Tuesday, July 31, 2012

Sickle Cell Disease

Today we heard about a patient with a sickle cell crisis.

Much has been written on the topic on this blog.

Check out a blogpost on Sickle cell anemia here

Acute chest syndrome is a dreaded complication, read all about it here

Monday, July 30, 2012

Pyogenic Liver Abscess

Today we discussed a case of pyogenic liver abscess. This is a very hot topic right now! Incidence increases with age, which may explain why we are seeing so many of these on general internal medicine wards. They most commonly involve the right lobe of the liver, as it is larger and receives more blood supply.

Causes of pyogenic liver abscess can be categorized as follows:

1. Biliary tract disease: ascending cholangitis caused by obstruction (stone, pancreatic or cholangioCA, stricture)

2. Portal vein seeding as a result of intraabdominal disease: this can be secondary to appendicitis, diverticulitis, bowel perforation, malignancy. May be accompanied by pyelephlebitis (suppurative thrombophlebitis of the portal vein).

3. Hepatic artery seeding: from systemic bacteremia with or without bacterial endocarditis

4. Contiguous focus of infection: gallbladder disease, subphrenic or perinephric abscess.

5. Traumatic: liver laceration, post-resection, post radiofrequency ablation, migrated foreign body (eg: fishbones through gastric antrum).

5. "Primary"=cryptogenic: Hypermucoviscous variants of Klebsiella pneumoniae are increasingly being recognized as a cause. This is seen most commonly in patients of Southeast Asian descent and has been associated with diabetes mellitus.

Microbiology of liver abscesses: Many are polymicrobial (especially if secondary to biliary tract disease or intraabdominal infections). Common pathogens are: E.Coli, Klebsiella pneumoniae, Strep (including Strep anginosus group- famous for abscesses), anaerobes.

Treatment is focused on source control=drainage of abscess. Broad-spectrum antibiotics (eg:ceftriaxone,flagyl) are used until a specific pathogen is isolated from drainage or blood cultures (positive 50% of the time). Antibiotics are initially intravenous, then stepped down to oral for a total 4-6 week course.

Check out this recent case from TGH with a review on the topic by our very own Wayne Gold and Derek MacFadden: Here

Friday, July 27, 2012

DKA Management

Above is a useful algorithm for the management of DKA, taken from CMAJ's 2003 paper (a classic and must-read for medicine residents):

Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state 

Added management pearls:

- Many people find it convenient to manage DKA by a flowchart updated ~hourly (although not everything needs to be checked hourly). You may want to record:
Time, Vitals, urine output, pH, HCO3, AG, Ket, Glu, K, PO4, IV fluid rate, insulin dose

-Ketones may increase even though the anion gap is decreasing. This is because beta-hydroxybutyrate (major ketoacid of DKA) is not detected by the ketone test. It is then metabolised to acetoacetate, which is detected.

-When calculating the anion gap, use the uncorrected sodium concentration. Note that even though we see hyponatremia in hyperglycemic states (and there is a "correcting calculation"), the anion gap reflects the balance between positively and negatively charged electrolytes in the extracellular fluid. Glucose is electrically neutral and does not directly alter the anion gap. However, glucose is osmotically active so water is pulled into the extracellular fluid. This has a dilutional effect on all extracellular electrolyte concentrations, both positive or negative, and so the anion gap is minimally altered.

- Use of bicarbonate is reserved for severe acidosis (pH<7.0) after 1 hour of rehydration

- Expect to see non-anion gap metabolic acidosis (ie. hyperchloremic) after AGMA resolves, because of loss of ketone bodies without H+ (i.e. loss of anion with Na+/K+ as cation). This is equivalent to the loss of a "potential bicarbonate". This lost bicarbonate is replaced by chloride ion (which is abundant in the saline we are giving).

Thursday, July 26, 2012

CN IV Palsy

Check out this Right CN IV Palsy- note that because CN IV innervates the superior oblique, the affected eye cannot look down and in - the patient will report improvement of diplopia with a corrective head position: tilting the head toward the opposite shoulder 

Tuesday, July 24, 2012

PFO/Stroke in the Young

This morning we discussed a case of stroke in the young. See a previous blog post on stroke in the young here.

Two specific points with respect to this came up:

1) In patients with cryptogenic stroke, does PFO closure prevent recurrent strokes?

