capsule à pure motor stroke

TIA

• Focal neurologic symptoms lasting less than 24 hours due to cerebral ischemia
• Head CT should be obtained in patients with stroke symptoms to distinguish ischemic vs. hemorrhagic
  • Thrombotic cause suspected à antiplatelet agent (aspiring) to prevent future events
  • Warfarin used to prevent future ischemic events due to cardiogenic emboli

Heat stroke

• Failure of body thermoregulation upon exposure to high environmental temperatures
• **look for very high core body temp (>105), dehydration, confusion, coma, dry flushed skin
• Symptoms = acute confusion, hyperthermia (>105), tachycardia, persisten epistaxis after exertion under direct sunlight

References:

Stroke; Cerebrovascular disease; CVA; Cerebral infarction; Cerebral hemorrhage; Ischemic stroke; Stroke – ischemic; Cerebrovascular accident; Stroke – hemorrhagic; Last reviewed: June 24, 2011.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001740/

 

Hemorrhagic Stroke with MCA Transformation

http://radiopaedia.org/cases/hemorrhagic-transformation-of-mca-stroke-1

 

Stroke risk factors and prevention

Stroke prevention; Preventing strokes; Last reviewed: April 30, 2011.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004662/

Compiled by: Debi Hickman

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

• It’s an indirect measure.
• It’s a late sign of increased ICP.
• It’s more subjective.
• It’s not a dynamic measurement.
• It’s not always practical.

Our earlier article on ocular ultrasound for measuring intracranial pressure was met with a common question. Primarily, why not just use papilledema as your initial assessment for intracranial pressure? This is what we are taught in medical school. Optic nerve disc swelling equals increased intracranial pressure (ICP). End of Story. Right? Not exactly…  While optic disc swelling can indicate increased ICP, it is an inferior measure of acutely elevated ICP. And here is why…

It’s an indirect measure

So just what are you detecting when you see papilledema? It’s not increased CSF pressure causing the optic disc to bulge under pressure. It’s actually the result of optic nerve compression by elevated CSF pressures. The backup of axonal transport caused by compression leads to swelling along the optic nerve and into the optic disc. It is not a direct measure, but a measure of a result of increased intracranial pressure. It is a measure of injury to the optic nerve after increased CSF pressure in the optic nerve sheath has already choked the optic nerve. I don’t know about you, but optic nerve swelling sounds like bad news to me.

On the other hand, ocular ultrasound uses optic nerve sheath diameter to detect increased intracranial pressure. As mentioned in the earlier article (which you should read if you are reading this), the optic nerve sheath is distensible and communicates with the subarachnoid space. By measuring optic nerve sheath diameter you are detecting ICP pressure changes transmitted to the subarachnoid space (and CSF) via the resulting optic nerve sheath distention. This is a much more direct measure of ICP.

It’s a late sign of increased ICP

Ok, so let’s assume for arguments sake you’re alright with using an indirect measure of detection when a more direct measure exists. What now? Let’s examine the time factor. Papilledema takes time to develop. It requires ICP to increase, fluid pressure in the optic nerve sheath to constrict the optic nerve, and axonal transport to back up enough to cause swelling at the optic disc. This can take hours to weeks to manifest. In an emergent situation your acutely ill patient may not have sufficient time to develop papilledema, but still have significantly elevated ICP. If you didn’t understand the pathophysiology of papilledema, you might take this negative exam finding as evidence of normal ICP. Papilledema is a late sign of increased ICP. As we are taught over and over, time is tissue. By the time you see papilledema badness has been going on for a while and tissue is being lost. This is not good!

With ocular ultrasound, you are observing CSF pressure in real time. ICP changes are transmitted to the CSF, including CSF in the optic nerve sheath. Optic nerve sheath diameter (ONSD) reflects distension caused by CSF pressure changes. Since ONSD changes occur concurrently with ICP variations, ONSD reflects the ICP at the time of measurement. This means you see changes in ICP as they develop, and not hours after the fact, using ocular ultrasound.

It’s more subjective

This is another biggie! When I learned physical exam, it took a week of abusing my ever-so-patient boyfriend to see an optic disc clearly on the fundoscopic exam. It took even longer to get used to what a normal optic disc looks like. Seeing the difference between a normal and slightly swollen optic disc through the tiny window of an undilated pupil is vulnerable to subjectivity. A typical emergency room fundoscopic exam doesn’t have a standardized measurement component either. What you think is papilledema someone else may not, so there isn’t much objectivity to it. Even the experts have poor inter-rater agreement on papilledema. When a panel of trained neuro-ophthalmologists were asked to rate the severity of papilledema from images, they only agreed 45% of the time. And this was in images! If the experts of neuro-opthalmology don’t agree on papilledema severity even half of the time, imagine trying to objectively assess a mentally altered patient with undilated pupils as a non-neuro-ophthalmologist. Not fun and definitely not objective.

