Diabetic Foot Ulcers

We discussed diabetic foot ulcers this morning. The best way to prevent these ulcers is early detection of diabetic neuropathy, which is best done with a brief history and screening with Semmes-Weinstein monofilament.

Use the monofilament in 8-10 anatomic sites recommended (see above picture). However, even testing 4 plantar sites on the forefoot identifies 90% of the patients with an insensate site. Monofilament testing is fairly sensitive (66-91% ) and has a very good NPV 94-95%.

Here is review article on preventing diabetic foot ulcers. 

Extended Light's Criteria

This morning we discussed an approach to pleural effusion.

 

One concept we discussed was the possibility of transforming transudative pleural fluid in patients receiving diuretic therapy to an exudate.

In such cases we can use the “extended Light’s criteria”, which is to calculate the total protein gradient (serum minus pleural fluid). The fluid is a transudate if the total protein gradient is greater than 31g/L.

Here is a previous post about the Light’s criteria with a review article by Dr. Light himself!

Bacterial Meningitis

This morning we talked about a case of bacterial meningitis.  This is a disease that is rare but has significant mortality and morbidity, so it is important to be familiar with how to diagnose and treat it. Here are a few key point we discussed this morning.

1. Do not delay antibiotics for procedures such as CT head or LP
2. Antibiotic doses of meningitis are different (and much higher) 
3. Even if the CSFcultures are sterilized by prior antibiotics, other clues such as degree of neutrophillia, CSF glucose level, or the gram stain can point toward bacterial meningitis
4. No everyone needs a CT head
5. IDSA recommendation for CT prior to lumbar puncture is below:
1. Immunocompromised state
2. History of CNS disease Mass lesion, stroke, or focal infection
3. New onset seizure Within 1 week of presentation;
4. Papilledema
5. Abnormal level of consciousness …
6. Focal neurologic deficit
7. fields, gaze palsy, arm or leg drift

 Here is a review from Lance on management of bacterial meningitis. 

**Gram stain CSF: GPC in pairs and short chains suggestive of Streptococcus pneumoniae

KEEP COOL

Given the extreme heat in Toronto recently, I want to bring your attention to a post I did about a year ago about heat stroke, when we were hit with a heat wave and increased admissions. This extreme weather causes no only heat stokes, but also exacerbations of many chronic cardiopulmonary disease.

ABCDE rule

Early recognition of melanoma is an important prognostic factor. To distinguish early melanoma from other forms of benign pigmented lesions, we can use the ABCDE rule.

• Asymmetry (if a lesion is bisected, one half is not identical to the other half)
• Border irregularities
• Color variegation (brown, red, black or blue/gray, and white)
• Diameter ≥6 mm
• Evolving: a lesion that is changing in size, shape, or color, or a new lesion

The diagnostic accuracy of the ABCD vary in different studies. In a retrospective study of 1140 lesions including 460 melanomas, the sensitivity in identifying a lesion as a melanoma was 97 percent when using a single criterion and 43 percent when using all five criteria jointly. By contrast, specificity was 36 percent for a single criterion and 100 percent for all five criteria.

CAM

This morning we discussed a case of delirium.  Although a common diagnosis, it is sometimes challenging to diagnose delirium, especially in patients with underlying dementia or depression. The Confusion Assessment Method (CAM) is a validated tool to help you identify delirium. 

The diagnosis of delirium by CAM requires the presence of features 1 AND 2 plus either 3 OR 4.

1. Acute onset and fluctuating course

2. Inattention

3. Disorganized thinking

4. Altered level of consciousness 

For admitted medical and surgical patients, the CAM has a sensitivity of 94-100% and a specificity of 90-95% for diagnosing delirium.

Here is a detailed explanation of Confusion Assessment Method (CAM).

RS3PE SYNDROME

RS3PE syndrome stands for remitting seronegative symmetrical synovitis with pitting edema.

This syndrome has many similar features to PMR. Patienst are often over the age of 50 and are seronegative. However, unlike PMR, many patients with RS3PE have sudden onset of polyarthritis, usually more prominent distally.

Patients with this disorder respond to low-dose glucocorticoids.

RS3PE also has been described as a paraneoplastic disorder that is associated with solid tumors and hematologic disorders.

Here is a good review article on PMR.

* Areas of pain in PMR

Doctor, my legs are so puffy!

This morning we discussed a case of new onset bilateral leg edema. 

Approach to is to think about one or more of the following etiologies: 1. increased capillary hydrostatic pressure (e.g. CHF) 2. decreased capillary oncotic pressure (e.g. nephrotic syndrome) 3. increased capillary permeability (e.g. inflammation)

As we discussed, focus your history on cardiac, hepatic, or renal disease, or drugs that affect any of those systems.

 Physical examination should focus on the pattern of edema. Is the JVP elevated? Is there pulmonary edema? Is there ascites? Is the edema localized or generalized? Is it pitting or non-pitting? Is it acute or chronic? Pattern of edema will help you narrow down your differential diagnosis.

  Here is a reference on the topic.

Romberg Test

This morning we talked about the Romberg test.

The ability to maintain a steady posture depends on input from 2 of the 3:
o vestibular apparatus
o eyes
o propioception from feet
The cerebellum coordinates the input from all three.

ROMBERG test tells you about problems in propioception or the vestibular apparatus.
The test start with the patient standing with heels together and eyes OPEN. If there is unsteadiness, then there is cerebellar ataxia. If the patient is steady, then ask the patient to stand with eyes CLOSED. Inability to stand for 60 seconds with eyes CLOSED is a positive Romberg sign, and reflects vestibular disease or sensory ataxia.

*The test was named after the German neurologist Moritz Romberg (1795-1873).

Ref: Evidence-Based Physical Diagnosis, McGee. 2007.

"what about my water pill, doctor?"

This morning we briefly talked about the mechanism of action of furosemide (lasix). This drug is a loop diuretics that inhibits the Na-K-2Cl channel in the thick ascending limb of the loop of Henle on the luminal side.

The efficacy of Furosemide is dose-dependent, but a plateau is reached in which even higher doses produce no further diuresis (when all the channels are saturated). The bioavailability of furosemide is only about 50%, so IV is twice as potent as oral. The drug is renally cleared.

IV therapy is preferred in patients with decompensated heart failure initially because drug absorption may be slowed by decreased intestinal perfusion and mucosal edema.

Furosemide is a sulfonamide drug so can cause hypersensitivity reactions, but patients with a history of allergy to sulfonamide antibiotics usually tolerate furosemide with little cross-reactivity.

Another side effect furosemide to be aware of is ototoxicity.

Here is a review article on diuretic therapy.

Pleural Effusion and Ultrasound

At Gel Rounds today, we discussed pleural effusion. The image above is the ultrasound image of a small right sided effusion. The top of the image represents the probe resting on the chest wall, the dark area (e) is the effusion. The Bright band between (e) and the liver is the diaphragm (d). The lung is seen superior and deep to the effusion.

Now that you know how to identify pleural effusion with the ultrasound, use it in addition to your physical exam when doing a bedside thoracentesis.

Prothrombin-Complex Concentrates (PCC )

This morning we discussed the use of PCCs in reversing the INR. PCC is the combinations of vitamin K-dependent coagulation factors (ie, factors II, VII, IX, and X). It is used to normalize the INR and acts more rapidly than FFP or vitamin K alone.

PCC available in Canada is Octaplex (there are more in the market). This is a human blood product derivative (not a recombinant).

Advantage of using PCC is the much lower volume load compared to FFP. Thrombotic complications (such as DIC or MI) have been reported with PCC, but this risk is difficult to quantify.

Vitamin K should be given if you need to completely reveres INR even when using PCC to avoid delayed secondary rise in the INR as the coagulation factors are metabolized (remember factor VII has a half-life of four to six hours in vivo).

The cost of INR reversal with PCC is between $1000-$3000 USD.

Here is a review on reversal of vitamin K agonist therapy.

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).