Answer: in a recent (NEJM 2012) unblinded multicenter study of 909 patients (ages 18-60yrs) randomised to closure or medical management (antiplatelet or anticoagulation at physician's discretion), there was no significant difference in the primary endpoint (composite of stroke or TIA in 2 years, death of any cause in 30 days, and death from neurological cause at 31 days to 2 years). See the study here.

2) One question that this brings up for me: does anticoagulation prevent recurrent strokes in patients with PFOs?

Answer: data and expert opinion are conflicted as to the optimal medical management of a patent foramen ovale in a patient with an otherwise cryptogenic stroke. In this study subgroup, patients were randomised to ASA 325mg or warfarin following stroke (250 cryptogenic out of a total 601 strokes). Of note, PFO was found in 39.2% (98/250) of patients with cryptogenic stroke, compared with 29.9% (105/351) in patients with known cause of stroke. Note that this is not a huge difference in prevalence between the two groups.

With respect to treatment, there was no significant difference in the time to recurrent ischemic stroke or death between those treated with warfarin and those treated with aspirin (P=0.49; hazard ratio 1.29; 95% CI 0.63 to 2.64; 2-year event rates 16.5% versus 13.2%).

There is some data suggesting that the presence of an atrial septal aneurysm along with a PFO confers greater risk.

The AHA Guidelines from 2011 are as follows:

- For patients with an ischemic stroke or TIA and a PFO, antiplatelet therapy is reasonable (Class IIa; Level of Evidence B). 

- There are insufficient data to establish whether anticoagulation is equivalent or superior to aspirin for secondary stroke prevention in patients with PFO (Class IIb; Level of Evidence B). (New recommendation)
- There are insufficient data to make a recommendation regarding PFO closure in patients with stroke and PFO (Class IIb; Level of Evidence C)

3) Finally: What the heck is CADASIL?

Answer from Harrison's:  
-  cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)
- inherited disorder that presents as small-vessel strokes, progressive dementia, and extensive symmetric white matter changes visualized by MRI.  
- 40% of these patients have a history of migraine with aura. 

See you tomorrow!

Monday, July 23, 2012

A tale of 2 cases - July 23, 2012

Thank you to team 8 for bringing 2 cases, and to Dr. Wayne Gold for hosting today’s morning report.  We discussed 2 interesting cases.

The first case involved a patient with a stroke.  We discussed that in patients already receiving ASA, neither Plavix (clopidogrel) nor Aggrenox (ASA + extended release dipyridamole) is superior to the other agent for preventing recurrent stroke, as demonstrated in the PRoFESS trial (Prevention Regimen for Effectively Avoiding Secondary Strokes) published in 2008 (Sacco RL, et al; PRoFESS Study Group. Aspirin and extended-release dipyridamole versus clopidogrel forrecurrent stroke.  N Engl J Med. 2008 Sep18;359(12):1238-51.).  They randomized 20322 patients and followed them for a mean of 2.5 years for the primary outcome of first recurrence of ischemic stroke.  No difference was found in the primary outcome (9% in the ASA + extended release dipyridamole group and 8.8% in the clopidogrel group; hazard ratio 1.01; 95% CI 0.92 to 1.11).  However, some patients may benefit from anticoagulation if there is known cardioembolic stroke risk such as atrial fibrillation, or apical thrombus.  In reality, the benefit of antiplatelet or anticoagulant therapy must be balanced against the individual bleeding risk of the patient.

We then discussed the differential diagnosis of episodic decreased level of consciousness post stroke.  The most prominent being post-stroke seizure (+/- accompanying post-ictal phenomenon).  Hemorrhagic conversions are less likely to present as transient decreased level of consciousness.  It is important to obtain imaging to rule out structural causes, EEG to assess for seizure, and to complete a metabolic work-up to rule out non-CNS causes.  Syncope is also in the differential diagnosis of episodic loss of consciousness and cardiac investigations (including the ruling out of dysrhythmias) may be warranted.

In the discussion of our second case, we discussed the principles of management of febrile neutropenia.  We discussed the importance of starting empiric broad-spectrum antibiotics first without waiting for results of cultures.  Minimum of blood and urine cultures, and chest x-ray should be obtained.  Other investigations should be directed based on patient’s presenting symptoms and physical exam findings.  Empiric therapy should cover gram positive organisms (including Staph aureus) +/- CNST (coagulase negative staph), AND gram negative organisms (including Pseudomonas).  Many institutions have empiric therapy guidelines based on local resistance pattern.  The Infectious Diseases Society of America (IDSA) Guideline on antibiotics used in febrile neutropenic patients can be found here.  (Freifeld AG. Clinical practice guideline for the use of antimicrobial agents inneutropenic patients with cancer: 2010 Update by the Infectious DiseasesSociety of America.  Clin Infect Dis. 2011 Feb 15;52(4):427-31.)