When I learned to measure ONSD to detect increased ICP, it took less than five minutes. It was fast, user friendly, and objective. Using the caliper function of the ultrasound machine, you can take precise measurements of ONSD. Those measurements have been extensively studied and compared to more invasive ICP monitoring methods. In symptomatic patients, an ONSD >5mm correlates to an ICP >20mmHg. In all patients, an ONSD > 5.7mm correlates to an ICP >20mmHg. No guessing necessary. And as discussed in the prior article, ONSD ultrasound is 100% sensitive and 96% specific for elevated ICP. Now that we know the numbers are objective and validated, what about ONSD measurement variability between users? Measurements can change slightly based the on angle of probe, angle of the patient’s gaze, etc. Despite that, ONSD measurements have good reproducibility between different users (it’s been studied) with a median inter-rater measurement difference of 0.25mm. In an optic nerve sheath at the upper limit of normal (5mm), 0.25 mm variation would only cause a 5% measurement variation. This means inter-rater ONSD measurements on typically overlap by 95%. This is starting to look like a no brainer (pun intended).

It’s not a dynamic measurement

Still not sure..? Papilledema doesn’t provide a dynamic means of monitoring ICP. Well developed cases of papilledema can persist for 6-10 weeks following resolution of elevated ICP. It’s not a great tool for monitoring ICP once papilledema occurs. If papilledema worsens, you can’t distinguish if it’s from worsening ICP or just the natural progression of the papilledema. It is a qualitative means of detecting elevated ICP. Basically it tells you the optic nerve was compressed (possibly by elevated ICP) at some point recently. Another reason not to rely on papilledema as your primary indicator of acute ICP elevation.

As mentioned above, changes in subarachnoid space pressure are reflected in distension of the optic nerve sheath by the CSF within it. This is a dynamic process, happening in real time. As ICP increases or decreases, so do ONSD measurements. This means ONSD reflects the current picture of ICP. For the patient that may develop increased ICP, you can track their ICP status over time with ocular ultrasound. Is ICP improving? Is it worsening? You can monitor this. ONSD measurements provide a quantitative assessment, so you can compare concrete values between ocular scans taken at different times. This makes them more ideal to detect differences in ICP over time.

It’s not always practical

Fundoscopic examination isn’t possible in some patients. A trauma patient with a mechanism consistent with increased ICP may also have ocular damage or periorbital swelling preventing visualization of the optic disc. In these cases papilledema can’t be used to detect increased ICP. Instead ocular ultrasound should be used. Using methods described in our earlier article, ICP can be assessed rapidly and non-invasively in the patient that isn’t even a candidate for fundoscopic exam.

Relevant Anatomy and Physiology

The optic nerve sheath contains the optic nerve and is a potential space that communicates with the subarachnoid space. As ICP pressure increases, the pressure is transmitted to the subarachnoid space and the CSF contained within it. CSF exerting greater pressure within the optic nerve sheath causes it to distend. However its capacity for distension is limited, causing elevated pressure to compress the optic nerve. To create visible papilledema, the pressure within the optic nerve sheath must be great enough to impede axoplasmic transport in the optic nerve. The resulting swelling moves along the nerve and into the optic disc where it is seen on fundoscopic exam. Now I’m just a medical student, but I’m guessing that compressing the optic nerve to the point of swelling is bad. Bad for the nerve. And bad for the patient.

The fundoscopic exam for papilledema detects optic nerve injury (disc swelling) caused by increased fluid pressure within the optic nerve sheath. Occular ultrasound measures the ONSD, which correlates to subarachnoid space/CSF pressure within the nerve sheath generated by ICP changes. ONSD measurement via ocular ultrasound detects increased ICP without requiring optic nerve compression and injury to occur. Now that’s a substantial improvement.

So What’s the Point of All This?

The fundoscopic exam is a great exam and has its place. However papilledema as a method of detecting acutely increased ICP is inferior to ocular ultrasound. Ocular ultrasound provides real time, quantitative measurements. Quantitative measurements make the exam objective and allow you to compare ICP changes over time. It also detects increased ICP earlier than the presence of papilledema, since papilledema takes time to develop. If you do see papilledema during a fundoscopic exam in a patient with suspected increased ICP, remember what a late and serious sign this is. However DO NOT rely on the absence of papilledema to rule out increased ICP. If you think your patient has increased ICP, do a bedside ultrasound. It’s fast, sensitive, objective, provides quantitative information, measures ICP in real time, and is easy to do. Need I say more?

