The Perfect Storm

This morning we discussed a case of thyroid storm. This is a life-threatening condition, characterized by exaggerated symptoms of hyperthyroidism.

Thyroid storm can present as first time presentation of thyroid disease, but more commonly seen in those with long standing history of hyperthyroidism triggered by infection, trauma, surgery, post-partum, or an iodine load.

Patients are often tachycardic with hemodynamic instability, and can have hyperpyrexia, altered LOC, and GI symptoms. Given the high mortality associated with thyroid storm (20-30%), a high index of suspicion should be kept in patients with history of thyroid disease.

Here is a review on thyroid emergencies.

Happy Holidays

On Monday in dermatology morning report we discussed SJS/TEN.

Here is a great reference that our presenter, Dr. A.D., has recommended.

Happy Holidays everyone and see you in January!

Drug-induced liver injury (DILI)

This morning we discussed drug-induced liver injury (DILI). Many drugs, both prescription and over-the-counter, can cause hepatotoxicity, so a careful medication history should always be obtained when a patient presents with liver enzyme abnormalities.

DILI can range from asymptomatic mild enzyme elevations to fulminate liver failure. Jaundice in addition to elevated enzymes is associated with a worse prognosis than that seen in the setting of isolated ezyme abnormalities (an observation known as "Hy's law").

The most important treatment for DILI is cessation of the offending drug.

Here is a review on DILI.

* H& E stain, liver biopsy, atorvastatin-induced acute hepatitis, Inflammatory cell infilteration of the liver parenchyma consistant with inflammation.

Hypersensitivity Pneumonitis

This morning we talked about hypersensitivity pneumonitis- also referred to as extrinsic allergic alveolitis.

This condition is an immunologic reaction of lung parenchyma to an inhaled agent, particularly an organic antigen. HP has been identified in various groups including farmers, bird handlers, carpenters, and those exposed to various industrial dusts. Mold exposure in poor housing can cause HP.

HP can present acutely with abrupt onset of fever, cough, dyspnea, and diffuse fine crackles. CXR may be normal or show transient patchy opacities. Subacute HP presents with gradual development of productive cough, dyspnea, fatigue, anorexia, and weight loss. Respiratory symptoms are more severe than with acute HP, and radiographic findings more extensive.

Removal from exposure to the inciting antigen leads to improvement in symptoms.

* Many adults and children suffer from chronic cough and respiratory symptoms secondary to mold exposure in poor housing in the Northern Ontario Cree community of Attawapiskat.

Here is the CBC photo gallery of the Attawapiskat Housing Crisit.

"once a chief, always a chief...."

This morning, we reviewed a case of HTLV-1 associated T-Cell lymphoma. The human T-lymphotropic virus (HTLV-I) is a retrovirus.

As we discussed, HTLV-1 is also associated with myelopathy, AKA tropical spastic paraparesis (TSP) which causes progressive weakness and spasticity of one or both legs with hyperreflexia.

HTLV-I is diagnosed by serum serology.

Treatment is not indicated for asymptomatic HTLV-1 infection.

*The title of this post has nothing to do with HTLV-1. I just liked Dr. HPK's quote from this morning!

Alcoholic hepatitis

This morning we reviewed a case of Alcoholic hepatitis at morning report.

Updated Post written by Dr. Wong

Alcoholic hepatitis takes place DURING significant alcohol use. They rarely seek medical attention because the hepatitis is mild and resolves on stopping alcohol for a few days. When they do present to ER, it is usually because symptoms persist despite abstinence. Patients rarely recognize jaundice, but in retrospect will have noticed dark urine.

Alcoholic liver disease can be recognized by the findings of AST > ALT, high GGT and high MCV.

Alcoholic hepatitis presents with AST 80-300 > ALT, low grade fever, a rise in WBC/left shift from baseline (baseline may be low), RUQ tenderness. Mild cases (normal INR) have an excellent survival prognosis. Severe hepatitis (INR > 1.9, Bilirubin > 100 or MELD > 21) has a high mortality risk and steroid therapy should be considered.

Therapy is Prednisone 40 mg OD x 4 weeks, no taper. Therapy is contra-indicated in the setting of infection, GI bleeding or renal failure.

Reassess after 1 week, stop if no improvement in bilirubin.

Nutrition with adequate calories is the other mainstay of therapy.

* Coloured light micrograph of a section through the liver of a patient with alcoholic hepatitis, inflammation of the liver due to heavy alcohol consumption. The normally regular cellular structure of the liver has been disrupted here, and large vacuoles of fat (yellow) are seen. The circular structures at centre are bile ducts.