We then discussed a rash in the setting of febrile neutropenia.  In general, the rash can represent a primary skin/soft tissue infection, or a secondary manifestation of a systemic infection.  The latter can be from hematogenous seeding (as in the case of Janeway lesions in infective endocarditis), immune mediated (e.g. disseminated gonococcal infection), activation of coagulation cascade (purpura fulminans), or toxin-mediated (as in staphylococcal toxic shock syndrome).  In our patient, we suspect the skin lesion is ecthyma gangrenosum.  In febrile neutropenic patients, this may represent a gram negative infection (commonly Pseudomonas).  Other infections (e.g. fungi [Candida, Aspergillus]) are also possible.  See this article by Yas Moayedi which summarizes mechanism of skin manifestation of systemic infection, other organisms that can cause ecthyma gangrenosum, and principles of management.  (Moayedi Y,Bunce PE, Sade S, Ghazarian D, Gold WL.  Fromthe outside looking in.  Am J Med. 2012May;125(5):457-60.).

Note that in most patients with skin infection, we do not routinely obtain aspirate and biopsy of the skin.  However, in a patient with febrile neutropenia, this is worthwhile as it has a higher yield of recovering the organism(s) responsible.  We chose to treat this patient with two anti-pseudomonal agents to ensure that there is at least one agent that is active against the organism should it later turn out that this patient had a resistant organism.  Once sensitivity known, antibiotics can then be tailored.

Your chief resident (Lauren) will return tomorrow.  Thank you for a week of interesting cases.  Terence

Friday, July 20, 2012

Vasculitis - July 20, 2012

Thank you to team 6 for bringing an interesting case and to Dr. Ho Ping Kong (“As brilliant as House, but nicer.”) for hosting.

Among other things (malignant hyperthermia can be diagnosed with muscle biopsy, nasopharyngeal cancer is EBV associated, etc …), we discussed a case of a woman with likely non-acute kidney disease, rash, and p-ANCA positivity.  This is suspicious for a vasculitic process.  We talked about that imaging (in addition to blood rheumatological markers) is an important part of a vasculitic work-up.  Of course, biopsy can be very helpful as well.

A commonly used classification scheme of systemic vasculitis is the “Chapel Hill” classification, named after the Internal Consensus Conference in 1994 where it was convened for this matter.  It is published in:  Jennette JC, Falk RJ,Andrassy K, Bacon PA, Churg J, Gross WL, Hagen EC, Hoffman GS, Hunder GG,Kallenberg CG, et al. Nomenclature of systemic vasculitides. Proposal of aninternational consensus conference. Arthritis Rheum. 1994 Feb;37(2):187-92.

We will briefly summarize the classification here, but you can get the full details from the actual article:
- Large vessel:  Giant cell (temporal) arteritis, takayasu arteritis
- Medium vessel:  Kawasaki disease, Polyarteritis nodosa
- Small vessel:  Churg-Straus syndrome, Wegener’s granulomatosis, microscopic polyangiitis, cutaneous leukocytoclastic angiitis, essential cryoglobulinemic vasculitis, Henoch-Schonlein purpura.

Churg-Straus, Wegener’s, and microscopic polyangiitis have strong associations with ANCA.

Have a fabulous Friday!

Thursday, July 19, 2012

Heart failure and sarcoidosis - July 19, 2012

Thank you to team 7 for bringing a fascinating case, and to Dr. Rakowski for hosting.

Today, we discussed a case of a patient with sarcoidosis who presented with heart failure.  Regardless of whether we think that is the true cause of our patient’s symptoms, cardiac manifestations of sarcoidosis is interesting.

I have included 2 references here:
- a review article from New England Journal of Medicine about sarcoidosis in general (IannuzziMC, Rybicki BA, Teirstein AS. Sarcoidosis.  N Engl J Med. 2007Nov 22;357(21):2153-65.).
- a review article about cardiac sarcoidosis specifically (Kim JS et al.  Cardiac sarcoidosis.  Am Heart J. 2009 Jan;157(1):9-21. Epub 2008Nov 12.).

Information from this blog taken from the above 2 references, and of course, what we talked about in morning report today.