References

-          Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med. 2003; 10: 376–381.

-          Blaivas M., Lyon M. (2008). Chapter 17. Ocular Ultrasound. In M. Blaivas, O.J. Ma, J.R. Mateer (Eds), Emergency Ultrasound, 2e. Retrieved October 14, 2012 from http://www.accessemergencymedicine.com/content.aspx?aID=102878.

-          Fox, Chris; Dawson, Matt. auth. “Ocular Ultrasound with Chris Fox.” Ultrasound Podcast. N.p., 30 2012. web. 14 Oct 2012. <http://www.ultrasoundpodcast.com/2012/04/episode-26-ocular-ultrasound-with-chris-fox/&gt;.

-          Gossman MV, February 15, 2012. Papilledema, Medscape. http://emedicine.medscape.com/article/1217204-overview (November 20, 2012)

-          Moretti R, Pizzi B, Cassini F, Vivaldi N. Reliability of optic nerve ultrasound for the evaluation of patients with spontaneous intracranial hemorrhage. Neurocrit Care. 2009; 11:406–410.

-          Sinclair AJ, Burdon MA, Nightingale PG, et al., “Rating papilloedema: an evaluation of the Frisén classification in idiopathic intracranialhypertension,” Journal of Neurology. 2012; 259: 1406-1412.

-          Soldatos T, Chatzimichail K, Papathanasiou M. Optic nerve sonography in the diagnostic evaluation of adult brain. Crit Care. 2008;12:R67. doi: 10.1186/cc6897.

Compiled by: Jennifer Cotton

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

Pathophys of DIC. Source: Lippincotts

DIC is a pathological process where tissue factor or other thromboplastic substances from endothelial cell injury are released into circulation-Leads to paradoxical formation of 1) microthrombi leading to organ failure and 2) hemorrhaging.

 Associated Clinical Causes

-Sepsis
-Trauma (especially neurotrauma)
-Cancer
-Shock
-Major Surgery
-Immunologic (transfusion/transplant reaction)
-Obstetric complications

Diagnosis

Can be complicated by the underlying causes, lab tests indicating DIC:

- Platelets <100,000 or recent rapid large decrease in number
- Prolonged PT and aPTT
- Elevated D-Dimer (>.5ug/ml)
- Schistocytes in blood smear
- Fibrinogen -if obtainable <1g/L (only in ~28% of pts)

A scoring system has been developed (click continued reading)

DDx: DIC, Hemolytic Uremic Syndrome, Liver Disease, Thrombotic Thrombocytopenic Purpura, Heparin-induced thrombocytopenia, HELLP syndrome in pregnancy

Treatment

Treat the underlying cause, platelet and blood factor replacement to treat bleeding can be used but won’t correct DIC. Heparin used when fibrin deposition is excessive and no risk of hemorrhage present (no petechiae or bruising).

Disseminated Intravascular Coagulation is a condition more commonly seen in intensive care situations, but can easily arise from emergencies in ED’s as well. It’s not something easily diagnosed, and is more common than the statistics show. Researchers now believe it to occur in 30% of severe sepsis cases, as many as 50 % of massive trauma patients, 10% of patients with metastatic tumors, and 50% of OB patients with abruptio placentae or an amniotic-fluid embolism (Levi).

Initially, DIC manifests as a microangiopathic hemolytic anemia, as a result of activation of the coagulation cascade from exposed subendothelium. The microthrombi formed become trapped in the vasculature, leading to ischemia of various organs and eventually their failure. Schistocytes are seen in blood smears due to RBC damage from the thrombi.

Paradoxically, hemorrhaging can occur. This is due to the massive amount of clotting, hence consumption of clotting factors, as well as activation of the fibrinolytic pathway (where the D-dimer elevation comes from). This condition manifests as petechia, ecchmoses, and classical oozing from IV sites and wounds.

