HOCM

Today we had a very information special guest morning report from the medical consults team. They discussed a woman with a new systolic ejection murmur, found to have hypertrophic obstructive cardiomyopathy on echo. They also discussed the complications of HOCM in pregnancy.

HOCM is a familial cardiomyopathy that results in marked asymmetric left ventricular hypertrophy (predominantly anterior ventricular septum) and diastolic dysfunction. In severe cases there is left ventricular outflow tract obstruction during systole, because the anterior (usually) leaflet of the mitral valve and septum actually meet. You may hear the term "systolic anterior motion" or SAM - this is what it is referring to.

Consequences of HOCM range broadly - from no symptoms whatsoever, to CHF and atrial fibrillation, to sudden cardiac death. Shortness of breath on exertion is the most common symptom. Predicting who will suffer serious consequences is difficult, but there are some generally agreed upon risk factors. These include:

1. Family history of HCM with sudden cardiac death
   
2. History of syncope or presyncope
   
3. Massive LVH (septal wall thickness >30 mm)
   
4. Previous (survived) sudden cardiac death
   
5. Nonsustained ventricular tachyarrhythmias (NSVT)
   
6. Abnormal blood pressure response to exercise

Physiologically we discussed how decreasing preload, increasing contractility, and decreasing afterload all worsen outflow obstruction.

Treatment also varies based on clinical presentation. Low risk asymptomatic patients do not require treatment. Betablockers and calcium channel blockers have a role in the symptomatic patient. Patients with CHF will likely require diuretics but this must be done cautiously as decreasing preload will worsen the outflow obstruction. Implantable cardioverter defibrillators can be used to prevent sudden cardiac death in a subset of high risk patients. Surgical treatment is generally reserved for patients who fail medical management and remain highly sympomatic.

See here for a review of management and risk stratification.

For those of you interested in preparticipation screening of athletes, here is an interesting article.

Have a good weekend and see you in a week!

Acute kidney Injury and HIV

Today we discussed an interesting patient with acute kidney injury in the setting of HIV, HCV, and DM II.

Acute kidney injury occurs more frequently in HIV+ patients than in HIV- individuals. This is distinct from the increased frequency of chronic kidney disease we sometimes see as the result of the HIV-associated glomerulonephropathies (ie HIV-associated nephropathy, IgA nephropathy).

The approach to renal failure remains the same: prerenal, renal, and postrenal. However, there are some specific causes that must be weighted more heavily or added to this list as a function of the patient being HIV+. For example:

Aside from the usual, prerenal causes must also include:

Pancreatitis (leading to 3rd spacing)

Cirrhosis/hepatorenal syndrome

Diarrheal illnesses

Renal causes must also include:

ATN

prolonged prerenal failure (not specific to HIV, but still the most common cause for ATN)

amphotericin B

aminoglycosides

pentamidine

ritonavir

cocaine

Acute tubulointerstitial nephritis

Several Abx, H2RB (ie ranitidine), NSAIDs

glomerular

HIVAN

IgA nephropathy

Immune-complex GN (ie cryoglobulinemia in the setting of HCV coinfection)

vascular

TTP, HUS

drug-induced

infection

crystal-associated nephropathy

sulfadiazine

indinivir

acyclovir

Aside from the usual, post-renal should also include:

nephrolithiasis (increased suspicion)

urethritis

retroperitoneal disease (ie lymphadenopathy)

infections (including fungal, TB-suspect in aseptic pyuria)

See here for a review that outlines the broad ddx.

Lastly, this study here looked at ARF in hospitalized HIV+ patients before and after the advent of HAART and found that HIV+ patients were more likely to have CKD, but also more likely to have ARF before and after HAART (adjusted OR 4.62 (4.3-4.95), and 2.82 (2.66-2.99), respectively. Age >65, DM, CKD, acute/chronic liver disease, and hepatitis co-infection were all statistically significant risk factors for development of ARF - interesting given that our patient had many of these. Interestingly, the incidence of acute renal failure was higher in the post-HAART era. Not surprisingly, in-hospital mortality was higher in HIV+ patients with ARF than in those without (OR 5.83 (5.11-6.65). Of course, it is difficult to say whether ARF is an independent predictor or more a marker of more severe illness.

Pituitary Apoplexy

Today we discussed a very interesting case of a 60M with pituitary apoplexy.

Pituitary apoplexy is hemorrhage, infarct, or both, of an underlying pituitary adenoma (less often a nonadenomatous gland) that results in ischemia and ultimately necrosis. The presentation can include: headache, nausea, vomiting, and ophthalmoplegias. The latter can include ptosis/dilated pupil/down and out eye (CN III), vertical diplopia (CN IV), and infrequently horizontal diplopia (CN VI). Visual field defects from expansion and compression of the optic chiasm can also occur. Subarachnoid bleeding can cause altered mental status and even coma.

Predisposing factors include: trauma, presence of an adenoma, hypotension, hypertension, previous pit irradiation, postsurgical, cardiac surgery, anticoagulation, treatment with dopamine agonists (ie bromocriptine), pituitary stimulation tests, and pregnancy (ie Sheehan's syndrome).

Differential diagnosis should include: SAH, meningitis, brainstem infarct, cavernous sinus thrombosis, migraine, Rathke's cleft cyst hemorrhage. If the presentation is primarily one of adrenal insufficiency, the other causes of adrenal insufficiency must be considered, and primary AI must be differentiated from secondary. See here for my previous post on adrenal insufficiency with links to a review article.

Once the pituitary has infarcted, pituitary function becomes impaired. This includes the production of ADH, oxytocin (posterior pituitary), and LH, FSH, TSH, GH, PRL, ACTH (anterior pituitary). Most important immediate concerns are the CRH-ACTH-cortisol axis, and IV hydrocortisone is required. Electrolytes must be closely monitored as patients may be hyponatremic, but the impaired ADH secretion can lead also to diabetes insipidus leading to brisk diuresis and hypernatremia. Patients will likely also need thyroid replacement. In secondary adrenal insufficiency (which this is), fludricortisone is typically not needed.

Workup includes MRI (sellar), electrolytes, urine lytes, TSH, PRL, other hormonal workup including LH, FSH, IGF-1, and AM cortisol (only helpful if it is very low). Cosyntropin stimulation test is only helpful when abnormal - if you have a high pretest probability, you would need more sensitive integrated hormonal tests.

See here for an interesting review of pit apoplexy.

IBD and malnutrition

Today we talked about a young man with acute on chronic diarrhea. We discussed the presentation of Inflammatory Bowel Disease, as well as the extraintestinal manifestations of IBD. We also chatted about the physical examination for malnourishment and splenomegaly.

1. Extraintestinal Manifestations of IBD:

MSK:

Seronegative spondyloarthropathy (oligoarticular, asymmetric, migratory, migratory; mostly peripheral but can be axial. Most often seen in Crohn's and is often associated with other extra-intestinal manifestations, namely ocular, skin, mouth).

Ocular:

Iritis/Uveitis/Episcleritis (from IBD)

Glaucoma/Cataracts (from prednisone)

Dermatologic/Mucosal:

Can be divided into 3 classes: granulomatous, reactive, and secondary to nutritional deficiency

Granulomatous

Perianal/stomal ulcers/fistulas

Abscesses

Reactive

Erythema Nodosum

Pyoderma gangrenosum

Aphthous stomatitis

Sweet's syndrome

Nutritional

Acrodermatitis enteropathica (looks like psoriasis, zinc-related)

Angular cheilitis (from Fe deficiency)

HepatobiIiary:

Primary sclerosing cholangitis (inflammation and fibrosis of intra- and extra-hepatic bile ducts)

Cholelithiasis (from GI loss of bile acids)

Fatty liver (from malnutrition)

Liver abscess (rare)

Heme:

Anemia (blood loss, chronic disease)

Thromboembolic events

Renal:

Acute renal failure (from ++ GI losses)

Nephrolithiasis (from both dehydration and hyperoxaluria)

Metabolic:

Osteoporosis

Drug-Induced:

Too many to list here, but there are many, depending on the agent used.

See here for a useful review.

2. We also discussed how to determine if a patient is malnourished. I don't need to tell you that the reason we worry about this is because malnourished individuals have higher risks of infection, poorer wound healing, poorer outcomes related to other illnesses (ie trouble weaning from ventilators in the ICU), and death.

Key features on history:

• weight loss >10% body weight in past 6 months
• abnormal dietary intake
• daily anorexia/nausea/vomiting/diarrhea for >2 weeks
• functional capacity.

Key features on physical exam:

• Loss of SubQ fat (manifest as skinny triceps, deltoid thinness, midaxillary line @ costal margin, and palmar/interosseous areas of hand)
• Loss of muscle (check the quadriceps and look for squaring of the deltoid muscle)
• Edema (ankle, sacral, ascites)

These findings must be used in combination to avoid false positives.

See here for the JAMA Rational Clinical Examination on this issue.

3. Splenomegaly: You're all very busy and this post is too long already - I am sure it will come up again, and I'll post more then!

Have a great weekend!

PJP Pneumonia & TMP-SMX reaction

Hope you enjoyed morning report today. Today we discussed an HIV+ man with a CD4 count of 4 who presented with a diffuse rash after being started on TMP-SMX for PJP pneumonia.

Adverse reactions to TMP-SMX are much more likely in HIV+ patients, thought to be because of systemic glutathione deficiency that renders HIV+ patients less able to deal with TMP-SMX metabolites.

TMP-SMX works by inhibiting bacterial synthesis of tetrahydrofolic acid - bacteria are obligate folic acid synthesizers, but we get it from our diet. The trimethoprim and sulfamethoxazole components do this through different mechanism.

Side effects include:

GI:

Nausea, vomiting, anorexia can occur, with glossitis, stomatitis, and diarrhea occurring less frequently. Hepatotoxicity is rare.

Derm:

Maculopapular rashes, urticaria, erythema, morbilliform lesions, erythema multiforme, purpura, and photosensitivity can all occur. Stevens Johnson syndrome and toxic epidermal necrolysis can occur, from the sulfa component.

Renal:

Elevated Cr (but retained GFR),hyperkalemia (careful with ACE/ARB!)

Heme:

Megaloblastic anemia in patients with low folate stores. Rarely agranulocytosis, granulocytopenia, anemia, thrombocytopenia

In HIV patients it is useful to think of reactions as either Hypersensitivity or Other. Hypersensitivity reactions typically occur 8-12 days after initiation, and include diffuse rash, rising LFTs, azotemia, nausea, vomiting, and diarrhea. SJS/TEN can occur.

Absolute contraindications to continuing or ever restarting TMP-SMX include SJS/TEN, severe hypersensitivity reaction, anaphylaxis, or severe cytopenias. In the absence of these concerns, it may be reasonable to try to treat adverse reactions symptomatically while continuing TMP-SMX or attempting dose escalation sensitization.

Treatment of PJP pneumonia is ideally with TMP-SMX 5mg/kg q8h, which has been shown to be superior to pentamidine. Alternatives to TMP-SMX include dapsone 100mg/d PO + trimethoprim 5mg/kg q8h PO x 21 days, or clinda + primaquine, or atovaquone, or pentamidine IV.

Here's a free freetext link to a useful review of TMP-SMX.

Here's a useful review of dermatologic manifestations of HIV.

Remember that in a patient with a CD4 count this low, a rash may be due to a number of causes, including:

HIV itself with it's myriad derm manifestations

Other Infection (gonococcal, varicella, syphilis)

Malignancy (lymphoma, Kaposi's Sarcoma)

Drug-reaction to ARVs (nevirapine, abacavir)

Drug-reaction to other Rx (TMP-SMX).

Hope you find that useful!

Vasculitis

I hope you enjoyed morning report today, where we presented a case of young woman with disseminated necrotic skin lesions ultimately found to be pANCA+ levamisole-associated vasculitis.

Here's a case report of 2 cases from NY published just this June. Similarly, we have had a string of such cases here in Toronto. As we
mentioned, levamisole is an anti-helminthic (veterinary) drug that has been tried for
immunomodulatory/antineoplastic purposes in the past. Increasingly it is being used to
cut cocaine, which we are seeing manifest as vasculitis and as agranulocytosis in our
patient populations. The patients described in this case report were also PANCA+, and
like our patient this morning, one's biopsy more consistent with a thrombotic process.
Interestingly, the other's biopsy was more consistent with a small-vessel vasculitis,
demonstrating that levamisole-induced vasculitis can have different manifestations on
biopsy.

See the CDC morbidity & mortality weekly report
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5849a3.htm for details of a series of
agranulocytosis reports to come out of the US. Note reference 6 - it's a case series out
of Canada. Note that several of these patients came to present because of acute febrile
illnesses, and many had pharyngitis.

Lastly, here's an old but great review article on vasculitis. Figure 1 is great
for getting a sense of which vessels are involved in this inflammatory process when we
say Small, Medium, and Large-vessel vasculitis.

Table 1 gives you a great framework for:
large vessel:Giant cell and takayasu's arteritis
medium vessel: PAN, Kawasaki's and Primary CNS vasculitis
small vessel: ANCA associated (sometimes called pauci-immune for the lack of
immune-complex deposition), immune-complex mediated (infectious and noninfectious), and
paraeneoplastic (with IBD as a separate heading).

I like this article's approach to diagnosis:
1) Diagnose that there is a small-vessel vasculitis in the first place
2) Now, figure out which one it is.
The presentations can be very similar, and it is important to look for clues to help
differentiate. Purpura, nephritis, abdominal pain, peripheral neuropathy, myalgias, and
arthralgias, and constitutional symptoms can be common to many of the vasculitidies, and
looking for clues (ie which organs are involved? Is there nasal involvement? Is derm the
primary problem?). Table 3 & 4 are useful for this.

Also, make sure to send: ANCA, antinuclear antibodies, complement, cryoglobulins, fecal
blood, antibodies to hepatitis B and C, rheumatoid factor, BUN, Cr, Urine R&M (for blood,
protein, and LOOK FOR CASTS - if the lab doesn't routinely do this, ask specifically or
spin it yourself).

I won't go in to too much more detail, as it's a broad topic. The best advice I can give
you is to review it again and again, whenever you have a patient with vasculitis.

Enjoy!

Drug safety, Publicly Funded Healthcare, Ascites

I hope you all enjoyed morning report today - we covered a variety of topics, and had some very interesting discussion - thank you all for participating! As Dr. Bell mentioned, so many of these topics interested me that I almost don't know where to start, but I will try to contain myself, and keep this concise.

We discussed a man with EtOHism and RA who presented to ER confused after being prescribed diazepam for insomnia.

1. Drug safety: We must always think about prescribing safety when discharging patients from hospital, and as we know there are certain medications that are known to be associated with morbidity and mortality, particularly in the elderly. There are many examples of this, but we have several 'local' studies looking at this: - Arch Intern Med 2008; 168(10):1090-6. (Dr. Bell's on this) found that relative to those who received no antipsychotic therapy, community-dwelling older adults with dementia who were newly dispensed an atypical antipsychotic therapy were 3.2 times more likely and those who received conventional antipsychotic therapy were 3.8 times more likely to develop any serious event (defined as event requiring hospital admission or death) during the 30 days of follow-up.

- CMAJ 2009; 181(12):891-6 (Dr. Dhalla's on this) looked at long-acting oxycodone prescribing, and found that from 1991 to 2007, prescriptions of oxycodone increased by 850%. Opioid-related deaths doubled, from 13.7 per million in 1991 to 27.2 per million in 2004. The addition of long-acting oxycodone to the drug formulary was associated with a 5-fold increase in oxycodone-related mortality (p<0.01).

2. Publicly funded healthcare: Our discussion of why this patient presented to the ER led to a discussion about primary care, and what the effect of disincentives (ie user fees) would have been on this patient. (I will state my conflicts of interest here - I am pro-medicare). Dr. Bell mentioned the RAND Health Experiment, which looked at 4
randomized insurance models: full coverage, and 25, 50, or 95% cost-sharing (or
copayments, the % being the percentage of medical costs that the patient has to pay). You can see why this study is cited by pro-privatization groups: there was fewer usage of health services by people who had to pay, and no significant difference was found in quality of care (defined as process measures decided upon by the analysts, potentially introducing some bias?). HOWEVER, you can also see why this study is cited by pro-medicare groups: highly effective services were underused just as much as less-effecitve services, and the quality of care in some ares DID suffer: free care led to improvements in HTN, dental health, vision, and other serious conditions (exertional CP, bleeding, LOC, unintentional weigh loss). The poor disproportionately experienced poorer quality of care in these areas. I am attaching a summary document on this study.

Another resource if you are interested in some of the evidence for publicly funded health care can be found at http://www.canadiandoctorsformedicare.ca/mustreadjournals.html

A particularly interesting article: Increased Ambulatory Care Co-payments and
Hospitalizations Among the Elderly, Amal N. Trivedi, Husein Moloo and Vincent Mor, The New England Journal of Medicine 362(4): 320-328, 2010.
Essentially, enrollees in plans that increased their copayments had significant increases in annual in-patient days, annual patient admissions, and the probability of any use of in-patient care, and were more likely to be black, of lower socioeconomic status and lesser educational attainment.

See http://www.canadiandoctorsformedicare.ca/e-rounds/e-rounds26.html for a more complete analysis.

3. Lastly, ascites. We'll have lots of time to talk about the physical exam so Ill send you that article later on (JAMA rational clinical exam). We discussed the role of albumin in cirrhotics with spontaneous bacterial peritonitis. A NEJM RCT of 126 such patients randomized to either IV cefotaxime alone or IV cefotaxime + albumin iven at a dose of 1.5 g per kilogram at the time of diagnosis, followed by 1 g per kilogram on day 3, showed that the group given albumin had less renal impairment and death up to 3 months out. Here's the study.

Phew! That's all for now!

Hypercalcemia

This morning we discussed an interesting case of hypercalcemia.

Key learning points included:

a) Patient confidentiality takes precedence over any legal issues the patient may have

b) Hypercalcemia: remember to ask about symptoms related to CAUSES and CONSEQUENCES. Most common causes are primary hyperparathyroidism (most common in incidental hypercalcemia and otherwise well outpatients), and malignancy (most common in sick inpatients).

A good way to classify etiology is:

Associated with high PTH:

- Primary, secondary, and tertiary hyperPTH

- Li ingesion

Associated with high vitD:

- Granulomatous disease (TB, sarcoid)

- Lymphoma

- Over-ingestion

Associated with normal vitD:

- Increased intake (milk alkali syndrome) - Decreased excretion (thiazides, familial hypocalciuric hypercalcemia)

- Increased bone turnover (hyperthyroidism, Paget's)

- Malignancy (PTHrP production, bony mets, osteoclast activation (in Myeloma))

Treatment is FLUIDS FLUIDS FLUIDS, IV bisphosphonate (watch in renal failure), calcitonin. Steroids may be a useful adjunct in non-TB granulomatous disease or known lymphoma.

Here's a great review article. Have a good weekend!

Pink Eye

I have no idea what we discussed today, as I was stuck at home with pinkeye.

