Fever in the returned traveller

Today we discussed issues related to fever in the returned traveller

Some points that came up:

The red herring effect:
Do not be completely distracted by the travel history and its accompanying exotic possibilities; remember to look for and exclude the common causes of fever (i.e. common bacterial and viral infections, etc).

Important points on history:
-detailed travel itinerary (for location, activities) and dates (for incubation periods)
-whether pre-travel advice and appropriate prophylaxis was obtained
-specific exposures: sexual history, fresh water, animals, mosquitos

The VFR effect
Travellers "visiting friends and relatives" (i.e. VFR) are a particularly high risk group for serious travel-related illness; they are less likey to seek pre-travel counselling and take indicated prophylaxis. In contrast, they are more likely to have high-risk exposures and waning immunity due to prolonged absence.

Selected features of specific diagnoses (not intended to be exhaustive!)

Malaria- any fever in returned traveller from tropics is malaria until proven otherwise. Diagnosis by thick (sensitive) and thin (specific) smears; send multiple. Falciparum is the most virulent type

5 Malaria Questions:
1) Where it was acquired, and the resistance patterns there
2) What type is it? (much more worried if falciparum)
3) What is the degree of parasitemia (% of RBCs carrying); > 5% can be fatal
4) Was the pt on prophylaxis, taking it properly?
5) Is this "severe malaria"; coma, severe prostration, anemia, ARF, severe jaundice, resp failure, hypoglycemia, shock

Dengue- Wide spectrum of clinical manifestations. Retrobulbar h/a, muscle and joint pain "break bone fever"; rash in 50%. Leukopenia and thrombocytopenia common. Dengue Hemorrhagic Fever is feared complication; more common in previously exposed.

Typhoid- Abdo pain, fever, chills. Evanescent "rose spots" on abdomen or trunk. Relative bradycardia for fever is classic. Diarrhea or constipation. May have leukopenia or leukocyosis, anemia, transaminitis. Diagnosis by blood or stool cultures. Bone marrow Bx is 98% sensitive.

Others: schistosomiasis, leptospirosis, rickettsial diseases, hepatitis A, hepatitis B, HIV seroconversion reaction...

Some useful links

Click here for VFR paper from JAMA
Click here for GeoSentinel survey for conditions by geographical location
Click here for Gideon website- input location, symptoms, duration and receive weighted probabilty of different diagnoses
Click here for CDC website

Aortic Stenosis

At physical exam rounds, we discussed aortic stenosis.

Some key points:

Possible findings:

Vitals- Narrow pulse pressure

Pulses- Carotid may have low volume (parvus) and slow rate of rise (tardus). Brachio-radial delay, apical-carotid delay

JVP- Elevated if R heart failure as consequence of pulmonary edema (late)

Precordial palpation- Displaced, sustained apex, palpable S4, thrill

Heart sounds- Diminished S2, paradoxically split S2, S4

Murmur- Mid to late- peaking crescendo-decrescendo systolic murmur loudest in aortic area radiating to R clavicle, R carotid, or apex (Gallavardin)


Findings shown to rule out or rule in AoS

Sensitive (used to rule out)

Any systolic murmur

Murmur radiation to R clavicle (JGIM) or R carotid (JAMA) - see references


Specific (used to rule in)

Pulsus parvus et tardus (JAMA and JGIM)

Decreased intensity of S2 (JAMA and JGIM)

Mid to late-peaking systolic murmur (JAMA and JGIM)

Brachio-radial delay (JAMA)

Apical-carotid delay (JAMA)












Flow diagram from Etchells et al


References:

Click here for JGIM bedside clinical prediction rule

Click here for JAMA article on abnormal systolic murmur

Alcohol-related Liver Disease

Art Deco glamorization of excessive martinis







Today we discussed issues related to alcoholic liver disease and SBP. Some points that came up:

Risk factors for SBP
1) Prior SBP
2) GI bleed
3) Child's C cirrhosis
4) Ascitic fluid protein 10g/L

When to suspect SBP (and therefore perform diagnostic tap)
1) Admission of all cirrhotic pts with ascites, regardless of reason for admission
2) Patients with ascites and with GI bleed routinely before abx (20% have SBP initially, 40% by discharge)
3) Patients with ascites and any of abdominal pain, rebound, vomiting, diarrhea, fever, leukocytosis, encephalopathy (although NB- abdo pain is often absent)

SBP diagnosis
Ascites PMN > 250 or WBC > 500. If WBC > 1000 or polymicrobial culture or protein > 10g/L, suspect secondary peritonitis (i.e. intra-abdominal persistent source- abscess, perforation, etc).

