Doctor my back hurts!

Today in Morning Report we reviewed a case of a 60F with acute onset of low back pain.

Remember the Red Flags of Back Pain:

1. Saddle anesthesia

2. Bowel/bladder changes

3. Constitutional symptoms (fever, chills, sweat, anorexia, weight loss)

4. Prior or current history of malignancy

5. Night pain

6. Hx of IVDU

7. Older age> 65 with new onset back pain

Why do we care about these red flags?

- Impending neurologic compromise

- Malignancy

- Abscess

The role of imaging in the management of low back pain: bottom line - in the absence of red flags, imaging for LBP doesn't significantly influence management and is associated with substantial cost.

http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/15031430 (use your UtorID for access)

A systematic review published in the Annals of Internal Medicine in 2004 concluded that in adults < 50 years old with no systemic symptoms (or red flags), symptomatic therapy without imaging is appropriate. In adults > 50 years, or those with systemic symptoms, routine bloodwork and plain radiographs are usually sufficient to rule out underlying systemic disease.

http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/12353946

Aphasia

Today in Morning Report we talked about a woman with acute onset of word-finding difficulties and recognition. Here is simple approach to aphasia:



*Remember: APHASIA = impairment in language. DYSARTHRIA = motor speech problem.



Broca's area and Wernicke's area are the main language areas located in the perisylvian language area, they are joined by the arcuate fasciculus.



*All aphasias have naming problems.

1) Can the patient repeat? (Assess repetition)
- Repeat after me: "no ifs, ands, or buts"

- if yes: perisylvian language area intact, therefore lesion in area around perisylvian language area = transcortical aphasia

• 2) Is the patient able to comprehend? (Assess comprehension, simple commands)


• easy questions: close your eyes, to more difficult: point to your nose with your right hand


• If yes: "Transcortical motor aphasia"


• If no: "Transcortical sensory aphasia"

- if no repetition: lesion within perisylvian language area

• 2) Is the patient able to comprehend?


• If yes: "Broca's aphasia"


• If no: "Wernicke's aphasia"

Summary:

Broca's Aphasia
- can understand, cannot repeat ("patient is frustrated")
- not fluent

Wernicke's Aphasia
- cannot comprehend, cannot repeat
- fluent (but non-sensical speech, not coherent) - word salad ("examiner is frustrated")

Transcortical Motor Aphasia
- like Broca's aphasia but CAN repeat
- usually lesion near Broca's area but not in the perisylvian area (in the frontal cortex)

Transcortical Sensory Aphasia
- like Wernicke's aphasia but CAN repeat

Global Aphasia
- cannot comprehend, cannot repeat, not fluent, cannot read, cannot write (usually mute)
- suggests large lesion affecting both Broca's and Wernicke's areas (ex. Large MCA stroke)

Anomic Aphasia
- difficulty naming but no other deficits
- does not localize

Conduction Aphasia
- cannot repeat, but everything else intact
- lesion in the Arcuate Fasciculus (the fibers that connect Broca's and Wernicke's); the two main areas are intact but the listening and the speaking parts of the brain can't connect

"Rapid Fire" MR

August 4, 2011 - Today we had "rapid fire" post-call morning report and reviewed several cases from last night. Here are some synopses:



Case 1. 57M mucosal bleeding. PMHx: APLA, ITP with splenectomy. Meds: Prednisone 15mg daily, no warfarin. O/E: petechiae, ecchymosis, cushingoid.



What do you think is causing his bleeding?



Investigations: Plt 285, INR 1.0, PTT 25.7, bleeding time >15s, U/A 2+ blood, creat 78



Does this change your differential diagnosis?



Remember the components of coagulation:
- factors, inhibitors (check via INR, PTT)
- Plt fxn (uremia, antiplt)
- fibrinogen
- vWF/factor 8 deficiency

Disorders of primary hemostasis:
- Acquired: antiplatelet agents (ASA, Plavix), thrombocytopenias (ITP, HIT, TTP), primary bone marrow diseases (myeloproliferative disorders, MDS, plasma cell dyscrasias), severe renal failure (so called "uremic platelets")
- Congenital: vWD, some platelet dysfunction disorders


Disorders of coagulation/fibrinolysis:
- Acquired: liver failure, Vit K deficiency, anticoagulant meds, factor inhibitors, scurvy
- Congenital: coagulation factor deficiencies (hemophilias), antiplasmin deficiency

Initial lab tests:
- CBC, liver enzymes, ABO blood group
- INR, aPTT, if abnormal: consider 1:1 mixing studies
- fibrinogen
- vWF antigen, ristocetin cofactor, factor VIII
- platelet aggregation test
- standardize bleeding time


***
Case 2. 58F 6-weeks post-THR (PMHx: JRA). Recent C. Diff treated with Flagyl, returning with worsening diarrhea, abdo pain.

C. diff recurrence - Definition: complete abatement of C. diff infection symptoms while on appropriate therapy, followed by subsequent reappearance of diarrhea and other symptoms after treatment has been stopped; must distinguish from persistent diarrhea without resolution during initial therapy.