But, in honour of WHY I have no idea, here's an article on diagnosing the "red eye"...something that is not only useful in primary care, as I have had patients with 'red eyes' many times on the wards - a useful differential diagnosis (and list of red flags) to have in your mind.

Red flags include: severe pain, need for topical steroids, vision loss, copious purulent discharge, corneal involvement, traumatic eye injury, recent ocular surgery, distorted pupil, herpes infection, or recurrent infections.

Adrenal Insufficiency

Wednesday's morning report focussed on adrenal insufficiency and endocrine causes of syncope (adrenal insufficiency and hypoglycemia being the most common of these, though hypocalcemia can cause hypovolemia and thus presyncope).

With respect to adrenal insufficiency, it's useful to review the hypothalamic-pituitary-adrenal axis, in that the hypothal produces corticotropin releasing hormone, which stimulates pit production of corticotropin or ACTH, which stimulates the adrenal gland to produce cortisol and androgen (and short-lived aldosterone).

I had to review the anatomy of the adrenal cortex, but as a quick reminder the zones are (from outside in): GFR - zona glomerulosa, fasciculata, and reticularis, which produce mineralocorticoids, glucocorticoids, and androgens respectively (salt, suger, sex is a good way to remember it).

Here's a review article (a bit old, but useful) - see table 1 for the causes of primary/secondary insufficiency. Table 2 highlights the signs/symptoms of adrenal insufficiency, emphasizing that this is a nonspecific presentation that requires looking for other clues (ie high K or low Na, hyperpigmentation) and actually remembering the diagnosis as a possibility. Very easy to miss. Dynamic testing (ie cosyntropin stimulation test) is necessary to make the diagnosis, though AM cortisol can sometimes be useful (or at least practical) in people in whom you have a very low index of suspicion and you are just ruling it out (ie the asymptomatic patient who has euvolemic hyponatremia). Remember, patients with adrenal insufficiency on treatment should probably have medicalert bracelets - something you can give them info on before they go.

TB encephalitis

Today we discussed a very interesting case of an HIV+ man with a CD4 count of 20, found to have CMV encephalitis and TB meningitis. Clinical pearls include: - sometimes, there ARE 2 diagnoses and Hocm's razor does not apply - TB meningitis can sometimes present with neutrophilic predominance in the CSF cell count, so do not be fooled. High PMNs with a negative CSF C&S should alert you to the possibility of TB meningitis.

Here's a review article on CNS TB. This is a broad topic that warrants lots more than 5 pages, but its a good start while you're busy on team.

Lastly, we didn't discuss too much about the role of steroids in TB meningitis. A cochrane review of 7 trials showed a small but significant mortality benefit in HIV-NEGATIVE patients (Prasad K, Singh MB. Corticosteroids for managing tuberculous meningitis. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD002244. DOI: 10.1002/14651858.CD002244.pub3); there is insufficient data to support use in HIV+ patients. A study in NEJM showed a mortality benefit in all-comers (no difference in longterm disability in survivors), but subgroup analysis in HIV+ patients showed nonsignificance. As expected, in this trial the case fatality was much higher in HIV+ patients at 65.3 percent, vs. 28.4 percent overall. (N Engl J Med 2004;351:1741-51)

Acute Renal Failure & ezitimibe

On Jul 12 we discussed an interesting case of renal failure in a patient with recurrent UTIs and recent lower GI bleeding.

Key learning points included:

1. Acute renal failure can be divided into prerenal (decreased renal blood flow), renal (intrinsic parenchymal damage), and postrenal (urine obstruction) causes. Of these, pre-renal causes are the most common. Key features on history include a detailed medication history, including any recent changes in potentially nephrotoxic or diuretic medications, as well as history of over-the-counter medications (ie NSAIDS) and recent Abx use (several can cause interstitial nephritis). We also need to remember to ask questions around the CAUSES of ARF and the COMPLICATIONS of ARF. Here's a review article from BMJ. Figure 1 gives a good list of investigations to order, but remember that this needs to be tailored based on history, physical, available investigations, and clinical suspicion. Remember to consult our nephro colleagues if the ARF is not improving despite your treatments, or if cause appears unclear.