Evidence-based prophylaxis in cirrhosis
1) Primary SBP prophylaxis in cirrhotic patients presenting with GI bleed: quinolone or ceftriaxone
2) Secondary prophylaxis of SBP: daily norfloxacin or weekly ciprofloxacin
3) Screening OGD at time of diagnosis, repeated q1-3 years depending on compensation
4) Non-selective B-bl (i.e. nadolol) for patients with varices (including those which have not bled) 5) Endovascular ligation (i.e. banding) for high-risk varices
6) Combination of B-bl and nitrates may slow progression of portal HTN
7) HCC screening by u/s q6-12 months for cirrhotic patients and high-risk HBV carriers
8) Hepatitis A and B vaccination for all patients with chronic liver disease

Alcohol withdrawal seizures
1) Generalized
2) Possibly recurrent (i.e. "rum fits")
3) Minimal post-ictal phase
4) Not followed by Todd's (suggests focality- suspect SDH, other focal abnormality)
5) Usually self-resolving

Wernicke-Korsakoff's syndrome
1) Ataxia - "magnetic gait"
2) Ophthalmoplegia- commonly bilat 6th CN. Possibly also 3rd CN
3) Amnesia- anterograde and possible mild retrograde (cannot learn new material; often confabulate)
1+2 = Wernicke's, 3=Korsakoff's


Some references
Click here for cirrhosis guidelines
Click here for esophageal varices / portal HTN guidelines
Click here for RCT on withdrawal sz treatment
Click here for evidence for empiric abx in cirrhotics with GIB

Meningitis

Gram positive diplococci in CSF which grew strep. pneumo

Today we discussed meningitis, a serious infection that requires prompt initiation of life or neurological function-saving therapy before confirming the diagnosis. Although the discussant was, well, substandard, some important points still came across

(for those not there, the discussant was me, so no emails necessary)

Some issues that came up:

Common sources of infection in nursing home patients:
1) Urinary tract
2) Pneumonia (would be 'healthcare associated'- different abx coverage)
3) Skin

Reasons for a patient not to improve despite appropriate abx for an infection:
1) Not receiving therapy (non-adherence, vomiting, etc)
2) Resistant organism
3) Wrong diagnosis
4) Source not being penetrated (e.g. underdosed, abscess)
5) Persistent source not dealt with (e.g. osteomyelitis, sacral ulcer)

Common organisms in meningitis:
1) St. pneumo
2) N. meningitidis
3) H. flu
4) Listeria

Order depends on patient; listeria more common in older, immunocompromised. Think of unusual causes in right setting (e.g. cryptococcus, TB). Even though cryptococcal meningitis (which may present subacutely) comes to mind in HIV, invasive st. pneumo infections are far more common in HIV than in the general population.

Important risk factors to ask about:
Travel, contacts, HIV RFs, sinus or ear infections, injection drugs, head trauma.
The lack of all of fever, altered mental status, or neck stiffness virtually rules out meningitis

Some physical exam points:
1) Kernig's and Brudzinski's signs were described a century ago in patients with end-stage TB meningitis. They have low sensitivity, but high specificity.
2) Jolt accentuation (i.e. patient turns own head horizontally at 2-3 /second) is 100% sensitive, but very non-specific. Therefore, lack of it essentially rules out the diagnosis (although the JAMA article excluded immunocompromised patients, so be careful)

Empiric treatment (i.e. before CT scan, before LP. Ideally after blood cultures)
1) ceftriaxone 2g (for NM)
2) vancomycin 1g (for SP- there is pen-resistant SP in the community)
3) ampicillin 2g (if suspect listeria)
4) dexamethasone 10mg (with antibiotics)- see references
5) +/- acyclovir if suspect HSV encephalitis (rash, sz, focal deficits)- need to hydrate aggressively
Tailor Abx once culture result back +/- HSV PCR is back


LP is mandatory! Even though Abx are started, you need a diagnosis.


Causes of very low CSF glucose
1) Bacterial meningitis
2) TB
3) Fungal
4) HSV encephalitis

Some references:

http://jama.ama-assn.org/cgi/content/full/282/2/175

http://content.nejm.org/cgi/content/abstract/347/20/1549

http://jama.ama-assn.org/cgi/content/full/296/16/2012

Vasculitis

p-ANCA immunofluorescence

Today we discussed the diagnosis and management of vasculitis, specifically ANCA-associated vasculitis. These diseases are rare, complex, multisystemic, and present many challenges to everyone involved (including those trying to blog about it). Good thing we had an expert!


When to suspect vasculitis?

