Never Look At Things In Isolation

Dear Bloggers

Whenever a set of lab data, radiology or other studies are looked at, they must be looked at in the context of the clinical picture of the patient.

I have often seen residents present a history and physical examination and then go off at a tangent because of the unusual findings of the lab data or the CT findings. The history and physical exam seem to be left behind and unimportant. Why ? In these instances, the history and physical examination have usually not been done adequately as in some peoples opinion, it cannot provide quantitative data that modern medical tests can [I would disagree!] The patient's history is a story of events and intangible to some doctors who need reference ranges and absolute numbers to make a decision e.g. CRP. The physical exam which involves tapping, feeling, probing and listening no longer seems to be as convincing as the BNP of 300. As a result, the history and physical are not being taken seriously enough and left behind in favour of labs, xrays and serum rhubarb.

Moreover, based on CT findings, sometimes residents provide an encyclopedic list of causes, for example, the 10 causes of 'ground glass' shadowing, which has no relevance to the history at all. They compartmentalize their thinking instead of integrating it with the history and physical.

In order to work out a differential diagnosis the doctor needs to keep the thorough history and physical examination in mind as the primary point about which the various tests can then be ordered and interpreted. With a good history and physical, the differential diagnosis can sometimes be whittled down to a few main causes quite quickly thereby avoiding expensive, needless and time wasting tests.

In order to develop better clinical and diagnostic thinking, junior doctors need guidance to understand what they hear in the history and what they see or have missed from the physical exam. Frequently, reviewing the patient on a senior round will reveal the true cause by the words that come from the lips of the patient. What the patient says can change the diagnosis in a second despite the CRP, BNP and LDH. The relevance of the tests is based on what is considered is wrong with the patient. This can only be determined by asking the patient what is wrong with them! It comes back to us asking the right questions ....

Remember, Common things are Common. Common things present Commonly. Hence, when a patient has preceding viral upper respiratory symptoms and then develops bibasal crackles, it is far more likely to be a primary viral or secondary bacterial pneumonia than a drug induced pneumonitis.

Never make a diagnosis purely from a radiographic image without the attached history and physical exam. The features on a CT might be accounted for by many causes and only a history can indicate which cause it is likely to be.

Speaking to, and examining the patient is free. It is immediate and gives much valuable information that cannot be derived from a CT scan or MRI.

Using a textbook to look up the various causes of XYZ disease is encouraged but if the listed cause does not fit the major features of the patient's presenting illness, then it is less likely to be the underlying disease (although not exclusively!)

Therefore, history, physical, lab studies and radiology need to be used to complement eachother and not used in isolation otherwise the patient's true condition gets lost in the confusion. Remember, lab studies and radiology should not be used to make the diagnosis. They should be used to confirm what you are already thinking and to support or refute your differential diagnosis.

Please consider....

Leeches, Placentas and Asthma

Dear Bloggers

I wanted to share a really unusual case with you. This relates to a female patient with many years of chronic asthma who was recently hospitalised in a distant hospital.

She had worsening asthma several days before admission and despite her wheeze improving with steroids and bronchodilator treatment, her SpO2 was low at rest.

Her physical examination was consistent with chronic obstructive lung disease evidenced by 'bounding pulses', a hypertrophied accessory respiratory muscles, tracheal 'tug', a 'barrel chest' and purse-lip respiration. She had mild polyphonic wheeze throughout both lung fields. Legs were mildly oedematous.

There was a concern why the SpO2 was not improving despite effective anti-asthma therapy.

Pulmonary embolism was considered a possibility and her Well's Prediction Score showed moderate risk. V/Q scanning was performed with both ventilation and perfusion parts completed. It revealed multiple pulmonary emboli. Hence, the cause for the low SpO2 had been found which had probably resulted in the exacerbation of asthma in the first place.

Lower limb ultrasonography revealed bilateral DVTs !!

However, not only that, some very strange areas of calcification had been noticed on the plain chest Xray. This is where things get even more interesting. The calcifications were only in the breast tissue and predominantly in the lateral tail of the each breast. It was considered that this might be old age related involutional change with subsequent calcification. However, the tissue affected was quite extensive. Macrocalcification is usually of no consequence. It is the microcalcification and laterality of such findings that make one suspicious of cancer.

When the patient was later asked about the breast abnormalities she revealed that she had received novel asthma treatment some years before which entailed the implantation of placental tissue into her breasts!!! Yes, believe it.

Quite frankly, the thought of leeches comes to mind, used in the dark ages as a treatment for every ailment by the apothocaries of their day. However, on doing further research, and let me tell you it was not so easy, it turns out that the first description on medline of such a technique was in Brazil in 1968. It also became an established alternative treatment in some institutions in Asia with it being reported as a potential therapy for chronic inflammatory disease even up to 20 years ago.

The mechanism with respect to how this novel treatment was supposed to work has not been fully elucidated but suffice it to say, that people underwent such trials of therapy to try and quiesce their chronic inflammatory disease.

This is not standard treatment and not supported by any of the major world respiratory societies. It is considered to be no better than standard pharmacological therapy.

Although this might not be at all relevant to the rest of the Western world, it is worth knowing for doctors practising in Asia who may see unusual areas of calcification in breast or other soft tissues in patients with chronic inflammatory diseases such as asthma, atopic dermatitis or even rheumatoid arthritis. Go back to your patient and ask about the soft tissue problem as they may just tell you they had such a treatment. Of course, common things being common, it is usually involutional change :-)

Just as Plombage treatment for Tuberculosis was commonplace in the UK (insertion of pin-pong balls into the chest of tuberculosis suffers to collapse the lung in the pre-antibiotic era) there are other treatments which have been performed in other countries to treat a variety of diseases. Placental tissue implantation for treating asthma is one of those interesting facets of medicine that one never expects to see. It makes medicine ever more exciting for me.

This is a very good example of why evidence based medical practise needs to be applied when considering investigation and treatment of patients. Without rigorous analysis of existing or new therapies and applying the use of the evidence to every day patient scenarios, we might still be giving patients potentially inefficacious treatments.

Now, where did I leave those leeches.....?

Prof Stein, Rheumatology and My Spin On Things

Dear Bloggers

Professor Stein, Rheumatologist, University of Florida, is well known to Japan and he has kindly commented on January's case. I would normally publish such comments as additions to the published cases but I think that Prof Stein's comments being so important deserve their very own spot on the blog.

Here are Prof Stein's comments below:

1. Pt's response to PSL was dramatic with decrease in her pains and increase in her activity level.

2. The PSL dramatic response represents a theraputic diagnosis, most consistent with PMR/GCA.

3. The American College of Rheumatology list 5 criteria for the diagnosis of Giant Cell Arteritis: 1) age of onset >/ 50 years, 2) New headache, 3) Temporal artery abnormality, 4) Elevated ESR and 5) Abnormal artery biopsy. The presence of any 3 has a sensitivity of 93% and a specificity of 91%.

4. This patient had 3 of these criteria in addition to the dramatic response to PSL.

5. The neuropathy the patient had has been rarely described in GCA as well as rare cases of associated nephritis

6. There is no evidence for a primary nephropathy in the patient, none for MPA; P-ANCA is non-specific inflammatory marker.

7. The case details omitted her now-presumed very limited pre-PSL daily activity level

8. Most of the suggested diagnostic tests were unnecessary and only added to her hospital costs; every patient considered for long term PSL must have a Tb evaluation.

9. In my experience Japanese physicians are not well informed about PMR/GCA; there is a great need for more rheumatologists in Japan.

I would like to comment as well.

Tuberculosis

Tuberculosis evaluation is very important in Japan. The rate of new Tb cases in Japan (a few years ago) was about 1 in 5,000 population compared to the UK which is about 1 in 8,000 new cases. The levels have apparently been decreasing in Japan whereas in the UK, they had been increasing but are now somewhat more stable. The reason for the rise in the UK is likely to be due to the large immigrant population. Japan has a more homogeneous population than the UK and fewer immigrants, although the level of Tb appears to be higher. I am uncertain why there is a higher level of Tb infection in Japan especially when there is an effective health care system in place. Perhaps others would like to comment?

Hence, as Prof Stein has mentioned, ruling out Tb prior to starting the steroids is a must. It must be done properly. Chest radiography, sputum microscopy and culture. Checking the PPD skin test is useful because a positive reaction means antibiotic therapy. Other tests can be done but which have various problems with specificity and sensitivity with attendant higher cost implications which include mycobacterial PCR and interferon testing.

Prof Stein also mentioned about over testing in this patient. He is correct. With a patient such as this, doppler ultrasonography of the temporal arteries and subsequent urgent biopsy would be necessary. Ensuring that Tb investigations were under way, steroids would need to be started urgently to avoid potential blindness if giant cell arteritis was really suspected. If Tb was also suspected e.g. cough, weight loss, sputum and CXR consistent with the diagnosis, many physicians would also commence anti-Tb therapy whilst awaiting the confirmatory Tb results.

Moreover, waiting for a biopsy result prior to starting steroid therapy is not an option in a case where GCA is high up in the differential diagnosis. In fact, steroids are advocated to be started before the biopsy if there is any potential for delay in obtaining a specimen. There is often a concern about being 100% correct about the diagnosis before starting treatments which, if delayed, can have serious adverse consequences on patients. Remember that delaying starting steroids in GCA can result in blindness. It is not something just written in the textbooks -- I have seen such a case.

Start Treatment as Soon As Deemed Clinically Necessary

Never delay life saving / organ saving treatments for fear of not wanting to be wrong. It is acceptable to give a patient with suspected heart failure the additional steroids and beta-stimulant therapy if they have obvious wheeze especially if they have a history of smoking or asthma and a physical examination consistent for both CHF and COPD. Don't just put it down to the cardiac wheeze of CHF as you will more often be wrong than right. Sometimes, patients have heart failure and COPD together. It comes down to history, physical examination, basic lab tests and basic radiology.

In another example, it is necessary to give broadspectrum antibiotics in patients with symptoms and signs of sepsis despite the lab data showing no rise in the CRP and absence of fever. Patients don't write the textbooks and the absence of some features does not preclude the condition existing. I know of one such case where a junior doctor did not appreciate the patient's low blood pressure and absence of fever despite the history of recurrent UTIs. The patient clearly had features of sepsis but the CRP was normal. However, blood cultures grew gram negative bacilli. Sepsis in the elderly can sometimes trick the doctor as it can present with so few signs, and is often a Baptism of Fire for the junior doctor.

Don't just rely on lab studies, they can sometimes be misleading. Put the pieces of the puzzle together to make the likeliest picture. Treat the serious problems first. Treatment should be based on what is likely and what cannot be immediately excluded quickly. Starting life saving treatment should be immediate and not delayed by the doctor wanting to be 100% right with the diagnosis e.g. suspected PE but unconfirmed by CT -- start heparin as soon as the diagnosis is strongly considered. Remember, the patient comes first and not the doctor's pride.

We cannot be 100% right all of the time. No one will think bad of you for treating all potential conditions that can cause the presenting symptoms and signs etc. It is a matter of protecting the patient from further harm from their condition.

The Balance of Tests Versus Treatments

It can be difficult to get the balance right between instituting tests and starting treatments. Over investigating patients does increase costs for the patient and at the same time, it seems to give physicians the confidence that certain diseases do not exist. I only wish the latter was true, but it is not. Not all tests are 100% accurate and in order to understand the investigation of a disease one needs to understand the limitation of the various lab studies and not over rely on them as is commonly done. In my experience, doctors often order a battery of tests without even considering why the tests are performed to use the 'labo' as a 'screening tool'. In my opinion, this is completely unnecessary, a waste of resources and in some cases it does not add to the identification of the problem. Tests should be ordered depending on what is considered to be wrong with the patient rather than what is done as a battery of tests.

For example, C-reactive protein is useful in only a minority of conditions such as some connective tissue diseases but in other respects it is unnecessary and expensive. I do not advocate its routine measurement. The measurement of LDH is again wasteful and lacks sensitivity and specificity. Yes, it can be measured in lymphoma where is can sometimes be very high. However, many, many other conditions also elevate the LDH level and it is somewhat like the CRP as it does not add to your diagnostic plan. Funnily, I have often heard of doctors saying ' Follow the CRP ' or ' Follow the CT '. I prefer to follow the patient.

If the diagnosis is still not clear after receiving back the information from the first set of tests, then proceeding with other specific tests can be justified. However, performing tests that simply reconfirm what you already know is pointless and wasteful e.g. chest CT scanning when a pneumonia has already been confirmed by history, physical and chest radiography. To say that it gives detailed images is correct but it DOES NOT usually add anything to diagnosis or treatment. Of course, if after a few days of treatment the fever is still swinging or the pneumonia clears to leave a mass then tumour or abscess can be investigated by CT. However, most pneumonias do not require a chest CT to confirm the diagnosis. History should guide you e.g. previous Tb, unsafe sexual practises, heavy smoker etc. Without history, we are lost and end up ordering the 'pan-man scan'.

In actual fact, a good history and thorough physical exam can tell you if there is pneumonia or effusion. Many UK GPs diagnose pneumonia and do not do blood tests (unless necessary) and may only send the patient to the hospital for a chest Xray (if deemed necessary). They start treatment based on the history and physical. Only the sick patients get referred for inpatient treatment.

Cultural Medical Practise

When we consider the practise of medicine we must also consider the cultural practises rather than just a rigid template of 'this is the way we do it in this country', because it may not be translatable in another culture.

For example, in Japan, there is much choice of where you can go to see a doctor. Basically, you can turn up in any hospital you like and see any doctor you like who specialises in the condition you think you have. This is not the case in the UK NHS system whereby you are usually allocated a GP servicing your local community and you are referred to the local hospital for outpatient consultations by your GP. You cannot just turn up in the outpatients. Of course, ER (A&E) attendances do not require an appointment in the UK. However, choice is lacking in the UK system.

Japanese hospitals are a mixture of public and private compared to the British which is predominantly public.

Because patients have so much choice in Japan, the adverse impact is that some ask for many tests and indeed, some expect the battery of blood tests, CT and MRI even if they are not always medically justified. Sometimes, the doctor can feel pressurised into performing unnecessary tests. Of course, patients are quite rightly concerned about potential types of illness but it is the role of the doctor to be the gate-keeper to stop patients having unnecessary annual CT scans and serum rhubarb evaluations to rule out the rarest of conditions. Remember, common things are common. Rule out the common things before trying to identify the zebra amongst the drove of horses.

Luckily, with the advent of the DPC system, which limits the amount paid for a particular condition, it will help to reduce overall costs to the Japanese Government for health care and also to the patient and their family who need to pay 30% of the overall medical costs. Therefore, over investigating patients is no longer a realistic option and doctors need to become more reliant on clinical skill with history taking and physical examination techniques. This can only be done through effective training at university and in the post-graduate residency training schemes.

Need for More Rheumatologists

Prof Stein also quite rightly says there should be more rheumatologists in Japan. As with palliative care and oncology specialists, rheumatologists are few and far between.

Many patients with rheumatology problems are seen by orthopedic doctors. Training as a rheumatologist is a medical sub-specialty rather than a surgical specialty. Such study requires an in-depth knowledge about systemic disease requiring many years of training in internal medicine. Hence, although orthopedic doctors do a sterling job to try and treat patients with connective tissue disease, they should be really seen by the rheumatology specialists for fine tuning of the diagnosis and therapeutics.

Unfortunately, drugs tend to be used at lower dosages in Japan. For example, methotrexate is commonly given at 5mg per week for rheumatoid arthritis whereas most UK / American rheumatologists would titrate the dose to the maximum tolerated to relieve the symptoms and destructive changes e.g. 15mg/week. It is not correct to think that just because a patient has a connective tissue disease e.g. rheumatoid arthritis, that they should expect to develop debilitating disease because that is the expected natural history of the condition. If DMARDs are going to be used, then they should be used according to evidence rather than eminence.

Summary

There are many differences between the Japanese system and the UK-USA systems.

It is clear to me that doctors need to have more skill in history taking and physical examination. More urgency needs to be taken over starting life / organ saving therapies rather than trying to be 100% correct at the outset with the attendant wait resulting in potential and real detriment of the patient. Patient's should not be over investigated and tests should be based on what is considered to be wrong with the patient and what serious diseases need to be ruled out quickly e.g. Tb. Treatments should be provided based on relevant evidence from history, physical, labs and radiology etc, to cover the various potential serious conditions e.g. heparin in suspected (unconfirmed) PE.

I come back to the use of the problem list and grouping technique, as taught by Prof Stein in his Problem Oriented System, in order to decide what are the likely causes of the various symtpoms and signs. By using this process, junior doctors can understand the various problems which aide them to make a diagnostic and therapeutic plan for patients.

Many thanks to Professor Stein for his very necessary comments.

Answer To January's Case

Dear Bloggers

Thank you for waiting for the answer to January's case. I was informed that it might have been a bit too difficult. However, residents still need to be able to understand all the problems in any patient case in order to construct a logical plan of further investigations and / or treatment.

Although this patient had many problems, it is not a rare occurrence for patients of advanced age to accrue disease which muddies the water when trying to make a diagnosis for a main problem; hence Ockham vs Hickham (see below). This is where clinical acumen, logical testing and using the mental probability assessment of common things being common and uncommon things being uncommon comes into play.

At the end of the day, it is sometimes necessary to obtain a biopsy to get the diagnosis - as Prof Lawrence Tierney says "Tissue is the issue". Let's see whether that was necessary in this case.

Professor Masami Matsumura who is well known to this blog for his excellence in problem solving has again astounded me with his opinion on this very difficult case.

We have to consider the contrast between Occam’s Razor and Hickham’s Dictum because this patient is a high aged woman. Did she have SINGLE disease or MULTIPLE diseases? She had multiple processes as follows;
1. Chronic inflammatory condition including neoplastic disease
2. Neuropathy
3. Masses in mouth and submucosa in upper GI tract
4. Heart failure
5. Emphysema

It is impossible to interpret ALL problems within SINGLE disorder. Firstly, I would focus on the chronic inflammatory condition and neuropathy.

Questions 1) Please make a full list of ALL the patient's problems and make assessments according to diagnostic grouping.

I listed problems as follows;
#1 Fever
#2 Weight Loss
#3 Sweats (suspect dehydration)
#4 Fatigue
#5 Normocytic anemia
#6 High ESR
#7 Foot numbness (L4, 5, and S1)
#8 Leg Pain (disappeared)
#9 Unusual scalp feeling
#10 Shoulder Pain (for several years)
#11 Fixed 'shotty' nodes in the groins
#12 Mass in oral cavity
#13 Submucosal mass in upper GI tract
#14 Dyspnea
#15 Tachypnea
#16 Hypoxia
#17 Tachycardia, Atrial Fibrillation
#18 Effusions
#19 Wet early crackles
#20 Cardiomegaly
#21 Pitting edema > 40 seconds
#22 Hypertension
#23 Quinke's sign
#24 ex-smoker
#25 Hyper-expanded chest
#26 Fibrotic change in the lung
#27 Elevated ALP
#28 Impaired Glucose Tolerance
#29 Insomnia
#30 Cataracts *I can’t interpret following finding correctly; Trachea .. with two-fingers appliable to the suprasternal notch I guess this finding was caused by emphysema. (correct - tracheal tug)

ASSESSMENT:
Chronic inflammatory condition including infection, neoplastic, or autoimmune disease should be considered from #1 Fever, #2 Weight Loss, #3 Sweats, #4 Fatigue, #5 Normocytic anemia, and #6 High ESR. This patient disclosed B symptom. Vasculitides, lymphoma, tuberculosis (TB), or infective endocarditis (IE) is suspected.
Interpretation of #7 Foot numbness is peripheral neuropathy. In this case, mononeuritis multiplex or polyneuropathy should be considered. Most likely etiology is vasculitides, especially polyarteritis nodosa. Microscopic polyangiitis is one of candidate. However, kidney function was normal and normal urinalysis except trace of protein was observed.
Vasculitides including polyarteritis nodosa is suspected from #8 Leg Pain. Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are suspected from #9 Unusual scalp feeling and #10 Shoulder Pain.
Lymphoma or another malignant tumor has to be ruled out because she disclosed #11 Fixed 'shotty' nodes in the groins, #12 Mass in oral cavity, and #13 Submucosal mass in upper GI tract.

Multiple myeloma is not candidate in this case. I would introduce one pearl of Dr. Tierney. “The three no’s of myeloma: no FEVER, no splenomegaly, no elevated ALP”

Heart failure is apparent because of #14 Dyspnea, #15 Tachypnea, #16 Hypoxia, #17 Tachycardia, Af, #18 Effusions, #19 Wet early crackles, #20 Cardiomegaly, and #21 Pitting edema >40 seconds. Her pulse character was consistent with atrial fibrillation (Af). WET EARLY CRACKLES at the base means early sign of heart failure. Pitting edema >40 seconds was derived from heart failure too. If patient's serum albumin is low, pit recovery time will be within 40 seconds with one exception if there is long standing pitting edema caused by low serum albumin. Long history of edema will cause tissue fibrosis.

Quinke's sign doesn’t mean high specificity of aortic regurgitation (Ar). However, aortic regurgitation due to hypertension is suspected. Of course IE must be ruled out. Interpretation of #24 Ex-smoker, #25 Hyper-expanded chest, and #26 Fibrotic change in the lung are emphysema.

My differential diagnoses are as follows:
Vascular: Less likely Infection: IE, TB (TB is always differentiated in feverish patient in Japan) Neoplastic: Lymphoma, Paraneoplastic syndrome
Autoimmune: Polyarteritis nodosa, Microscopic polyangiitis, PMR/GCA, Still’s disease, SLE, Wegener’s glanulomatosis, Sarcoidosis, Churg-Strauss syndrome
Toxic: Less likely
Metabolic: Diabetes Trauma/Degenerative: Less likely
Iatrogenic: Less likely Idiopathic: Less likely
Congenital: Less likely plus she had Af, HTN, Ar, heart failure, and emphysema.

2) What other laboratory study or studies would you consider performing in this patient?

I would order the following tests; LDH, blood glucose, HbA1C, ferritin, P-ANCA, C-ANCA, and ANA Three sets of blood cultures Cardiac echo to confirm vegetation and kinetics of heart muscle Sputum acid fast stain and cultures for TB Angiogram of celiac, mesenteric, and renal arteries Biopsy of sural nerve and mass in mouth if possible Submucosal mass in upper GI tract should be carefully monitored ALP should be monitored

3) What is your top suspected diagnosis for the MAIN problem in this patient and how would you establish the definitive diagnosis?

In Japan, microscopic polyangiitis is not so rare. Polyarteritis nodosa and Wegener’s glanulomatosis are rare in Japan. But I highly suspect polyarteritis nodosa in this case. I refer one of criteria of Polyarteritis Nodosa. She might have three criteria (bold & italics: 1, 4, and 5). 1990 Criteria For the Classification of Polyarteritis Nodosa

1. Weight loss; 4 kg Loss of 4 kg or more of body weight since illness began, not due to dieting or other factors

2. Livedo reticularis Mottled reticular pattern over the skin or portions of the extremities or torso

3. Testicular pain or tenderness Pain or tenderness of the testicles, not due to infection, trauma, or other causes

4. Myalgias, weakness or leg tenderness Diffuse myalgias (excluding shoulder and hip girdle) or weakness of muscles or tenderness of leg muscles

5. Mononeuropathy or polyneuropathy Development of mononeuropathy, multiple mononeuropathys, or polyneuropathy

6. Diastolic BP >90 mm Hg Development of hypertension with diastolic BP higher than 90 mm Hg

7. Elevated BUN or creatinine Elevation of BUN >40 mg/dl or creatinine >1.5 mg/dl, not due to dehydration or obstruction

8. Hepatitis B virus Presenece of hepatitis B surface antigen or antibody in serum

9. Arteriographic abnormality Arteriogram showing aneurysms or occlusions of the visceral arteries, not due to arteriosclerosis, fibromuscular dysplasia, or other noninflammatory causes

10. Biopsy of small or medium-sized artery containing PMN Histologic changes showing the presence of granulocytes or granulocytes and mononuclear leukocytes in the artery wall

For classification purposes, a patient shall be said to have polyarteritis nodosa if at least 3 of these 10 criteria are present. The presence of any 3 or more criteria yields a sensitivity of 82.2% and a specificicy of 86.6%. BP = blood pressure; BUN = blood urea nitrogen; PMN = polymorphonuclear neutrophils. Lightfoot RW Jr, Michel BA, Bloch DA, Hunder GG, Zvaifler NJ, McShane DJ, et al. The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. Arthritis Rheum 1990;33:1088---93.

PMR/GCA is suspected too. However, these diseases don’t disclose neuropathy. