Treatment of Latent TB

Treatment of latent tuberculosis infection: An update. 

Lobue. Respirology (2010) 15, 603–622

http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1843.2010.01751.x/abstract


This article provides a good review of existing trials conducted on the efficacy, safety, cost effectiveness, and compliance of latent TB treatment regimens. 


The author concludes that: 

As long as 9months INH remains the standard therapy, LTBI treatment will remain expensive with a greater than desirable risk of adverse events and have suboptimal public health impact, because of poor acceptance by many patients and providers. At the moment, this regimen is considered the regimen of first choice, but two acceptable alternatives are 4 months of INH plus rifampin or 4 months rifampin mono-therapy. Of the two alternatives, the 2-drug regimen has been tested in more trials, and has equivalent completion, toxicity, and effectiveness as 6–9 months INH. Therapy with 4 months rifampin alone has significantly better completion, and signifi- cantly lower toxicity than INH. These are very impor- tant advantages, but effectiveness remains uncertain as this regimen has not been tested as extensively in randomized trails. 

Treatment for people with exposure to MDR-TB remain poorly studied. Current recommendations (CDC and Francis J. Curry National Tubercu- losis Center) are based on expert opinion of likely susceptible drugs based on MDR-TB's resistance patterns but are not evidence-based; there have been no clinical trials for the use of these regimens in contacts of patients with MDR TB. 

CDC Guideline:

Candidates for the Treatment of LTBI

Persons in the following high-risk groups should be given treatment for LTBI if their reaction to the Mantoux tuberculin skin test is ≥5mm:

• HIV-infected persons
• Recent contacts of a TB case
• Persons with fibrotic changes on chest radiograph consistent with old TB
• Patients with organ transplants
• Persons who are immunosuppressed for other reasons (e.g., taking the equivalent of >15 mg/day of prednisone for 1 month or longer, taking TNF-aantagonists)

In addition, persons in the following high-risk groups should be considered for treatment of LTBI if their reaction to the Mantoux tuberculin skin test is ≥10 mm:

• Recent arrivals (< 5 years) from high-prevalence countries
• Injection drug users
• Residents and employees of high-risk congregate settings (e.g., correctional facilities, nursing homes, homeless shelters, hospitals, and other health care facilities)
• Mycobacteriology laboratory personnel
• Persons with clinical conditions that make them high-risk
• Children under 4 years of age, or children and adolescents exposed to adults in high-risk categories

Has Oseltamivir Been Shown to Be Effective for Treatment of H5N1 Influenza?

EDITORIAL COMMENTARY

Has Oseltamivir Been Shown to Be Effective for Treatment of H5N1 Influenza?

http://www.journals.uchicago.edu/doi/full/10.1086/656317
This issue of JID features an article by Adisasmito et al. It reviews previous clinical report, case series etc to determine whether oseltamivir is effective for treatment of H5N1 influenza.

In total, 308 cases were identified from 12 countries: 41 from Azerbaijan, Hong Kong SAR, Nigeria, Pakistan, and Turkey (from clinical records); 175 from Egypt and Indonesia (from various sources); and 92 from Bangladesh, Cambodia, China, Thailand, and Vietnam (from various publications). Overall crude survival was 43.5%; 60% of patients who received 1 dose of oseltamivir alone (OS⁺) survived versus 24% of patients who had no evidence of anti‐influenza antiviral treatment (OS⁻) ( ). Survival rates of OS⁺ groups were significantly higher than those of OS⁻ groups; benefit persisted with oseltamivir treatment initiation 6–8 days after symptom onset. Multivariate modeling showed 49% mortality reduction from oseltamivir treatment.

It is interesting to note that 14 cases in the Adisasmito report were treated with higher than standard dosages and 7 (50%) survived; 20 were treated for longer than 5 days (median, 7 days) and 15 (75%) survived. In view of the need for better treatment and the safety data available on higher dosages (150 mg twice daily) and longer durations of oseltamivir treatment, it seems reasonable to adopt the WHO proposed treatment of a higher dosage and duration of 10 days for H5N1 influenza and possibly all cases of influenza pneumonia. Finally, parenteral treatment with either the unapproved peramivir or zanamivir preparations may be best for this severe disease.