Click for larger view. Source: emedicine

Reference:

Emergency Medicine Updates. Nov, 23. 2009. Web. http://emupdates.com

Levi, MD. Marcel. “Disseminated Intravascular Coagulation.” Medscape Reference. Web. 12 Nov 2012. http://emedicine.medscape.com/article/199627-overview

Levi, MD, Marcel. and Hugo Cate, MD. “Disseminated Intravascular Coagulation”. New England Journal of Medicine. 341.8 (2006): 587-592.12 Nov. 2012. https://residents.lsuhsc.edu/no/neurology/docs/DIC%20NEJM [1].pdf

Nickson, Chris. “Disseminated Intravascular Coagulation.” lifeinthefastlane.com 12 Nov 2012.

http://emedicine.medscape.com/article/779097-diagnosis

Compiled by: Nick Mancuso, M1

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

• Pain:  Paroxysmal stabbing pain affecting one or more divisions of the trigeminal nerve
  

• rarely bilateral, and never on both sides at the same time
• may last for days or weeks and patient may remain pain free for many months after pain subsides
• Signs and symptoms:  usually no accompanying neurological problems, sometimes blunting of pinprick over affected region
• Triggers: speaking, brushing teeth, washing face, eating, cold wind, touching a “trigger spot”
• Mostly affects females and patients 50+ yrs of age

Investigation

• CT or MR scan to exclude CPA lesion or demyelination

Acute Attack Treatment = Phenytoin 250 mg IV for relief for hours- 3 days

First line Agent =  Carbamazepine 100mg 1-2 times per day, with increase of 100-200mg every 3 days up to a maintenance dose of 400-800mg

This post will go into a bit more detail about causes and treatment options for managing patients with trigeminal neuralgia coming into the ED.

Causes

• Root or root entry zone compression
  • Arteries impinging on trigeminal nerve root as it enters Pons
    

• Tumors between the Pons and Cerebellum (the cerebellopontine angle or CPA) can compress CN V nerve roots

Management

• Anticonvulsants: Carbamazepine, gabapentin
• Tricyclic antidepressants: Amitriptyline
• GABA-enhancing drug: Baclofen
• Procedures
  • Nerve block
    • alcohol or phenol (temporary relief)
  • Avulsion of supraorbital or infraorbital nerves
    • more long-term relief, but permanent damage
  • Trigeminal root section
  • Microvascular decompression
    • separation of blood vessels in contact with trigeminal nerve root or root entry zone at cerebellopontine angle by inserting non absorbable sponge
    • no nerve damage necessary
  • Radiofrequency thermocoagulation
    • electrical stimulation of inserted needle at trigeminal ganglion identifies location of trigger spot when it matches site of tingling
    • radiofrequency thermocoagulation with general anesthetic creates permanent lesion
  • Balloon Gangliolysis
    
    

A 2011 Cochrane Intervention Review evaluated the “analgesic efficacy and adverse effects of carbamazepine for acute and chronic pain management (except headaches),” finding that carbamazepine is, in most cases, effective for short term pain relief:

“Carbamazepine is effective for relieving chronic pain caused by damage to nerves, either from injury or disease, although the data available to support this is limited. Anticonvulsants (also known as antiepileptics) are a group of medicines commonly used for treating ‘fits’ or epilepsy, but which are also effective for treating pain. The type of pain which responds well is neuropathic pain, e.g., postherpetic neuralgia (persistent pain experienced in an area previously affected by shingles), trigeminal neuralgia, and painful complications of diabetes. About two-thirds of patients who take carbamazepine for neuropathic pain can expect to achieve good pain relief in the short term, and two thirds can expect to experience at least one adverse event.”

Source:

Wiffen PJ, Derry S, Moore RA, McQuay HJ. Carbamazepine for acute and chronic pain in adults. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD005451. DOI: 10.1002/14651858.CD005451.pub2.

Another 2011 Cochrane Intervention Review assessed the various neurosurgical techniques commonly used in treating trigeminal neuralgia.  Their findings emphasize the need for more research in order to help guide patients with trigeminal neuralgia in choosing the best neurosurgical option:

“There is either no, or very low quality, evidence for most neurosurgical procedures for the treatment of trigeminal neuralgia because of the poor quality of the trials. All procedures result in some pain relief (with or without medications) and there is good evidence to show that ablative procedures result in sensory loss. There is no evidence to assess the effect of surgery on quality of life and no evidence of the economic costs. There are no RCTs on microvascular decompression which from observational data gives the longest pain relief periods. Thus there is little evidence to provide the patient with guidance as to the most effective surgical procedure for the management of trigeminal neuralgia and this is in line with the study by Spatz 2007 on decision making. Thus any future high quality trials in this area are likely to lead to a highly significant impact on practice.”

Source:

Zakrzewska JM, Akram H. Neurosurgical interventions for the treatment of classical trigeminal neuralgia. Cochrane Database of Systematic Reviews 2011, Issue 9. Art. No.: CD007312. DOI: 10.1002/14651858.CD007312.pub2.