Sarcoidosis is a granulomatous disease that can affect many organs.  Most of us have heard of pulmonary manifestation and lymph nodes involvement.  The classic Lofgren’s syndrome consists of arthritis, erythema nodosum, bilateral hilar adenopathy.  This occasionally shows up in Medical Jeopardy and morning reports.

Cardiac infiltration most commonly occurs in LV free wall, intraventricular septum, and conduction system.  Because of this, it may manifest as:
- conduction abnormality and dysrhythmias (palpitations, syncope, sudden death)
- cardiomyopathy (heart failure symptoms such as dyspnea, orthopnea, peripheral edema)

But another reason for patients with sarcoidosis to have heart failure is right heart failure secondary to their pulmonary disease, as well as valvular regurgitation (especially MR from papillary muscle dysfunction).  Pericardial diseases are rare but have been reported.

As we discussed and saw in our patient today, echocardiography and cardiac MRI are important imaging modalities in these patients.

Also discussed in morning report today, aggressive investigation of dysrhythmias and pace-maker/ICD implantation is usually recommended if electrical system involved.  Treatment of sarcoidosis with corticosteroids for heart failure is usually warranted.

We did not really touch on this today, but for general management of heart failure, we refer you to the Canadian Cardiovascular Society Heart Failure Guideline program here.

Thank you for a great morning report and have a thrilling Thursday!

Wednesday, July 18, 2012

Colorectal cancer and spinal cord compression - Wednesday, July 18, 2012

Thank you to team 8 for bringing the case and to Dr. Raymond Jang for hosting today’s special Oncology morning report.

We discussed colorectal cancer and one of the oncological emergencies, namely spinal cord compression.

You can read more about colorectal cancer here.

For spinal cord compression, we discussed that functional status at presentation predicts outcome.  Urgent MR whole spine (not necessarily with contrast) is the preferred imaging modality (as clarifying the number of lesions may have therapeutic implications).  We discussed that in the acute setting, dexamethasone (10 mg IV x 1, followed by 16 mg/day [can be in divided doses]) and pain control are the usual medical treatment for the internist.  However, these patients require URGENT radiation oncology assessment and/or neurosurgical intervention.

We discussed about a randomized control trial that suggested selected patients with a single site of lesion may benefit (better neurological outcome) from neurosurgical intervention and radiation when compared to radiation alone.  The trial (Patchell RA et al.  Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised trial.  Lancet. 2005 Aug 20-26;366(9486):643-8.) can be accessed here.  The primary outcome was the ability to walk and statistically significantly more patients in the surgery followed by radiation group (84%) achieved this outcome than the radiation only group (57%, p=0.001).

However, this is not the only consideration and expert opinion from radiation oncology and neurosurgical colleagues will be helpful.

Tuesday, July 17, 2012

Shortness of breath - July 17, 2012

Thank you to team 5 for bringing the case and to Dr. Andrea Page for hosting.

Today, we discussed a case of an elderly man from a long-term care facility who presented with shortness of breath.  The differential diagnosis was quite wide, and we had the opportunity to discuss a few of them.

From an infectious perspective, this man is at risk of Health Care Associated Pneumonia (HCAP).  The significance being that he may be at risk for infections by organisms that may not be usually thought of the Community Acquired Pneumonia setting.  The Infectious Diseases Society of America (IDSA) Guideline (2005) about this topic can be found here and it lists the following as risk factors for HCAP:
- Hospitalization for 2 days or more in previous 90 days
- Residence in a nursing home or extended care facility
- Home infusion therapy (including antibitoics)
- Chronic dialysis within 30 days
- Home wound care
- Family member with multi-drug resistant pathogen

Dr. Page reminded us that much of the literature is based in the U.S. environment and that local ecology of organisms (rate of drug resistant organisms) may be quite different.  It is important to consider the local experience here.  If you are interested in this concept, here are 2 recent review papers:  Am J Med (2011) and Curr Opin Infect Dis (2012).

Also, it is important NOT to forget viral causes of pneumonia.  A recent Lancet paper on this topic can be found here.  You can find flu activities in Ontario and Toronto in the Flu Bulletin here (For 2 weeks ending July 7, 2012, Toronto showed sporadic activity).  For the 2 weeks ending on July 7, 2012, parainfluenza virus and entero/rhinovirus had the most number of positive specimens.

We also discussed briefly that patients born in the pre-war period (in Canada and Europe) are at risk of TB.