Hypomagnesemia

This morning we reviewed a case of severe hypomagnesemia .

Patients often present with generalized weakness and non-specific complaints, but VENTRICULAR ARRYTHMIA and neurologic finings such as delirium and coma can also occur.

ETIOLOGY
- GI losses: diarrhea
- Renal losses: renal failure or renal magnesium wasting due to drugs such as diuretics, aminoglycosides, or cisplatin, or rare genetic causes such as Gitleman's disease
- Alcohol: causes renal tubular dysfunction and urinary loss of Mg.
- Decrease PO intake

**Think of Magnesium depletion in refractory hypokalemia or unexplained hypocalcemia.

MANAGEMENT:
Route depends on severity and renal function

If hypomagnesemic-hypokalemic ventricular arrhythmias: give 50 meq of IV magnesium slowly over 8 to 24 hours and repeated as necessary to maintain the plasma magnesium concentration above 0.4 mmol/L or 0.8 meq/L.

Oral replacement is adequate for asymptomatic patient.

Treat the underlying disease.

Hypertensive Emergency

We discuss the approach to and management of hypertensive emergency.

Here is a previous post on that topic.

Neurosyphilis (in non-HIV patient)

This morning we discussed a case of rapidly progressive dementia, likely secondary to neurosyphilis.

Neurosyphilis can occur early or late. It may occur with primary, secondary, or tertiary syphilis. Early neurophysilis can present as stroke, meningitis, meningoencephalitis, cranial nerve deficits, hearing loss (otosyphilis), or visual loss (oculosyphilis). Late neurosyphilis occur decades later and can presents as general paresis, dementia with psychosis (rapidly progressive), or tabes dorsalis (posterior column involvement, bowel, bladder dysfunction).

Syphilis Screen:
CMIA-Chemiluminescent Microparticle Immunoassay (serum)- T.pallidum (IgG/IgM)
VDRL-Venereal Disease Research Laboratory-no longer done at UHN labs.
RPR - Rapid Plasma Reagin Test. Detects total IgG/IgM antibody to syphilis (T. pallidum). Automatically done by lab if CMIA is reactive.

CMIA and PRP are called “syphilis screen” in EPR

Confirmatory Tests:
TP.PA- Treponema pallidum particle agglutination.
FTA.ABS- fluorescent treponemal antibody. Positive confirmatory test(s) are often reactive for life

CSF examination (not done at UHN lab, sent to PHL):
• CSF VDRL is specific but not sensitive
• CSF FTA-ABS is sensitive but not specific

Here is a review of syphilis.

Click here for the Ontario Public Health Lab algorithm for interpreting the MANY permutations and combinations of lab results

* A U.S. Army Educational Commission Poster about Neurosypilis, 1918.

Epidural Abcess

This morning we discussed a case of fever with back pain and our differential included epidural abscess.

If you're thinking about an epidural abscess, you need to image the spine. MRI is the best modality as it is sensitive to pick early signs of inflammation. CT with IV contrast is an acceptable alternative if MRI is not available. Plain X-ray may show changes of advanced osteomyelitis or discitis but is not used to diagnose an epidural abscess.

Here is a previous post and a reference on Epidural Abscesses.

Once in a while my heart flutters really fast...

This morning we discussed a case of CHF decompensation secondary to atrial flutter with rapid ventricular response.

Atrial flutter is an arrhythmia of organized atrial activity that is not a sinus rhythm. It can be seen its own or sometime as a transition arrhythmia between sinus rhythm and atrial fibrillation.

Any disorders predisposing to atrial fibrillation can cause atrial flutter including thyrotoxicosis, obesity, the sick sinus syndrome, pericarditis, pulmonary disease, and pulmonary embolism. Mitral valve prolapse and cardiac surgery are also risk factors for developing atrial flutter.

Atrial flutter is very similar to atrial fibrillation its clinical presentation and should be treated the same in terms of rate control and anticoagulation. Ablations therapy is very successful for atrial flutter, however, so long-term antiarrhythmic medications are infrequently used.

Here is review on managment of Atrial Flutter.

* the hallmark of atrial flutter on ECG is the saw-tooth pattern (also referred as a picket fence pattern).

Light's Criteria for Pleural Effusion

Today at morning report we discussed the Light's Criteria.