Compiled by: Karl Echiverri, M1

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

• Alteration of conscious (97%)
• CSF Pleocytosis (97%)
• Fever (90%),
• Personality Change (85%)
• Headache (81%)
• Seizures(67%)
• Vomiting (46%)

In newborns it typically presents 6-12 days after birth with general lethargy, poor feeding, and/or seizures and is HSV-2.

Diagnosis

CSF should be taken immediately when HSE is suspected and sent for a PCR study. This is the gold standard and is sensitive 94-98% and specific 98-100%.

Lab studies are non-specific. Imaging (CT and MRI) and Electroencephalography abnormalities can take days to a week to appear on scans.

• CSF in patient with HSE will have elevated WBC, RBC, elevated protein, and normal glucose level with lymphocytic pleocytosis
• MRI findings if present would demonstrate temporal lobe lesions
• Electroencephalography (EEG) has characteristic periodic high-voltage spike wave activity emanating from the temporal lobes and slow wave complexes are highly suggestive of HSE.

Treatment

IV acyclovir should be started immediately , before PCR results confirm, because its toxicity is rather low and HSE prognosis is poor untreated. In adults 10-15mg/kg q8h x14-21days, 3 months-12years 20mg/kg x10 days, neonates 30mg/kg/day.

In keeping with the theme of turning what basic science we are learning in class into clinical scenarios, Sakib suggested I write up a piece on HSE relating to our Infectious Disease class. Struggling to stay focused through learning tons of boring viral info, bacteria, fungi, etc. I wondered what we’ll ever need to know again, especially in emergency medicine. There are actually quite a lot of emergencies that can arise, and HSE is one.

HSE is the most common cause of sporadic fatal encephalitis in the US (Meyer). HSV is a dsDNA virus in the Herpesviridae family, of which there are 8 types that affect humans. HSV-1 and HSV-2 are spread when an infected person is shedding virus during the primary infection or a secondary infection. The viron fuses with a cell’s plasma membrane where it uncoats and a Viral Host Shutoff protein is expressed. Herpesvirus then replicates using sequential control of protein synthesis expressing mRNA for first alpha, then beta, then gamma proteins. Herpes is well known for its characteristic of viral latency, where it remains dormant in cell bodies of neurons, safe from immune cell destruction.

Primary illness with HSV1&2 is typically the most severe illness, latent ones not as severe. 90% are symptomless, 9% minor illness, 1% have severe illness with gingivostomatitis, the most common symptom. Infections “above the belt” are usually (but not always) HSV-1 and “below” HSV-2.

PCR is used diagnostically to differentiate 1&2 and is the gold standard, because the viruses differ in 50% of their DNA. Immunocytochemistry and Western Blot can be used but are less accurate.

HSE

In regards to diagnosis, the presentation is described above. It has a somewhat non-specific presentation, but needs to be treated immediately. Untreated, death can occur in 7 days, which can vary with severity. The pathogenicity is not known, neither is the mechanism of cell damage leading to encephalopathy.

A short list of differential should include:

• Meningitis
• Infective encephalitis causes
• Abscesses
• Intracranial tumors

CSF analysis is used to diagnose. CT and MRI don’t show abnormalities for several days. On CT changes in temporal or frontal lobe are seen as low density lesions after 3-4 days. In T2 MRI, early involvement of white matter is seen. The inferomedial portion of the temporal lobe is most commonly affected on MRI (Anderson).

62-year-old woman with confusion and herpes encephalitis shows T2 hyperintensity involving right temporal lobe:

source = eMedicine

Acyclovir is used to treat. When HSE is suspected it should be started immediately, however in one study at an academic emergency medicine institution showed only 29% of patients were given acyclovir with presentation of HSE1 (Benson).

What better way to end this post than to get a quick review on serious CNS infections from Scott Weingart at EMCrit podcast

• Podcast on serious CNS infections = http://emcrit.org/podcasts/meningitis/
• http://crashingpatient.com/medical-surgical/cns-infections.htm/

References

Anderson, DO, Wayne. “Herpes Simplex Encephalitis Treatment & Management.” Medscape Reference. 07 2011

Benson PC, Swadron SP. Empiric acyclovir is infrequently initiated in the emergency department to patients ultimately diagnosed with encephalitis. Ann Emerg Med. Jan 2006;47(1):100-5. [Medline].

Meyer Jr., M.H. et al., 1960. CNS Syndroms of “Viral” Etiology. Am. J. Med. 29, 334-247.

Compiled by: Nick Mancuso, M1

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!