Other non-infectious causes including cardiac (heart failure, ischemia, pericarditis), volume overload from renal disease, pulmonary embolism, primary respiratory illness (COPD, interstitial lung disease) are also important considerations.

Monday, July 16, 2012


As a bonus, we discussed meningitis today and the benefits of steroids.

Here is a very digestible nugget on meningitis, from Yas Moayedi and Dr Gold himself:
Acute Bacterial Meningitis in Adults

Reminder of the Infectious Disease Society of the Americas (IDSA) guidelines on steroid use in bacterial meningitis in adults:

- Give dexamethasone (0.15 mg/kg q6h for 2–4 days with the first dose administered 10–20 min before, or at least concomitant with, the first dose of antimicrobial therapy) in adults with suspected or proven pneumococcal meningitis.
- Continue dexamethasone for 4 days only if CSF Gram stain reveals gram-positive diplococci, or if blood or CSF cultures are positive for S. pneumoniae.
- Adjunctive dexamethasone should not be given to adult patients who have already received antimicrobial therapy, because administration of dexamethasone in this circumstance is unlikely to improve patient outcome.

Have a groovy day!

HIV Potpourri

Today we had an exhilarating morning report with so much high-yield content it's hard to know where to begin.

1) One highlight was a review of opportunistic infections and their corresponding CD4 levels.
Here is a diagram which summarizes it:

The usual prophylactic regimens:
- Septra for PJP if past PJP, CD4<200 or history of esophageal candidiasis. Dapsone or atovaquone are the best alternatives.
- Septra also covers Toxoplasma
- Azithromycin for MAC at CD4<50

Here is a link to the CDC Guidelines for Prevention and Treatment of HIV positive adults. 

2) Also touched on was treatment of PJP infection in a patient with HIV
- Septra DS- 2 tabs Q8 hours
  Can also use IV Septra, trimpethoprim/dapsone or clinda/primaquine

- Addition of steroids: several trials showing a clear mortality benefit in moderate or severe pulmonary dysfunction
- These guidelines (from 1990!) are still current:
- start steroids with anti-PJP antimicrobial if PaO2 on room air <70mmHg OR Aa gradient (always on room air) >35mmHg
- start as early as possible, within 24-72 hours of antibiotic therapy
- 21-day tapering oral regimen of prednisone
- 21 days of antimicrobial therapy

Thursday, July 12, 2012

Is heparin better than LMWH in the initial treatment of cerebral venous sinus thrombosis?

Shout out to Team 7 for this great clinical question!

A recent unblinded randomised controlled trial of 83 patients in India showed (note both groups were bridged to acenacoumarol, a vitamin K antagonist)
- significant reduction in in-hospital mortality with LMWH compared to IV heparin
- non-significant improvement in functional status at 3 months with LMWH compared to IV heparin

Here is the link

Keep in mind that this is a very small study.

However these findings were consistent with what had been previously suggested in a prospective cohort study.

The bottom line? There is no data to suggest that IV heparin is better than LMWH in cerebral venous sinus thrombosis. In fact, there is some data suggestive of just the opposite.


Today in morning report we talked about fever.

Elevated body temperature can be caused by many things:

1. Infection- bacterial, viral, parasitic

2. Inflammatory (ie cytokine-related, "bad humours")
- autoimmune conditions
- cancer, especially lymphoma
- pulmonary embolism, thrombophlebitis
- post-endovascular procedure
- transfusion-related (IVIG very commonly)
- serum sickness
- Stevens-Johnson/Toxic Epidermal Necrolysis
- sarcoidosis
- familial mediterranean fever

3. Heat Stroke

4. Drugs:
- amphetamines and other sympathomimetics
- anticholinergic
- sometimes the antibiotic you are giving can cause fever (eg: tazocin) don't forget about this!

5. Specific hyperthermic drug syndromes:
- Neuroleptic malignant syndrome
- Serotonin syndrome
- Malignant hyperthermia

6. Endocrine
- thyrotoxicosis
- pheochromocytoma

7. CNS hemorrhage

Note that even rhabodymyolysis itself can cause fever- possibly the cause in our patient today. Remember to think about most likely causes, but keep the broad differential in mind!

Have a great day!

Wednesday, July 11, 2012

Code Status Discussions

Today we talked about how to frame code status discussions in the context of patient's goals and priorities.

One question which often comes up is how to ask about code status and whether CPR, intubation and life support need always be offered.