1) Multiorgan involvement otherwise unexplained

2) Systemic symptoms (constitutional, etc. ) otherwise unexplained

3) Organ ischemia or infarction (bowel, renal, myocardial, etc)

4) Common condition in uncommon age group (MI, pulmonary edema, etc.)


How to classify vasculitis:

May classify by vessel size, by complement levels, by ANCA associated or not, and other features. Most commonly vessel size (Chapel Hill classification)

Large: Takayasu's, GCA

Medium: Kawasaki's, isolated CNS

Medium +/- small: PAN, Churg-Strauss, Wegener's

Small: HSP, cryoglobulinemia, hypersensitivity, microscopic polyangiitis


Basic features of some vasculitides (not intended to be exhaustive!)

Takayasu's:
pulse deficits, fever, malaise; may cause aortitis or dissection

Giant cell:
>50, sudden onset of pain, stiffness, fever, temporal h/a. Often pulse deficits, aortitis, aortic insufficiency

Kawasaki's
children with acute onset rash, fever, conjunctivitis. Often associated with coronary arteritis

Wegener's
fatigue, malaise, fever, inflammation of sinuses, kidneys, lungs. Also often cutaneous vasculitis. Often cANCA +ve

Microscopic polyangiitis
leukocytoclastic vasculitis, glomerulonephritis, hemoptysis, abdo pain. Often p-ANCA +ve

Churg-Strauss
Asthma, eosinophilia. Renal involvement is rare. p-ANCA often +ve

PAN
Assoc with HBV or HCV antigenemia. Fatigue, HTN, fever, renal failure, rash, mononeuritis multiplex. Marked HTN is classic for acute onset. May present as testicular pain.


Non-vasculitic causes of ANCA positivity

IBD, autoimmune hepatitis, CF, TB, many drugs (esp. PTU, methimazole, hydralazine, minocycline).

Some references for vasculitis diagnosis and management

http://www.bmj.com/cgi/content/full/338/apr22_2/b1461

http://jama.ama-assn.org/cgi/content/full/298/6/655

http://content.nejm.org/cgi/content/short/348/4/333

Welcome!

Welcome to Tangents, the Toronto Western Hospital morning report blog.

This was the idea of Isaac Bogoch, one of last year's CMRs, and I'd like to continue his great work this year.

The goal is to briefly summarize the topics discussed and give you links to some more detailed resources if you're interested.

Please feel free to give me any feedback on how to make it more useful to you.

David

UGIB

On Tuesday, we discussed issues related to upper GI bleeds.

Gastric ulcer with ASA tab in it!

Issues that came up:

DDx
-Ulcer (NSAIDS, H pylori) DU in 2nd/3rd part of duodenum suggests Zollinger-Ellison. Gastric ulcer: think of gastric cancer
-Varices (EtOH, hepatitis). High pressure venous system = big bleed
-Mallory-Weiss tears: vomiting hx. This is partial, vs. Boerhaave: rupture
-Esophagitis/gastritis (reflux, NSAID)
-Portal HTN gastropathy (like varices in stomach)
-Others: Dieulafoy's lesion, epistaxis, many others.

Checklist approach to acute UGIB management
1) Large bore IV access- at least 2
2) Group and screen, be ready to transfuse
3) Reverse any coagulopathy
4) PPI- IV or PO
5) Octreotide if known varices or high probability of variceal etiology
6) GI consult, possible urgent endoscopy

H. Pylori:
Acquisition: usually from childhood due to contaminated drinking water. Spread can occur person to person, especially within households.
Diagnostic tests:
Serology: Sensitive, but does not differentiate active vs. past infection
Urea breath test: Differentiates active vs. previous infection
Biopsy: Gold standard

Ferritin in Fe deficiency:
From Guyatt et al:
Likelihood ratios of Fe def (compared to gold standard of bone marrow bx):
Ferritin: LR
>100: 0.13
45-100: 0.46
18-45: 3.12
<18: 41.47
Cutoff of 41 is 98% Sn and 98% Sp

Some useful references- may need U of T computer to access full text.

Diagnosis of Fe deficiency:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2178409&dopt=Abstract http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1993290&dopt=Abstract

UGIB management:

http://content.nejm.org/cgi/content/full/359/9/928

http://www.cmaj.ca/cgi/content/full/174/10/1433

Dont decompensate......

Decompensated Cirrhosis / encephalopathy consider:

• SBP and other infection
• portal vein thrombosis
• variceal haemorrhage / upper GI bleed
• constipation
• narcotics / medications
• dehydration
• hypokalemia
• hepatocellular carcinoma

Here is a link for a recent article on cirrhosis management : Lancet. 2008 Mar 8;371(9615):838-51.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-4S0JSP4-15&_user=1166899&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000051839&_version=1&_urlVersion=0&_userid=1166899&md5=5581813824abf0c779fe91e89e3be860

Isnt it ELITE!!