In summary, the combined experience with oseltamivir treatment by Adisasmito et al supports the belief that oseltamivir given orally at approved dosages for 5 days is beneficial for treatment of H5N1 influenza, particularly if treatment is started early in the course of illness. However, improvement in therapy is needed, and available data suggest oral therapy with a higher dosage (150 mg twice daily) and a longer duration (7–10 days) or parenteral therapy with peramivir or zanamivir are likely to improve on the standard oral oseltamivir treatment regimen.

Mycology online - good collections of fungus database including pictures

Webpage - Mycology online published by University of Adelaide.
It contains photo gallery of fungus, description, identification, laboratory methods, and guidelines for therapy
http://www.mycology.adelaide.edu.au/

Survival of Hep C in syringes may explain high transmission amongst IVDUs

An article in JID published by Paintsil et al. 2010 hypothesized that the efficient transmission of HCV among IDUs may be partly due to the ability of the virus to remain viable in contaminated syringes for prolonged periods. (It is estimated that the probability of transmission of HCV per exposure to a contaminated syringe is 5‐fold to 20‐fold higher than that of HIV transmission).  

To test this hypothesis, they developed a microculture assay that allowed us to propagate HCV from small residual volumes contained in the dead space of syringes used by IDUs, and to determine the effects of storage at different temperatures for prolonged periods on the viability of HCV in syringes.

The authors found out that Insulin syringes failed to yield viable HCV beyond day 1 at all storage temperatures except 4°, in which 5% of syringes yielded viable virus on day 7; Tuberculin syringes yielded viable virus from 96%, 71%, and 52% of syringes after storage at 4°, 22°, and 37° for 7 days, respectively, and yielded viable virus up to day 63. 

Conclusions.The high prevalence of HCV among injection drug users may be partly due to the prolonged survival of viruses in syringes and the syringe type. . Our findings may be used to guide prevention strategies.

Further studies are also needed to determine whether higher HCV transmission amongst IVDU are due to differences in viral infectivity / inoculum size required to cause infection.  

http://www.journals.uchicago.edu/doi/full/10.1086/656212

Pneumococcal vaccination in HIV infected adults - would choice of vaccine differ?

J Infect Dis. 2010 Oct 1;202(7):1114-25.
http://www.ncbi.nlm.nih.gov/pubmed/20795819

In HIV infected patients, risk of pneumococcal infection is high and vaccination is recommended.  
The 23-valent pneumococcal vaccine is generally recommended for HIV-infected patients - previously recommended for patients with CD4 counts ≥200 cells/mm³, studies evaluating its efficacy have yielded mixed results (ACC Sep 1 2000, Jan 1 2001, and Jul 27 2005). Then, a study from AIDS clinical care suggested that protection benefit may be greatest in patients with CD4 <200 (http://www.medscape.com/viewarticle/563686). 


Nevertheless, immune response, even after revaccination with the 23-valent polysaccharide vaccine (PPV) are low among human immunodeficiency virus (HIV)-infected adults.

This study determined whether revaccination with the 7-valent pneumococcal conjugate vaccine (PCV) would enhance these responses.  HIV patients (median CD4 533cells/mm3 who's had PPV 3 - 8 years earlier were compared with non-HIV infected population, revaccinated wtih PCV or PPV.

RESULTS: HIV-infected persons demonstrated a higher frequency of positive antibody responses to PCV than to PPV (57% vs 36%) (P = .004) and greater mean changes in the immunoglobulin G concentration from baseline to day 60 for serotypes 4, 9V, and 19F (P < .05, for all), but not for serotype 14. However, by day 180, both outcomes were similar. Responses to PCV were greater in frequency and magnitude for all serotypes in HIV-uninfected adults, compared with those in HIV-infected adults.

CONCLUSIONS FROM AUTHOR: Among persons with HIV infection, revaccination with PCV was only transiently more immunogenic than PPV, and responses were inferior to those in HIV-uninfected subjects with primary vaccination. Pneumococcal vaccines with more robust and sustained immunogenicity are needed for HIV-infected adults.

What does the current 2009 AIDS guideline say:
Guideline now recommends pneumococcal vaccination when CD4 <200, but efficacy is not yet fully established. Re-vaccination after immune reconstitution CD4>200 can be considered but efficacy and duration of protection is not fully known. Revaccination every 5 years may be considered although definite data supporting this recommendation is lacking.