Light's criteria for exudative effusion are any of
protein level pleural:serum over 0.5
LDH pleural:serum of over 0.6
pleural LDH over 2/3 upper limit of normal for serum

The combination of the three criteria has a higher sensitivity, but a lower specificity, than each individual criterion. Light's criteria are sensitive for exudate; may have transudates falsely called exudates. If clinical appearance suggests transudate but Light's criteria says exudate, measure albumin in serum vs. pleural fluid. If serum albumin is over 12 greater than pleural fluid almost all have transudative.

Our case had a bloody effusion, which narrows Ddx somewhat to cancer, PE, trauma, infection (inc. pneumonia, TB)

Here is a review of Pleural Effusion by Dr. Light himself!

*A large left sided pleural effusion as seen on an upright chest X-ray.

Ascites

At Gel Rounds we discussed ascites.

Some key points:

Most sensitive findings (i.e. make it unlikely if not present):
1) flank dullness
2) bulging flanks
3) shifting dullness
4) peripheral edema
-history of increased girth, weight gain, ankle swelling

Most specific findings (i.e. make it likely if present)
1) fluid wave
2) shifting dullness

An approach to the examination in liver disease (besides examining the liver itself)

1) Signs of decompensated liver disease
-jaundice, scleral icterus, dark urine (high bilirubin)
-petechiae, ecchymoses (coagulopathy)
-edema (hypoalbuminemia)
-asterixis, level of consciousness (encephalopathy)

2) Signs of portal hypertension
-ascites
-splenomegaly
-dilated abdominal veins (extreme of this is caput medusae)
-hemorrhoids

Reference:

Click here for JAMA rational clinical exam on ascites.

* using the ultrasound, we looked at the Pouch of Morrison, which is a potential space between the liver and the right kidney. This is the first spot to check if you suspect a small amount of ascites. The picture shows Morison's pouch with fluid present (red arrows).

Pericarditis

At physical exam rounds today, we reviewed Pericarditis.

Clinical presentation: usually a sudden onset of retrosternal chest pain with a pleuritic component to it, often relieved by sitting up. You may hear a pericardial rub - this is classically described as a triphasic high-pitched sound. The 'tri' refers to 1. atrial systole, 2. ventricular systole, and 3. ventricular diastole.

ECG: may show diffuse, concave ST elevations that do not fit any particular vascular territory. PR depression is also seen.

Treatment: In most cases of idiopathic pericarditis, high dose NSAIDS are effective. Steroids and colchicine also may have a role.


Here is a review article on the topic.

Rhabdomolysis

This morning we discussed a case of rhabdomyolysis.

Here is a previous blog post on the topic.

*myoglobinuria

Miller Fisher Syndrome

Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy characterized classically by ascending weakness and absent reflexes. GBS is a heterogeneous disease with several variants. Miller Fisher Syndrome (MFS) is a variant that presents with opthalmoplegia, ataxia and areflexia.

In patients with GBS, CSF has elevated protein and normal WBC. In about 85% of patients with MFS antibodies against GQ1b (a ganglioside component of nerve) is positive, though this testing is not routinely performed.

Here is review of Guillain-Barre Syndrome.

* Dr. C. Miller Fisher, Canadian neurologist who first described the MFS variant of GBS in 1956. He was a stroke neurologist who contributed greatly to our understanding of lacunar stroke, and strokes related to atrial fibrillation.

SSRI and SIADH

This morning we talked about the association between SSRIs and SIADH.

The article we talked about was a review, by Dr. Liu, of case reports involving various SSRIs and hyponatremia. This study found that the majority (83%) of patients with this complication were over the age of 65. The average time to onset of hyponatremia was 13 days (range 3 to 120 days). This finding has since been confirmed through a prospective study.

Take home message is that elderly patients are at increased risk of hyponatremia associated with SSRIs.

Here is the abstract for the above article.

Here is a great review article about SAIDH.

Mitral Regurgitation

In physical exam rounds yesterday, we examined a patient with mitral regurgitations.
Here is a previous post on Mitral Regurgitation.

*Doppler ultrasound of the heart showing mitral regurgitation: there is abnormal leakage of blood backward (blue is flow away from the probe) through the mitral valve during systole.

Antimitochondrial antibody

Antimitochondrial antibody is present in 95% patients with Primary Billiary Cirrhosis. The antibody assay is 95% sensitive and 98% specific for PBC (except if it's done by indirect immunoflorescence).

There has been suggestion that the presence of antimitochondrial antibodies may predict the eventual development of PBC in asymptomatic people based on a small study. About 13% of first-degree relatives of patients with PBC have circulating antimitochondrial antibodies, suggesting they may be susceptible to developing PBC. The clinical significance of this finding remains to be determined.