The College of Physicians and Surgeons of Ontario has a policy statement on the matter which you can read here. Some excerpts:

"When it is clear from available evidence that treatment will almost certainly not be of benefit or may be harmful to the patient, physicians should refrain from beginning or maintaining such treatment. Any recommendation not to initiate life support, or to withdraw life support, should be discussed with the patient or substitute decision-maker, and family if there is consent."

"If the patient or substitute decision-maker, or family if there is consent, insists on a course of treatment that the physician feels will not be of benefit to the patient, the physician may offer to transfer care of the patient to another facility or care provider who is willing to provide that treatment. This option should be considered only after alternative methods of conflict resolution have been exhausted."

Conflict between healthcare providers and patients and/or their families on this topic can lead to stress on high levels of stress on both sides. If tensions really escalate, sometimes the media gets involved. This recent W5 Segment is an example of this.

Tuesday, July 10, 2012


Today we discussed the case of a man with pericarditis. 

See here for a discussion of the causes of pericarditis.

Pain in pericarditis is usually retrosternal, acute onset, and pleuritic. Often worse supine, improves leaning forward

Physical exam may show pleural rub (mono, bi, or tri-phasic)- each phase corresponds to movement of pericardium. Triphasic rub corresponds to three stages: atrial systole, ventricular systole and ventricular diastole.  Also look for Kussmaul's sign (suggests constrictive pericarditis) and signs of tamponade: JVP findings, pulsus paradoxus.

ECG in pericarditis vs. MI: In MI, uncommon to have diffuse STE however could happen if large antero-inferior infarct. The key differences are: in pericarditis have concave up ST segments, lack of reciprocal changes, only ST depression is avR (rather than avL in inferior MI), PR depression, T-inversions only occur once ST segment returns to baseline (unlike in MI).

Poor prognostic factors- consider 2D echo +/- admission:
-subacute onset
-elevated troponin (implies myocardial involvement)
-tamponade suspected (no kidding...)

Every pt should have CBC, troponin., Other tests are guided by evaluation.

If no specific cause found (majority of cases), options include
-high dose ASA (2-4g/day)
-ibuprofen (1600-3200mg/day) or other high dose NSAID

In recurrent pericarditis, colchicine or prednisone are often effective.

Click here for a NEJM review of pericarditis
Click here for JAMA Does this patient have cardiac tamponade?

Monday, July 9, 2012

CMA Driving Guidelines

In addition to the discussion below about jolt accentuation and other tests for meningeal irritation, check out the CMA's driving guidelines.

We discussed patients who have had a TIA- as you can read on this website there is no clear time period during which patients cannot drive- they need to be seen by a physician and if no neurological deficits persist can go back to driving.

Patients with a stroke should not drive for at least one month- however how long exactly depends on the physician's assessment of their deficits and risk of recurrence.

This website is a great resource as it is nearly impossible to remember all the times for every condition you will encounter. http://www.cma.ca/determining-fitness-to-drive

How are your meninges?

Today in morning report we discussed a case of a patient with fever, headache, and focal neurological signs. Those in the room were appropriately concerned about a CNS cause.
Could this patient have meningitis or something else (such as blood in subarachnoid hemorrhage) irritating his meninges?

Symptoms suggestive of meningeal irritation are: headache, neck stiffness, photophobia, cranial nerve palsies. These, in addition to fever/chills and other infectious symptoms can suggest a diagnosis of meningitis.

In meningitis, clinical history does a poor job of leading us to the diagnosis. Neck stiffness on history has a sensitivity of only 28%.

For physical exam, Kernig's and Brudzinski's signs have poor sensitivity and specificity (based on little data) for meningitis.

Jolt accentuation of headache is quite sensitive (97%) based on one study of 54 patients with fever and headache, making it a good ruling-out test if it is negative. To perform the test, ask the patient to shake their head from side-to-side at about 2-3Hz and ask them if their headache is better, the same or worse. If it is not worse, this significantly decreases the likelihood of meningitis.

It generates a positive likelihood ratio of 2.4 and negative likelihood ratio of 0.05 for CSF pleiocytosis (increased cell count). In order to use a likelihood ratio, you multiply the pre-test probability by the LR to get the post-test probability. See the image below for a visual of this calculation:

You can read more about this in the JAMA Rational Clinical Exam Article "Does This Patient Have Acute Meningitis" follow link here http://jama.jamanetwork.com/article.aspx?articleid=774331#JRC80004T4