Here is a link to the ELITE morning report ..... ILD

http://chiefmedicalresident.blogspot.com/2009/06/day-343-interstitial-lung-disease.html

Pneumocystis jirovecii pneumonia

PJP is the most common AIDS deifining opportunistic infection in HIV-infected individuals. The presentation in most people (>85%) includes fever, progressive cough and dyspnea. It is generally subacute developing over days to weeks. Other constitutional symptoms are common.

Radiology:

A large percent of initial CXR imaging is normal in people with PJP. As the disease progresses diffuse bilateral interstitial or alveolar infiltrates develop. Discrete infiltrates, cysts, nodules and pleural effusions have been described. If a patient suddenly deteriorates dont forget to think about the pnumothorax which is not an uncommon complication of this disease (see above). a HRCT maybe very helpful in times when the CXR is normal.

Diagnosis:

The diagnosis is confirmed based on demonstration of PJP in sputum (sens 50-90%) or BAL (sens >95%). Laboratory data is not particularly helpful for diagnosis but the 2 most common abnormalities are an elevated LDH and low CD4.

Treatment:

Anti-PCP treatment....first line is TMP-SMX - other considerations include tolerance, iv vs oral therapy. Duration 21 days.

Steroids: As people typically worsen 3-5 days into treatment with an inflammatory response, steroids become the standard of treatment in severe infection. This is defined as a PaO2 <70>35 on ABG. The original studies in this area came out of Toronto so check out this link.....

http://ovidsp.tx.ovid.com/spa/ovidweb.cgi?WebLinkFrameset=1&S=ELAFFPJJMDDDNMAANCFLNCJLJICKAA00&returnUrl=http%3a%2f%2fovidsp.tx.ovid.com%2fspa%2fovidweb.cgi%3fMain%2bSearch%2bPage%3d1%26S%3dELAFFPJJMDDDNMAANCFLNCJLJICKAA00&directlink=http%3a%2f%2fgraphics.tx.ovid.com%2fovftpdfs%2fFPDDNCJLNCAAMD00%2ffs047%2fovft%2flive%2fgv039%2f00005220%2f00005220-198808001-00007.pdf&filename=The+Possible+Role+of+Corticosteroid+Therapy+for+Pneumocystis+Pneumonia+in+the+Acquired+Immune+Deficiency+Syndrome+%28AIDS%29.

" The possible role of corticosteroid therapy for pneumocyctis pneumonia in the acquired immune deficiency syndrome" J Acquir Immune Defic Syndr. 1988;1(4):354-60

Milk 'does the body good'

Today we reviewed how to interpret a blood gas. There are many ways to do this but the approach generally follows a few simply steps....here is an example:

6 simple steps…

1. What is the pH?
2. Is the primary disturbance respiratory or metabolic?
3. Is there appropriate compensation?
4. If this is a metabolic acidosis is there an anion gap?

• what is the delta – delta?
• is there an osmolar gap?

5. what is the A-a gradient?

We also had a brief discussion of 'milk alkali syndrome' which is a syndrome characterized by the triad of hypercalcemia, alkalosis and renal insufficiency. This syndrome is most often precipitated by excessive ingestion of calcium carbonate preparations in predisposed individuals. In the acute presentation of this syndrome the patient develops symptoms within a week of the treatment. They have symptoms of hypercalcemia, including nausea, vomiting, weakness, and mental changes with psychosis or depressed sensorium. The also have severe metabolic alkalosis, a normal to elevated plasma phosphate concentration, and acute renal insufficiency. Withdrawal of milk and alkali leads to rapid relief of symptoms and the return of normal renal function.

Acute Yellow Atrophy

Fulminant Hepatic Failure is the acute rapid injury of the liver characterized by dysfunction with impaired synthetic dysfunction and encephalopathy in a person with a previously normal liver or well compensated liver disease. There are a number of etiologies and one easy to remember mnemonic is :

A - Acetaminophen, hepatitis A, autoimmune hepatitis
B - Hepatitis B
C - Cryptogenic, hepatitis C
D - Hepatitis D, drugs
E - Esoteric causes - Wilson's disease, Budd-Chiari syndrome
F - Fatty Infiltration - acute fatty liver of pregnancy, Reye's syndrome

Drugs - either Tylenol or idiosyncratic reactions to other medications - remain the number one cause of FHF (fulminant hepatic failure) in North America. Please see attached link for some additional information about some drugs which have been implicated.

http://emedicine.medscape.com/article/177354-overview

Do you have a sweet tooth??