Use of HPV vaccine in HIV-infected men - Journal of Infectious Diseases

By Wilkin et. al. 2010

Use of HPV vaccine in men should be considered to prevent development of HPV related anal cancers. A

a single‐arm, open‐label, multicenter clinical trial was performed to assess the safety and immunogenicity of the quadrivalent HPV (types 6, 11, 16, and 18) vaccine in HIV‐1–infected men. 

Men with high‐grade anal intraepithelial neoplasia or anal cancer by history or by screening cytology or histology were excluded. Men received 0.5 mL intramuscularly at entry, week 8, and week 24. The primary end points were seroconversion to vaccine types at week 28, in men who were seronegative and without anal infection with the relevant HPV type at entry, and grade 3 or higher adverse events related to vaccination.

Results showed that vaccine was well tolerated, and showed successful seroconversion: for all 4 types: type 6 (59 [98%] of 60), type 11 (67 [99%] of 68), type 16 (62 [100%] of 62), and type 18 (74 [95%] of 78). No adverse effects on CD4 counts and plasma HIV‐1 RNA levels were observed.

Conclusions.The quadrivalent HPV vaccine appears safe and highly immunogenic in HIV‐1–infected men. Efficacy studies in HIV‐1–infected men, especially in preventing anal cancer, are warranted.   

http://www.journals.uchicago.edu/doi/abs/10.1086/656320

Good Medical PodCasts

These are free PodCasts that can be downloaded from the itunes, featuring online audio summaries of the latest launched medical journals. 

In Singapore however access to Podcasts are restricted. 

You can overcome this by signing up a 'UK / US account', and then search for these items for download. 

Alternatively, you can visit the journal's official website and listen online, for some of them.  

• USF Division of Infectious Diseases PodCst
• SCCM PodCast - iCritical Care
• New England Journal of Medicine
• JAMA
• Lancet Infectious Diseases
• Lancet
• BMJ

Candida Score (CS) for discriminating between candida colonisation and invasive candiasis (non neutropenic patients)

Leon.C et al. Crit Care Med 2009; 37: 1624-1633

A prospective multi-centre study assessing the usefulness of CS for discriminating between candida spp. colonisation versus invasive candidiasis (IC) in non neutropenic and critically ill patients, enrolled 1107 patients admitted for at least 7 days. 

Fungal diagnosis was confirmed based on cultures, serum 1-3-beta-D-glucan adn anti-candida antibodies (some patients). 

Score: (0 = absent, 1 = present)

TPN 1

Surgery 1

Multifocal colonisation 1

Severe sepsis 2

CS >3 is at increased risk of IC (8.5%); with sensitivity 77.6% and specificity 66.2%, Positive predictive value 13.8%, and negative predictive value 97.7%. 

Early antifungal therapy may be considered. 

Risks of higher scores: 4 (16.8%); 5 (23.6%). 

Risk is 2.3% only, if score <3 and author concludes that IC is highly improbable in such patients.

http://www.ncbi.nlm.nih.gov/pubmed/19325481

Ventilator management for hypoxemic respiratory failure attributable to H1N1 novel swine origin influenza virus

Ramsey.C.D. et al. Critical Care Medicine 2010: 38

This article looks into patients who develop severe respiratory failure from pandemic Novel H1N1 influenza needing mechanical ventilation.

Mechanical ventilation using lung-protective strategy and previous trials including the ARMA trial/ ARDS Network protocol, were reviewed here: with low tidal volumes (Vt 6ml/kg), plateau pressures (<30 - 35cm H2O), and optimal PEEP aiming SpO2 88-90%.  However, trials are lacking in H1N1 patient groups and the author comments that physician preference on ventilator settings vary.

In some patients with severe persistent hypoxaemia (SpO2 <88-90% with high PEEP and FIO2>0.8), alternative methods of ventilation are discussed, such as high-frequency oscillatory ventilation (HFOV), airway pressure release ventilation, and prone positioning, are reviewed.  At present, data of each of these methods are still very limited thus choice depends on perceived benefit v.s. risks.

The author discouraged the use of NIV, as it was not successful in the majority of severe hypoxia from H1N1 and majority of patients still required mechanical ventilation eventually.  There has been concerns that NIV can increase the risks of H1N1 transmission by generating more aerosol.  It "may be considered for patients with milder disease whose anticipated need for ventilatory support is short".  The author explained the reason for poor results of NIV in critically ill patients may be due to greater proportion of type 1 than type 2 respiratory failure, as NIV demonstrated more consistent benefit in avoiding intubation among patients with hypercapnic as opposed to hypoxaemic respiratory failure (e.g. CCF, COPD exacerbations, pulmonary edema, and immunocompromised).

http://journals.lww.com/ccmjournal/Fulltext/2010/04001/Ventilator_management_for_hypoxemic_respiratory.8.aspx

Change of Blog Title

Previously this blog was dedicated to MRCP exam resources, but it will be converted to a ID blog from today onwards

HLA-DR sub-types and associated autoimmune conditions

HLA DR sub-types
HLA-DR is a major histocompatibility complex, MHC CLass II cell surface receptor, encoded by the human leukocyte antigen complex on chromosome 6.
HLA-DR is important for understanding of graft-versus host disease, organ transplant rejections, and also involved in several autoimmune conditions, disease susceptibility and disease resistance.

HLA-DR molecules are upregulated in response to signalling. In the instance of an infection, the peptide (such as the staphlococcal enterotoxin I peptide show in the two illustrations) is bound into a DR molecule and presented to a few of a great many T-cell receptors found on T-helper cells. These cells then bind to antigens on the surface of B-cells stimulating B-cell proliferation.

References:
HLA types associated with disease: http://en.wikipedia.org/wiki/HLA_DR
British Transplant Society - Publishes guidelines on ethics, criterias, and guidelines on various transplants: http://www.bts.org.uk/

Drugs that cause prolonged QT interval

Drugs commonly asked in MRCP exams:
Quinidine
Erythromycin, clarithromycin
Amiodarone
Sotalol
Tricyclic antidepressants
Chloroquine
Phenothiazine
Non-sedating anti-histamines
Ciprofloxacin

ECG: Causes of Axis Deviations

The normal axis is generally between -30 and +90 degrees.Right axis deviation is defined as axis located between 90 degrees and 180 degrees. Left axis deviation defined as the axis located between -30 degrees and -90 degrees.
The left table summaries the easy way to determine the cardiac axis (http://sitemaker.umich.edu/ecgtutorial/axis)

Left axis deviation
Left bundle branch block
Atrial spetal primum defect
Wolf-parkinsons white disease Type A
Inferior MI
Left anterior hemiblock
(N.B: LVH itself does not cause Left axis deviation)

Right axis deviation
Maybe normal variant in young adults
Right bundle branch block
Acute right heart strain - e.g. PE
Left posterior hemiblock
Right ventricular hypertrophy - e.g. Chronic lung disease +/- pulmonary hypertension
Dextrocardia
Anterolateral Myocardial Infarction
Wolff-Parkinson Wright Syndrome Type B
Atrial septal defect secundum
Severe pulmonary stenosis
Fallot's tretralogy / VSD

Tutorial link: https://courses.stu.qmul.ac.uk/smd/kb/resources/ECG_workshop/session2.htm