Here is a great review on Primary Billiary Cirrhosis.

*Immunofluorescent stain shows antimitochondrial antibodies on a liver biopsy specimen.

Endocarditis

This morning we discussed a case of subacute bacterial endocarditis secondary to Strep viridans.

Here is a previous post on endocarditis with some great review referrences.

* Viridans Streptococcus is a term for a large group of commensal streptococcal bacteria that are either α-hemolytic, producing a green coloration on blood agar plates (hence the name "viridans", from Latin "vĭrĭdis", green), or nonhemolytic.

Hypertension

This morning we discussed a case of Hypertensive Emergency.

Here is a previous post on this topic.

* William Harvey (1578–1657)the first physician who described the systemic circulation of blood being pumped around the body by the heart in his book "De motu cordis" which became the basis for our current understanding of hypertension.

Hypophosphatemia

Hypophosphatemia is secondary to decreased intestinal absorption (such as in Vit D deficiency), increased urinary excretion (such as in hyperparathyroidism), or shift into the cells (such as in refeeding syndrome).

Symptomatic hypophosphatemia occur when serum phosphate concentration reaches 0.64 mmol/L. Worrisome symptoms of hypophosphatemia are related to ATP depletion, causing metabolic encephalopathy, impaired myocardial contractility, respiratory failure due to weakness of the diaphragm, a proximal myopathy, Rhabdomyolysis, dysphagia, ileus, and hematologic abnormalities.

Hypophosphatemia should be replaced aggressively even if the patient is not overtly symptomatic, since develop myopathy and weakness.

IV phosphate is potentially dangerous, since it can precipitate with calcium causing hypocalcemia, renal failure due to calcium phosphate precipitation in the kidneys, and possibly fatal arrhythmias. So, if IV therapy is necessary in the patient with severe symptomatic hypophosphatemia, it should be given by slow infusions (over a long period of 4-12hrs).

Paraneoplastic Erythrocytosis

There are 5 types of tumor commonly associated with the overproduction Epo:

1. Hepatocellular carcinoma: Epo elevation doesn’t always cause erythropoiesis because of RBC production inhibition by malignancy.

2. Renal cell carcinoma: In about 1-5% of patients.

3. Hemangioblastoma

4. Pheochromocytoma

5. Uterine myomata: clue will be absence of anemia in patients with menorrhagia. RBC overproduction is reversed following myomectomy.

*Contrast-enhanced MRI image of a patient with Hb=194, showing renal cell carcinoma(arrow).

HIV and Pneumococcal Disease

Although we automatically think about opportunistic and atypical infections in immunocompromised patients, it is important to note that , similar to non-HIV infected patients, Streptococcus pneumoniae, is the most common bacterial pathogens of CAP in patients with HIV.

As was discussed this morning, HIV infection substantially increases the risk of invasive pneumococcal infection, particularly among those patients with a low CD4 count <200, and those not on therapy. This increased risk may be partially explained by the observation that HIV infected individuals have a predisposition for pneumococcal nasopharyngeal colonization.

For this reason, the Centers for Disease Control and Prevention (CDC) recommends that all HIV–infected patients be vaccinated (preferably early in the disease while they still have the ability to mount an effective antibody response).

Here is a review on the topic.

Invasive pneumococcal disease in patients infected with HIV: still a threat in the era of highly active antiretroviral therapy. Jordano et al. Clin Infect Dis.38(11):1623.

* Chest radiograph of an HIV positive individual with a CD4 cell count above 200 cells/mm3, revealing right upper lobe consolidation. Sputum and blood cultures were positive for Streptococcus pneumoniae.

Hypercalcemia associated with Malignancy

We discussed a case of hypercalcemia this morning and reviewed the mechanisms by which malignancy can cause hypercalcemia.

1. Direct metastases to bone: These mets trigger the production of inflammatory cytokines and stimulate ostoclasts. Sometimes osteoclasts are directly stimulated by tumor cells via Osteoclast Activating Factors (eg IL6) in multiple myeloma or lymphoma.

2. PTH related peptide: this is the most common cause of hypercalcemia from non-metastatic solid tumors. Classically in squamous cell lung Ca

3. PTH: this is rare! only a few case reports of PTH being released from tumors

4. Calcitriol: a very common mechanism for hypercalcemia in the lymphomas.

Here is a great review article.
*CT scan of a patient presenting with Ca=3.1, who subsequently was found to hav have small cell lung cancer.