Hi everyone,

I missed what was undoubtedly a fabulous discussion about insulin resistance on Monday. I have linked the new Diabetes Guidelines and an amazing article on DKA for you to this web page.

http://www.diabetes.ca/for-professionals/resources/2008-cpg/

Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state

CMAJ 2003;168(7):859-66

http://www.cmaj.ca/cgi/reprint/168/7/859

How can somthing so little cause something so big????

Above is a picture of leishmaniasis - visceral leishmaniasis is one of the causes of massive splenomegaly which can be distinguished from the listed causes of splenomegaly below by the fact that they are highlighted RED

Hematologic
Lymphoma, usually indolent variants
Acute and chronic leukemias (CML)
Polycythemia vera

Myelofibrosis
Multiple myeloma
Essential thrombocythemia
Acute and chronic hemolytic anemias (thalassemia)
Sickle cell diseas

Malignancy
Hematologic (see above)
Primary splenic tumors
Metastatic solid tumors

Infection
Viral - hepatitis, infectious mononucleosis, cytomegalovirus
Bacterial - salmonella, brucella, tuberculosis (MAC )
Parasitic - malaria, schistosomiasis,toxoplasmosis, leishmaniasis (Kala-azar)
Infective endocarditis
Fungal

Collagen Vascular Disease
Sarcoid
Systemic lupus erythematosus
Rheumatoid arthritis (Felty syndrome)


Infiltrative
Malignancy (infiltrative, primary tumor, metastatic tumor)
Gaucher's disease
Niemann-Pick disease
Amyloid
Glycogen storage disease
Langerhans cell histiocytosis
Hemophagocytic lymphohistiocytosis


Congestive
Cirrhosis
Heart failure

Thrombosis of portal, hepatic, or splenic veins

The internist's tumor.....

Renal cell carcinoma is often dubbed the 'internist's tumor' likely because of the many paraneoplaastic syndromes that have been associated with this cancer. The classic triad of "hematuria, flank pain and abdominal mass" as a presentation occurs generally in <10%>

Clinical syndromes....

1. anemia: can have the picture of anemia of chronic disease and precede the diagnosis of RCC.

2. hepatic dysfunction / STAUFFER's Syndrome: may be the result of liver mets but in the case of Stauffers syndrome occurs without any clear evidence of metastases and may be reversed by nephrectomy.

3. Fever: in up to 1/5 of people with additional constitutional symptoms

4. hypercalcemia: from bony mets, increased prostaglandins or PtHRP

5. erythrocytosis

6. thrombocytosis

7. AA amyloidosis

8. other hormonal overproduction....gonadotropins, human chorionic somatomammotropin, an ACTH-like substance, renin, insulin, glucagon

Do you see what I see......

The art of fundoscopy remains an important skill. When talking about hypertension some potentail changes include:

Mild Retinopathy : Retinal arteriolar narrowing, arteriolar wall thickening or opacification (copper wiring), and arteriovenous nicking (see above picture)

Moderate Retinopathy: Hemorrhages, either flame or dot-shaped, cotton-wool spots, hard exudates, and microaneurysms (see above)

Severe Retinopathy: Some or all of the above, plus optic disc edema (papilledema- see below)

All 'myx'ed up....

When discussing a case of hypothyroidism it important to consider the differential of hypothyroidism.....

Causes of Hypothyroidism:
Primary:

• Hashimotos
• RAI
• Surgery
• Subacute Thyroiditis
• Excess Iodine Intake
• Meds: lithium, amiodarone
• Iodine deficiency

Secondary Hypothyroidism (pituitary)
Tertiary Hypothyroidism (hypothalamus)
Peripheral Resistance to thyroid hormone

Investigations:

• TSH, FT3, FT4
• Anti-thyroid antibodies (anti-thyroglobulin, anti-TPO)
• Complications: CBC (normocytic anemia), lytes (hypoNa), fasting lipids, CK

Treatment:
L-thyroxine replacement (start at 25 - 50 mcg daily & increase slowly)
25 mcg daily for those with CAD, 50 mcg daily for elderly (age > 50)
full dose (usually 1-2mcg/kg daily) for young pt’s with no CAD
Titrate q 4wks based on TSH, FT4


Consider severity of hypothyroidism…..? myxedema coma:

Clinical Features:

-hypothermia
-hypotension / bradycardia
-hypercarbia
-hypoNa
-hypoGlu
-elevated CK

Management of this emergency……30-40%mortality!

• Admit to monitored setting
• Supportive
• Support ventilation as needed
• Monitor ABG’s
• Support BP with fluids / pressors
• Passive warming
• iv glucose for hypoglycemia – ± stress steroids, test for concomitant adrenal insufficiency
• Watch Na- likely SIADH

Specific:

• L-thyroxine iv bolus, followed by daily dosing (iv/PO)
• Adrenal insufficiency may be precipitated so hydrocortisone until plasma cortisol is known
  can have associated primary adrenal or secondary adrenal insufficiency
• Treat underlying cause (consider broad-spectrum Abx until cultures back)
• Refer to Endocrine

What is the colour of 1% milk???

When discussing the differntial diagnosis of meningitis you must always consider entities other than bacterial. Please see below for a review of a more unusual cause of meningitis: MUMPS.

Mumps is a single stranded RNA virus which is a member of the paramyxovirus genus. The incidence of Mumps infection has dramatically reduced since the introduction of the live attenuated vaccine in 1967. Despite this, there continue to be sporadic outbreaks.

The transmission of the virus is viral respiratory droplet, direct contact and fomites. The incubation period is 14-18 days from exposure to onset of symptoms. The peak of contagion is just before the onset of parotitis.

Clinical features of mumps include a non-specific viral prodrome of low grade fever, malaise, headache, myalgias and anorexia. Within 48 hours the onset of the classic parotitis begins. This is present in 95% of cases due to direct infection of ductal epithelium. The swelling can last up to 10 days.

Complications:
Some of the more serious complications of mumps include meningitis, encephalitis, orchitis. The orchitis is the most common complication in adult men appearing in close to 1/3 of cases. Symptoms include testicular pain, swelling, erythma of the scrotum. Oophoritis occurs in approximately 7% of post-pubertal females.
Aseptic meningitis is the most frequent extrasalivary complication. An assymptomatic pleocytosis can be seen in >50% of patients with clinical mumps. Clinical aseptic meningitis is seen in 4-6% of patients. This most frequently manifests as headache, low grade fever and nuchal rigidity. CSF has 10-2000 WBC (mostly lymphocytes), elevated total protein and mildly depressed glucose.
Other complications include encephalitis, deafness, GBS, transverse myelitis and facial palsy. Less frequent complications include thyroiditis, myocardial involvement, pancreatitis, interstitial nephritis and arthritis.

Diagnosis can be made on the classic presentation of parotitis. Other pertinent tests include leucopenia, relative lymphocytosis and serum amylase elevation. Specific testing for mumps include IgM mumps, significant rise in IgG titres, isolation of mumps virus. PC of affected fluid (e.g. CSF) is also an option.
Treatment is symptomatic.

Lets stick together....

The agglutination of AIHA - cold agglutinins

Autoimmune hemolytics anemias (AIHA) are grossly divided up based on the type of antibody produced by the reaction. IgG antibodies which react with protein antigens of the surface of RBCs at body temperature are referred to as “warm agglutinins”. This accounts for approximately 80% of AIHA.

The etiology of warm agglutinin AIHA is variable with most cases being idiopathic. Conditions which may be associated with this disease are:

• viral infections
• secondary to autoimmune disease - eg. SLE
• secondary to lymphoproliferative disorders – CLL, Hodgkins
• drug induced – hapten mediated (eg PCN) vs true anitbody mediated (e.g. methyl dopa)
• allogenic blood transfusion

The diagnosis is based on the demonstration of autoimmune destruction using the Coombs test. With the DIRECT COOMBS, the RBCS of the patient are washed free of adherent proteins and are reacted with antiserum or monocloncal antibodies prepared against various immunoglobulins and complement.

Clinically the anemia tends to be symptomatic. On exam patients tend to be jaundice, pale and have mild-moderate splenomegaly.

Blood film is characterised by spherocytes.

The hallmark of treatment once the diagnosis is confirmed is corticosteroids (1mg/kg predisone). Options for refractory disease include splenoctomy and for those not able to tolerate / not wanting surgery…immunospupressive / cytotoxic therapy including azathoprine, cyclophosphamide, cyclosporin and rituximab.

Do I look fat??? or am I inflammed.....

The consequences of alcohol are not just fatty liver and cirrhosis....you need think about alcoholic hepatitis as the prognosis of severe cases can be quite poor....

Alcoholic hepatitis should be suspected in a patient with heavy alcohol use and certain clinical / laboratory findings which differentiate this entity from just fatty liver.

Clinically the patients classically present with fever (low grade), hepatomegaly, jaundice and anorexia. When examining the liver you may notice increased size, tenderness and listen for a bruit over the liver because you just might hear one! At least a third of these patients have ascites and signs of chronic liver disease. Because the symptoms may be also seen in conditions such as SBP it is important to keep a wide differential. Alcoholic hepatitis is often a diagnosis of exclusion.

Laboratory abnormalities expected in alcoholic hepatitis include the typical transaminitis abnormalities in chronic liver disease with additional elevation in ALP, GGT and bilirubin. A liver biopsy is generally not needed in the diagnosis but if performed would show:

• liver necrosis
• mallory bodies
• infiltrative neutophils
• perivenular distribution of inflammation

Treatment of alcoholic hepatitis includes abstinence from ETOH as well as supportive measures such as management of withdrawal symptoms and vitamin supplementation. The overall prognosis of the acute condition can be assessed using MADDREY’s DISCRIMNANT FUNCTION (Maddrey’s Score)

Discriminant Function = 4.6x (PT-control PT) + (serum bilirubin (umol/L) / 17)

If the value is greater than 32 there is a high short term mortality (eg. one month mortality >35)

There are multiple trials with mixed results about the efficacy of steroid therapy for higher risk patients with a poor prognosis (including 2 positive metanalyses and one negative). The current recommendations from gastroenterology society guidelines are:

Corticosteroids (preferably prednisolone) should be used in patients with severe alcoholic hepatitis in whom the diagnosis is certain. Severity is defined as a discriminant function > 32 and/or hepatic encephalopathy. The efficacy of steroids has not been adequately evaluated in patients with severe alcoholic hepatitis who also have concomitant pancreatitis, gastrointestinal bleeding, renal failure, and active infection.

Sources say his tan was from Cape Cod.....

Primary Adrenal Insufficiency / Crisis

Clinical Presentation:

• symptoms depend on the rate of decline of function and superimposed illness
• must have a high suspicion as the presentation can be non-specific including nausea, vomiting, fatigue, weakness, fever and confusion
• more specific aspects of the presentation include a history of weight loss, hyperpigmentation (scars, bucal mucosa), less commonly hypoglycemia
  other autoimmune diseases may be present

Underlying Etiology of Primary Adrenal Insufficiency

• Autoimmune (Addison’s or autoimmune polyglandular dz especially type II “Schmidts syndrome”)
• Infection: TB, HIV, fungal, CMV
• Cancer/metasteses
• Hemorrhage – Waterhouse-Friedrichsen (GC) or anticoagulants
• Infarct – APLA
• Drugs: ketoconazole, mitotane
• Adrenomyeloneuropathy – X-linked

On Exam:

• hypotension
• reduced BMI
• hyperpigmentation
• hypogonadism – with changes in hair distribution patterns in women

Laboratory Features

• CBC (eosinophilia, lymphocytosis)
• Lytes: hyponatremia from decreased aldosterone (primary) or cortisol/increased ADH (secondary), hyperkalemia, hypercalcemia
• Glucose: hypoglycaemia – more common in secondary due to glucocorticoid deficiency
• Non-anion gap metabolic acidosis

Diagnosis

• Should be made with serum measurements of renin, ACTH and cortisol at baseline
  diagnosis is confirmed by a cosyntropin (ACTH) stimulation test.

Treatment

• In a ‘crisis’ needs to be initiated before the diagnosis is confirmed (due to hypotension etc)
• short term : dexamethasone 4-8mg iv bolus can be used as it doesn’t interfere with the stim test assays
• in patients with previous established disease hydrocortisone may be preferred due to mineralocorticoid activity
• long term: glucocorticoid therapy with hydrocortisone, prednisone, dexamethasone + mineralocorticoid therapy with flourinef
• consider: adrogen replacement in select circumstances
• *** counselling re illness, surgery, pregnancy and stress steroids
• ***medical alert bracelet

Who turned the lights out???

When thinking about altered level of awareness there are many possible approaches. A simple mnemonic is 'DIMS' . See below for the breakdown of what each letter stands for:

Drugs:

•Withdrawal : ETOH, benzodiazepines, narcotics, nicotine, antipsychotics

•Intoxication / interaction: anticholinergics (gravol), benzodiazepines, narcotics

Infections:

•urine, bacteremia, pneumonia, meningitis, encephalitis

Metabolic:

•Endocrine: Hypoglycemia / hyperglycemia, Thyroid

•Major organ failure: Lung; ­ hypercarbia, hypoxia, Kidney, Liver

•Electrolytes: ­ hypomagnesemia, hypercalcemia, hyper/hyponatremia

•Other: thiamine def.  B12 def. niacin def

Structural:

•Stroke : ischemic / hemorrhagic

•Subarachnoid hemorrhage

•Subdural hemorrhage

•Subacute: abscess, tumor

•Seizure (post ictal)

The differential 'Slaps' you in the face

When one talks about approach to new polyarthritis in the ER the differential diagnosis is quite extensive but should include.......

Infectious:

• viral (see below)
• bacterial (disseminated gonococcal, endocarditis...)
• lyme disease
• fungal

Inflammatory:

• SLE, RA, Stills Disease, IBD, psoriatic
• Sarcoidosis (Lofgrens)
• serum sickness reaction
• acute rheumatic fever

Finally....Always important to remember a bit about parvovirus B19 and the various clinical presentations.....

Erythema Infectiosum (5th disease)

• Incubation 4-28 days
• Prodrome: low grade fever, h/a, mild URTI
• Characteristic rash (3 phases): Slapped cheek appearance (facial flushing), Diffuse macular erythema, Central clearing of macular lesions – lacy, reticulated appearance
• Rash disappears over 1-3 wks but can wax and wane (sun exposure, exercise, heat, stress)

Arthropathy

• Females > males, adolescents > children
• likely post-infectious resolves in 2-4 wks
• range in symptoms from arthralgia with morning stiffness to frank arthritis
• most common: hands, writsts, knees, ankles

Aplastic crisis

• Transient arrest of erythropoiesis and absolute reticulocytopenia – sudden fall in hemoglobin in pts with chronic hemolysis (RBC life shorter)
• Incubation period for transient aplastic crisis is shorter – occurs coincident with viremia

Chronic Anemia:

• Immunocompromised

Fetal Infection:

• Nonimmune fetal hydrops and intrauterine fetal demise, risk fetal loss
• Monitor for signs of fetal anemia / hydrops – U/S with Doppler to measure peak systolic flow velocity in MCA

Myocarditis:

• Rare cause of lymphocytic myocarditis

Other cutaneous:

• PPGSS – papular-purpuric gloves and stocking syndrome – fever, pruritis and painful edema extremities

Have you seen the "Light"

The etiology of pleural effusions is a classic internal medicine question and as always a very popular morning report topic. ‘Light’s Criteria’ suggest an effusion is an exudate if it has any of:

• pleural protein / serum protien >0.5
• pleural LDH/ serum LDH >0.6
• pleural LDH > 2/3 upper limit of normal serum LDH

which is nicely detailed in the article:

Pleural Effusion. Light RW; NEJM 2002 vol 36 no. 25 1971

http://content.nejm.org/cgi/reprint/346/25/1971.pdf

Conversely, it has been suggested that the etiology of a pleural effusion may be better determined using liklihood ratios of various biochemical parameters. Theoretically this would better incorporate the pretest probability of an exudative and the absolute level of additional parameters including cholesterol, bilirubin and albumin which have some evidence as individual tests. Further, this avoids dichotimizing an effusion into transudate / exudate based on a single cutoff value. If intereted see:

Multilevel Likelihood Ratios for Identifying Pleural Exudatie Pleural Effusions. Heffner JE, Sahn S and LK Brown. Chest 2002 (121) 6: 1916-1920.

http://proquest.umi.com/pqdweb?index=36&did=134337871&SrchMode=3&sid=1&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1239631354&clientId=53675&aid=1

Progressive Multifocal Leukoencephalopathy

PML is a demyelinating disease of the CNS caused by reactivation of the polyomavirus JC (JC virus). It is found almost exclusively in immunosuppressed patients (only case reports of immunocompetent people). It is most commonly thought of in the HIV population (especially with CD4 <200) however should also be considered in other immunocompromised patients such as those with myeloproliferative / lymphoproliferative disorders.

This disease is a progressive multifocal disease involving the white matter of the CNS. It typically presents with subacute neurologic deficits including altered mental status, motor deficits, ataxia and / or visual symptoms. About 20% will eventually have seizures.

Although a brain biopsy is gold standard, diagnosis of PML is generally made on clinical grounds with supportive imaging and presence of JC virus in CSF. CT scan may show multiple hypodense patchy or confluent regions. MRI shows decreased T1 lesions or increase signal on T2 weighted images. An LP sent for JC virus – PCR is helpful. Without HAART the sensitivity of CSF PCR was 70-90% however in patients on treatment the yield is lower. Although brain biopsy is gold standard for diagnosis it is generally deferred due to high morbidity.

The prognosis of PML is poor with median survival (IN HAART TREATED PTS) approximately 1.8 years. Median survival is much less in non-treated HIV patients and <3 months in people with PML who are not HIV infected (myeloproliferative disorders etc.)

What a crisis!

ps...here is the reference / link for the article discussed....

The Lancet, Volume 356, Issue 9227, Pages 411 - 417, 29 July 2000

http://proquest.umi.com/pqdweb?index=4&did=57582446&SrchMode=1&sid=1&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1238693865&clientId=53675