Causes of Extrinsic Allergic Alveolitis

Commonly asked extrinsic allergic alveolitis:
Bird fancier's lungs: Parakeet, pigeon, chicken, turkey proteins etc from avian droppings or feathers
Cheese worker's lungs: Penicillum casei
Chemical worker's lung: Isocyanates from polyurethane foam, varnishes, lacquer
Coffee worker's lung: from Coffee bean dust
Compost lung: Aspergillus
Contaminated basement (Sewage): Cephalosporium
Farmer's lung: Thermophilic actinomycetes in mouldy hay, grain, silage
Fish food / meal lung: ? ageng from fish food
Hot tub lung: Cladosporium sp from mold on ceiling
House worker / cleaner: Bacillus subtilis enzymes from detergents
Humidifier or airconditioner lung (Ventilation pneumonitis): due to aureobasidium pullulans, candida albicans, other microorganisms from contaminated water in humidification or forced-air conditioning systems
Lab worker's lung: From rat urine
Lycoperdonosis: due to puffball spores (Lycoperdon)
Farmer's lungs (Micropolyspora faeni)
Malt worker's lung (Aspergillus clavatus or fumigatus)
Maple bark disease: Cryptostroma corticale from maple bark
Miscellaneous Medications lung disease: amiodarone, bleomycin, efaviren, hydralazine, hydroxyurea, isoniazid, methotrexate, paclitaxel, penicillin, procabazine, propranolol, sulfazsalazine
Pituitary snuff taker's lung: due to animal protein from pituitary snuff
Potato riddler's lung: thermophilic actinomycetes, aspergillus from mouldy hay around potatoes)
Sauna taker's lungs: Aureobasidium sp & other organisms from contaminated sauna water
Sausage worker's lung: Penicillium nalgiovense from dry sausages
Tobacco worker's lung: Aspergillus sp from mould on tobacco
Wood worker/ trimmer's lung: due to Rhizopus sp, Mucor Sp, aspergillus sp from contaminated wood dust
Sugarcane or Bagassosis Lung (Thermophilic actinomycetes from 'moldy' sugarcane)
Mushroom worker's lungs (Thermophilic actinomycetes from mushroom compost)
BAL: Shows increased lymphocytes in EAA (Eosinophils not typically elevated in blood).

MRCP Part II - some useful notes

Prolonged APTT
- Heparin
- Anti-phospholipid syndrome
- Haemophilia
* When Factor VIII level normal, this suggests diagnosis of Haemophilia B (IX deficiency). Bleeding time, thrombin time, and PT will be nomral

4 'Ts' for Anterior Mediastinal Mass
- Thymoma
- Teratoma / Germ Cell Tumour
- Thyroid
- Terrible Lymphoma

Causes of TTP - causes
- Infection (e.g. Gastrointestinal, genitourinary sepsis; rocky mountain spotted fever, anthrax)
- Pregnancy, oral contraceptives
- Drugs related (Clopidogrel, ticlopidine, ciclosporin, tacrolimus, quinine, high-dose chemotherapy) possibly due to antibody formation
- Autoimmune / vasculitis (SLE)
- HIV infection
- Metastatic Cancer
- Recent cardiovascular procedures (Catheterisation, angioplasty, vascular bypass, prosthetic heart valve)
- Severe hypertension (>200 / 120 mmHg)

* Aetiology - due to deficiency of ADAMTS 13, a metalloproteinase found in plasma responsible for cleaving the ultra-high molecular weight forms of von Willebrand factor secreted by endothelial cells, contributing to pathogenic platelet aggregation & adhesion.
* Classical manifestations: thrombocytopenia, purpura microantiopathic haemolytic anaemia, neurological findings (confusion, delirium, seizures, hemiparesis, aphasia, malaise, fatigue), renal failure, fever (variably present). Additionals inclue nausea, vomiting, abdominal pain, hypertension, arthalgias, splenomegaly. Mortality high. Severity estimated by degree of anaemia, thrombocytopenia, and LDH.
In contrast to HUS, HUS tends to have higher platelets, more severe renal failure, and neurological manifestations absent.
* Laboratory features:
- Anaemia-mild to very severe
- Thrombocytopenia - invariably present may be very severe
- Blood film - polychromasia (increased young red cells), nucleated red blood cellls
- Raised serum LDH
- Increased indirect (unconjugated) bilirubin
- Reduced haptoglobin
- COOMBs test negative
- ADAMTS 13 activity decreased
- Proteinuria, microscopic haematuria
- Elevated urea, creatinine.
- PT, APTT, fibrinogen - may be normal or mildly abnormal (If major consumption of clotting factors, diagnosis of TTP doubtful; prolonted APTT suggests circulating anticoagulant - lupus anticoagulant or antiphospholipid syndrome)
- ANA - present in ~20 %
- COmplement, platelet associated IgG usually normal

Normal Reference Values of Blood Count Differentials
'Nobody Likes My Education Background'
Neutrophils 60%
Lymphocyes 30%
Myelocytes 6%
Eosinophils 3%
Basophils 1%
(60, 30, 6, 3, 1 %)

Approach to bilateral parotidomegaly

'SLAM' the face

(S)
- Sjogren's disease (Look for dry eyes / month)
- Sarcoidosis (hilar lymphadenopathy, lupus pernio, hepatomegaly)

(L)
- Lymphoma / Leukaemia (anaemia, oral ulcers, bruising, hepatomegaly, splenomegaly, lymphadenopathy)

(A)
- Amyloidosis
- Alcoholic excess (evidence of chronic liver disease, neuropsychiatric manifestations, CAGE questionnaire)

(M)
- Mumps (also examine male genitalia)& many infections (e.g. HIV, EBV, CMV, coxsackie A, influenza, TB)
- Metabolic (starvation / bulimia, hyperlipidaemia) & endocrine (e.g. DM, chronic pancreatitis, acromegaly, hypothyroidism)

Reading of this weekend from ward-round

Few interesting cases were seen in today's ward-round
1. A 60-year old lady who's previously well with only known hypertension was admitted with 1 month's history of progressive bilateral glove-stocking distribution of sensory loss, tingling pain, and proximal / distal muscle weakness. Examination showed wasting of small hand & feet muscles, power 3 in all 4 limbs, generalised hyporeflexia & hypotonia in all 4 limbs, CN VII / XII palsy, and mild bilateral ptosis. Otherwise, ECG, cardiovascular, GI, and urological symptoms were unable. Patient is currently investigated for nerve conduction abnormalities, and herself & family are uncertain about this thus deferred. Possible diagnosis include CIDP v.s. other causes of peripheral sensory-motor polyneuropathy
Reading:
- CIDP on emedicine

2. Found out from renal that statin-induced myopathy is more common in nephrotic syndrome. A young man in his mid-thirities was admitted for headache which turned out to be a cerebral sinus thrombosis. His cholesterol was noted to be very high thus recommended to increase his simvastatin to atorvastatin 80mg. Baseline LFT was normal, however his renal team came by and recommended his dose to be reduced because of increased rhabdomyolysis risk
- Further raeding on FDA

The Lunatic Lament - Story of Syphilis

There was a young man of Back Bay
Who thought syphilis just went away.
And thought that a chancre
Was merely a canker
Acquired in lascivious play.
Now first he got acne vulgaris,
The kind that is rampant in Paris
It covered his skin
From forehead to shin
And now people ask where his hair is.
With symptoms increasing in number,
His aorta's in need of a plumber
His hear is cavorting
His wife is aborting
And now he's acquired a gumma.
Consider his terrible plight -
His eyes won't react to the light
His hands are apraxic.His gait is ataxic.
He's developing gun-barrel sight.
His passions are strong as before
But his penis is flaccid, and sore.
His wife now has tabes
And sabre-shinned babies
She's really worse off than a whore.
There are pains in his belly and knees.
His sphincters have gone by degrees.
Paroxysmal incontinence,
With all its concomitants,
Brings on quite unpredictable pees.
Though treated in every known way,
His spirochetes grow day by day.
He's developed paresis,
Converses with Jesus,
And thinks he's the Queen of the May."

By Isaac Asimov
This poetic manifest reveals the myriad of sickening phenomenon arising from this chronic, indolent infection.

Further reading:
1. Links to emedicine on neurosyphilis

Simple approach to ABG interpretation

Have came across numerous ABG interpretation books, and so far this frame work provides the easiest & fastest application. Adopted from BMJ / TTSH Intensive care handbook.
Hope you may find this helpful too (note inter-personal preferences may vary)

Reading: Procalcitonin

Today I was asked to order procalcitonin test for a patient with suspected infection.
The patient was well, no particular localising symptoms currently. However approximately 2 weeks ago he was treated as probable meningoencephalitis with improvment of headache & diplopia. Lab results returned normal, and an informative lab message showed:

" Procalcitonin: +ve if elevated suggestive of bacterial / parasite / fungal infections. It may not be raised in localised infection, chronic inflammation, or chronic autoimmune diseases. It is not usually elevated in fracture / surgery, and rarely exceeds 5. Procalcitonin begins to rise after onset of infection in 2hrs, peaks in 12 - 24 hours, and 1/2 life 22 - 29 hours".

Attacked reference: wikipedia (inside contain reading links)

Mnemonics - Extensor plantars & absent ankle jerks (PG)

Sex can make those 'F***ing' ankles clutch down (From anonymous author)

Sub-acute combined degeneration of the cord (B12 deficiency)
Cauda equina lesion
Motor neuron disease
Tabes Dorsalis *syphilis*
Frideriech's ataxia
CVA + Diabetes

Menomoics - Autonomic Drugs

Anticholinergic drug side-effects:
"Know the ABCD's of anticholinergic side-effects"
- Anorexia
- Blurred vision
- Constipation / confusion
- Dry mouth / dilated pupils ('ANTI' constriction)
- Sedation / urinary stasis


Cholinergics - "IF you know these, you will be 'LESS DUMB'"
- Lacrimation
- Excitation of nicotinic receptors
- Salvation
- Sweating
- Diarrhoea
- Urination/micturition
- Broncho-constriction
* 'Con' stricts the pupil

Neurology reading of the week: GBS, CVA, Peripheral neuropathy

First day in neurology's encountered with few interesting cases:
- Stroke
- Guillain Barre Syndrome
- Peripheral neuropathy - secondary to amyloidosis

Please click on the links below
1. GBS on eMedicine: See my summarised sheet on google docs
2. Stroke (NEJM Review)
3. Peripheral neuropathy

Presentation of the week - ECG changes in a poisoned patient

This week was asked to prepare a talk on ECG rounds. The topic that I chose was ECG changes in a poisoned patient. It is interesting to know how different drugs (especially anti-arrhythmics) can cause ECG changes and it can help us appreciate the myocardial electrophysiology.
Hope you'll find this helpful.

This Weeks' Reading

The important and interesting theme of this week is deficiency anaemias, something which is frequently encountered in almost any field of medical specialty.
For review:
1. Iron deficiency anaemia
2. B12 and folate deficiency anaemia
3. Interesting read: BMJ editorial on difficulty in distinguishing anaemia of chronic disease from other causes

Summary sheet - Assessment of an acutely poisoned patient

Here's one of my earliest works on making summary sheets, on how to approach a patient with suspected acute poisoning - focusing on history taking and investigations.
Hope this will provide an interesting & useful read.
Comments welcome!

Summary sheet - Polymyalgia Rheumatica

Polymyalgia is one of the most common inflammatory rheumatic disease characterised by pain and stiffness of proximal muscles (especially in the shoulder girdle) in elderly Caucasians and requires long-term treatment with glucocorticoids. There is strong relationship with giant cell arteritis.

This summary sheet provides a quick-glance format for key facts on PMR - its diagnosis, important differentials, and management methods which will be helpful for clinical practice and exam purposes.

Comments welcome.

Reading - Pulmonary Hypertension in Critical Care

Last week's reading was on pulmonary hypertension.
( Roham TZ et al. Managing strategies for patient with pulmonary hyertension in the ICU. Critical Care Medicine 2008)
This paper highlights that pulmonary hypertension and concomitant right ventricular failure present a particularly difficult diagnostic and therapeutic challenge in haemodynamically unstable patients in the ICU.

The categories of underlying aetiology can be sub-divided into those that causes:
1) pulmonary arterial hypertension;
2) associated with significant venous or capillary disease;
3) secondary to left heart disease;
4) Due to lung disease or hypoxaemia
5) due to thrombotic / embolic diseases

There are few important learning messages from this paper:
1) Fluid resuscitation must be carefully initiated because intravascular depletion (hence low pre-load) or over-load can worsen haemodynamics.
2) Mechanical ventilation - especially at high tidal volume and high PEEP can worsen pulmonary hypertension and hence haemodynamics (Target PEEP 5 - 8).
3) Effective treatment relies on ability to accurately identify the underlying cause - from history, thorough examination, and appropriate investigations (ECHO; the gold-standard cardiac catheterisatio; ECG, CXR etc) and address the primary cause.
4) Although studies of inotropes and vasodilators in pulmonary hypertension (especially in ICU) are limited, the use of dobutamine, inhaled nitric oxide, and IV prostacycline have the greatest support in the literature). As for other treatments, relies on good understanding of their pharmacokinetics / dynamics and co-morbidities of the patient being treated.
5) The use of vasopressors should be carefully titrated to their lowest effective dose due to higher risk of side-effects without extra treatment benefits. Such important side-effects include tachycardia, increasing cardiac oxygen demand, profound hypotension, and arrhythmias.

New summary sheet - pulsus paradoxus de-mysti-fied

Been experimenting with my mac's OmniGraffle for building diagrams.
I'm highly impressed with this software's user-friendliness & graphics interface.
Please feel free to have a read, hope you'll find this useful.
Comments welcome!
(Please click my summary sheets column on the right side for more slides)

Ward round 9 Apr 2008 - Ischaemic Colitis

The disease of this week is ischaemic colitis. It is sometimes a challenging disease for physicians to make a correct diagnosis and initiate the definitive treatment - yes, is to transfer the patient to the surgeons STAT.
Textbooks describe the classical features of extremely severe abdominal pain out of proportion with physical examination findings. However patient (especially the elderly, long-standing diabetics) may present with vague or atypical symptoms, and may not mount any inflammatory or febrile response (typically raised CRP, fever). Sometimes may be a patient with long-standing atrial fibrillation or vascular disease who suddenly deteriorates.

My first patient was a gentleman who was admitted to cardiology from A&E for preliminary diagnosis of fast atrial fibrillation & acute pulmonary oedema. His past medical history consists of long-standing diabetes mellitus type II complicated by neuropathy & nephropathy, hypertension, hyperlipidaemia, ischaemic heart disease underwent a bypass many years ago, and chronic atrial fibrillation on warfarin treatment but very good INR control. He has been well otherwise & compliant with his medications until the week before admission when he started to complain of increasing fatigue, breathlessness, and reduced appetite due to a vague 'uncomfortable & sinking feeling' down his lower abdomen. He was haemodynamically stable and afebrile, but breathless at rest with respiratory rate 26 per minute, saturatioin 98% breathing 50% oxygen. Abdominal examination found only mild right upper quadrant and epigastric pain.
His haematology & glucose investigations were unremarkable, however his biochemistry revealed unexplained severe high-anion gap metabolic acidosis, renal & liver failure with markedly raised ALT, AST, Bil, CK, Cr, and mildly raised amylase. It is highly unusual to find such abnormal results in patients purely with cardiac or pulmonary diseases, and we must suspect other underlying causes. Indeed, cardiac enzymes in series showed no rising trend. He was given IV maintenance fluids and empirical antibiotics for possible sepsis. The on-call surgeons were informed to evaluate our patient for suspected acute abdomen especially ischaemic colitis. CT with contrast subsequently confirmed the diagnosis of multiple infarcts in the colon and kidneys. He was sent for urgent laparotomy.

Learning points:

• Suspect fatal ischaemic colitis in the differential diagnosis of abdominal pain - especially in the context of patients with high risk factors.
  
• Cardiac or pulmonary diseases frequently present with 'abdominal discomfort' and may be difficult to distinguish from acute abdominal disease processes.
  
• Severe ischaemic colitis may manifest atypically with minimal abdominal findings.
  
• Clinicians should have a low threshold of suspicion for ischaemic bowel in patients with unexplained severe metabolic acidosis.

Further reading:
1. Early diagnosis of ischaemic colitis in a patient with severe metabolic acidosis.
2. Ischaemic colitis on emedicine

Best wishes for JM's trip to Delhi for his MRCS exams!

He will be leaving from 14 - 21 Apr for his exams, please wish him best of luck!

Please take this moment to read up a few things about Delhi:

1. Malarial prophylaxis
2. FCO information for travelers (India)
3. About Delhi (Lonely Planet)
4. CDC's traveler's health (India)

Interesting readings for next week (Theme: Critical care medicine)
Pulsus Paradoxus (Plus how to measure properly!!)
Management of pulmonary hypertension in critical care
Management of delirium in the ICU and a good quick summary sheet published by its authors
which highlights the diagnosis of delirium requiers
1) acute onset of fluctuating altered mental status &
2) inattention
PLUS
3) disorganised thinking OR 4) Altered level of consciousness.

Homework: please summarise the KEY points each topic to no more than 1 A4 sheet, or 7 minutes short presentation.

Good luck and have a smooooth MRCP exam for all candidates!

The blog master's currently out of service
Be back after examination's over
Wish me (all everyone of you) luck!