2. We also discussed the evidence for ezitimibe. No benefit in progression of Aostenosis (SEAS study), and no benefit in carotid intima thickness - I am not sure to be honest how clinically relevant that knowledge is! We do know that ezitimibe has not been shown to have a mortality benefit for primary or secondary prevention.

HIV/HCV coinfection & decompensated liver failure

Thanks to Dan for presenting a very interesting patient with decompensated liver failure in the context of HIV/HCV coinfection and concurrent alcoholism. We covered a few different topic areas today:

1. The importance of recognizing the broader context of a patient's life and thus the illness with which they are presenting to you. Dr. Hwang did a great job of highlighting this fact, and acknowledging the importance of the social determinants of health in a patient's illness. Here's a very interesting systematic review to come out of SMH on the positive impact of housing status in HIV patients on patient outcomes including medication adherence, health behaviours, and utilization of services. Note the authorship!

2. We also discussed the approach to a patient with decompensated liver failure and management principles. Decompensated liver disease is a constellation of clinical findings that can include all or some of: encephalopathy, coagulopathy, renal failure, rising LFTs, worsening ascites, and jaundice. Whenever someone presents to you in this way, it is important to ask WHY they are decompensating. You must rule out spontaneous bacterial peritonitis (done by doing a paracentesis and sending fluid for cell count/diff and C&S, with a neutrophil count of >250 suggesting SBP), as well as rule out UGIB. Other causes include medication/diet nonadherence, constipation, portal vein thrombosis, other infection, and development of a hepatoma (AKA hepatocellular carcinoma). I really like table 5 in the Lancet article for a list of cirrhosis complications and their management.

3. Lastly, we discussed the management of ascites. Here's a NEJM review on this topic, as well as an image I really like on paracentesis. Key principles include:

a. Mechanism of ascites: cirrhosis leads to hepatic resistance to portal flow, which ultimately causes portal hypertension, formation of collaterals, and shunting of blood systemically. As this develops, local vasodilator production (Nitric Oxide mostly) leads to splanchnic vasodilation and the 'transudate' that is ascites.

b. Management must include consideration of liver transplantation - at least consider whether they are a candidate, as patients with ascites have poor prognosis in the absence of transplantation.

c. Ongoing management requires a low Na diet, diuresis (typically with spironolactone starting at 100mg OD and furosemide starting at 40mg OD, with particular caution around the risk of inducing prerenal failure). Florence Wong, another SMH staff, has a great practical article on how to titrate your diuretics to 24h urine collection: Hope you find this information useful! Have a great evening and enjoy the sunshine (with sunscreen :)).

COPD, CHF

Today(Jul 6) we discussed a 69M with a history of COPD and CHF, coming in with SOBOE that was ultimately felt to be secondary to his CHF. We discussed several different issues, including the clinical examination for COPD & ascites, analysis of thoracentesis, and the differential diagnosis for someone presenting with shortness of breath.

With respect to a few specific issues:

1. Here's a summary of a recent Cochrane review on LABA/steroid vs tiotropium. Essentially, it's a mixed bag, with significant flaws in study design indicating that further study is needed.

2. Here's a link to a recent systematic review on PE in COPDE, that sites the Annals of Internal Medicine article from 2006 that I mentioned today in morning report (Ann Intern Med. 2006 Mar 21;144(6):390-6). Overall, the prevalence of PE was 19.9% but almost 25% in patients who ultimately required admission. Presentations were very similar between patients who did and did not have PE. Thus, it is important for us to calculate probability of PE in our patients when they present with COPDE.

3. The JAMA "Does the clinical examination predict airflow limitation" is from 1995 and I am unable to pull it up. However, there is a succinct ppt presentation online that summarizes it well:

I should also correct myself - the barrel chest was more sensitive than I had realized.