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