Treatment of C. diff:
Initial episode: Flagyl 500 mg PO TID x 10 to 14 days
Alternative ($$$): Vanco 125 mg PO QID x 10 to 14 days

First relapse: repeat treatment as in initial episode (Flagyl)

Second relapse: tapering course of PO Vanco, +/- probiotics (Saccharomyces boulardii 500 mg orally twice daily).

***
Case 3. 78M from ICU post hypercapneic resp failure due to severe COPD

NB: The traditional teaching of supplemental oxygen decreasing the "drive to breathe" in CO2-retaining COPDers, is incorrect. The current thinking is that therapy with supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates the Haldane effect (decreased carriage of CO2 by oxyhemoglobin when compared with reduced hemoglobin), resulting in changes in physiologic deadspace and worsening hypercarbia.

Published in:
Hanson, C William III et al. Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease. Crit Care Med 1996; 24(1): 23-28.

***
Case 4. 50F 6-week abdo pain, diarrhea. CT abdo shows: Terminal ileitis.

What is your differential diagnosis?

DDx terminal ileitis:
- Crohns (#1, 2, 3!)
- infectious (especially Yersinia, TB)
- spondyloarthropathies
- vasculitides
- ischemia
- neoplasm
- medication-induced (especially NSAIDS)
- eosinophilic enteritis

Elevated CK

Rhabdomyolysis

August 2nd, 2011 - Morning Report

Definition: the rapid breakdown of striated muscle with subsequent release of cellular contents into the extracellular fluid and circulation.

Fun fact:
First description of Rhabdomyolysis is thought to be in the Book of Numbers (Bible or Torah) after the Israelites ate quail and were poisoned. Scholars believe this to be due to cicutoxin from the Hemlock plant that the quail were believed to feed on.

Elevated CK
- CK-MM muscle
- CK-MB heart
- CK-BB brain

DDx for elevated CK-MM (rhabdo)
1. Crush: compartment syndrome; lying on ground immobile
2. Drugs:(statins - risk significantly increases with co-use of fibrates, ecstasy, heroin, cocaine, neuroleptics - NMS), malignant hyperthermia
3. Ischemia: DVT with compartment syndrome, arterial embolus
4. Exertion: seizure, marathoners, muscle builders (think fit vs non-fit)
5. Inflammatory: polymyositis (personal or famil hx of autoimmune disease?), dermatomyositis (look for an underlying tumor)
6. Infection (especially viruses like EBV, coxsackie), Legionnaire's disease
7. Genetic: most common is McArdle's disease (congenital myophosphorylase deficiency), Tarui disease (phosphofructokinase disease), carnitine deficiency
8. Endocrine: hypo > hyperthyroid

*The schematic above showing the causes and complications of rhabdomyolysis was taken from the article: Cervellin G, Comelli I, Lippi G. Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med. 2010 Jun;48(6):749-56.

Clinical features:

- classic triad: muscle pain, brown pigmented urine (myoglobinuria), weakness seen in <10% of patients

- can be asymptomatic with only elevated CK

- myalgias, pain, pigmented urine, fever, malaise, tachycardia, nausea/vomiting

- AKI can be seen if CK>5000

- complications: renal failure, DIC, and death in ~5% of cases

- urine myoglobin is not useful in diagnosis

- CK is the biochemical gold standard

- other investigations: elevated AST>ALT, LDH, UA

Treatment:

- FLUIDS!

- little support for the use of mannitol, Lasix, or bicarb

- manage the electrolyte derangements (hyperkalemia, hypocalcemia)

- severe hyperkalemia may require dialysis - shifting with insulin may not work if extensive tissue damage led to rhabdo

Moderate-intensity exercise (HR 55-90% max) is enough to elevate CK levels to the mid-thousands, particularly if "eccentric muscle contractions" like weight lifting or running downhill. More info can be found in the article:

Latham J, Campbell D, Nichols W, Mott T. Clinical inquiries. How much can exercise raise creatine kinase level--and does it matter? J Fam Pract. 2008 Aug;57(8):545-7.

Geripsych Morning Report

This morning we discussed some common geripsych issues...

Form 1
- any physician can fill out within 7 days of seeing a patient
- mandates mental health assessment, can hold patient up to 72 hrs to do this
- mental health assessment does not have to be done by a psychiatrist; can be done by any physician comfortable with this assessment
- if patient deemed unsafe, next steps either: 1) put on Form 3 if involuntary, or 2) patient can stay voluntarily
- rarely use Box B (except psychiatrists who know the patient well because addresses patient's history)
- must give pt the Form 42: notifies the patient of why they're being held and by what authority (otherwise illegal to detain them)

Agitation
- clarify what agitation means and whether it warrants treatment
- treatment responsive versus non-treatment responsive
- treatment non-responsive: example -> wandering doesn't warrant treatment - there's no specific treatment except zonking them out
- treatment responsive: yelling, behavior driven by psychosis, striking/violence
- non-pharmacologic therapy: some "agitated" patients just need something to do like fold towels or stuff envelopes
- pharmacotherapy:

1. Atypical antipsychotics: mainly oral
- Risperidone: highest EPS, least sedating, ex: 0.25 OD or BID
- Olanzapine: most anticholinergic therefore avoid in elderly, mid EPS, mid sedating
- Quetiapine: Lowest EPS, most sedating, causes orthostatic hypotension (huge variation in dose, 6.25-200mg! Start low go slow, first couple days will have sedation)

Here is the Results portion of the article: L.B. Ozbolt; M.A. Paniagua ; R.M. Kaiser Atypical Antipsychotics for the Treatment of Delirious Elders. Journal of the American Medical Directors Association (January 2008), 9 (1), pg. 18-28

"Results: Risperidone, the most thoroughly studied atypical antipsychotic, was found to be approximately 80% to 85% effective in treating the behavioral disturbances of delirium at a dosage of 0.5 to 4 mg daily. Studies of olanzapine indicated that it was approximately 70% to 76% effective in treating delirium at doses of 2.5 to 11.6 mg daily. Very few studies have been conducted using quetiapine; it also appears to be a safe and effective alternative to high-potency antipsychotics. In comparison to haloperidol, the frequency of adverse reactions and side effects was found to be much lower with the use of atypical antipsychotic medications. In the limited number of trials comparing atypical antipsychotics to haloperidol, haloperidol consistently produced a higher rate (an additional 10% to 13%) of extrapyramidal side effects."

2. Typical
- Haldol: can be given po/im so gives you options, most EPS, least anticholinergic (ex 0.5-1mg po q4h prn); NB Haldol iv better for EPS but less safe from cardiac perspective ie long Qt
- Loxapine: slightly sedating, available in liquid form

3. Other
- Trazadone: good for nighttime restlessness

Stimulants in Depression:
- use for depression in the medically ill elderly who are anergic (apathetic) as opposed to sad, ex: flat affect, fatigued, low energy, no interest in eating in patient with no history of depression
- one week to titrate up and if it's going to work you expect it to work quickly within first week
- options: Buproprion or SSRIs
- NB: can use mirtazapine to stimulate appetite but caution because can increase cholesterol

Leukemia Cutis

Today at morning report we discussed rash and acute leukemia.

Rash (or other dermatologic complaints) are often difficult for internists to deal with, as we often lack a lot of experience with them. However, going back to basics, a few key points to make are:

(1) A description of the rash is important. This includes the features of the lesions (i.e. macules, papules, plaques, nodules, bullae, etc), a description of the distribution (localized vs. diffuse, major regions of the body affected, areas spared) and the progression of the lesions over time. It is also important to describe the associated symptoms - fever, pruritis, pain, parasthesia or anasthesia, etc.

(2) Rule out acutely dangerous things. A few key rashes internists should know about are:

• Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis
• Pemphigus
• Infections of skin/soft tissue (in particular, necrotizing fasciitis)
• Purpura fulminans (meningococcemia)
• Staphylococcal toxic shock
• Viral exanthems (Note that varicella, measles, etc can be severe and even fatal in adults, especially the elderly)

(3) If in doubt, stop all possible offending drugs and get an urgent dermatology opinion and biopsy.

We talked in more detail about leukemia cutis, a disease caused by infiltration of the skin with leukemic cells. The Canadian Medical Association Journal recently published a short case report with images (although in a child) on this syndrome. Leukemia cutis may portend a worse prognosis in adults with AML.

Management of Ascites

Today at morning report, we discussed the management of ascites.

I wanted to share with you some guidelines and literature:



Chronic Outpatient Management of Ascites

1. Sodium restriction (88 mmol/day [2000 mg/day])


2. Diuretics (oral spironolactone with or without oral furosemide).


3. Fluid restriction only if serum sodium is less than 120 to 125 mmol/L.

Chronic Outpatient Management of REFRACTORY Ascites

1. Serial therapeutic paracenteses.


2. Postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L.


3. For large-volume paracenteses, an albumin infusion of 6 to 8 g/L of fluid removed can be considered.


4. Transjugular intrahepatic portasystemic stent-shunt (TIPS) may be considered in appropriately selected patients who meet criteria similar to those of published randomized trials.

Who Needs SBP Prophylaxis?

1. Anyone who has had SBP before.


2. Anyone with cirrhosis admitted with a variceal bleed. See the NEJM paper


3. Anyone with cirrhosis, ascites ascitic protein less than 1.5, creatinine greater than 106 mmol/L OR BUN greater than 8.9 mmol/L), serum Na less than 130, MELD greater than 9 points with bilirubin greater than 3 mg/dL.

One question that came up was whether prophylaxis should be daily or intermittently. Both regiments have been shown to be of benefit in clinical trials, but there is concern that intermittent dosing will lead to bacterial resistance and therefore the preferred regimen according to the AASLD is daily.

Renal Failure in Ascites

Erik mentioned using albumin in patients with SBP. The major evidence supporting this practice is from an article published in the NEJM in 1999 which randomized patients with SBP to either antibiotics alone or antibiotics with albumin. The investigators found a statistically significant reduction in renal dsyfunction and mortality with this regimen.

There was aslo a recent review article on renal failure and cirrhosis in the NEJM.

See the AASLD Guidelines for more information on the management of ascites.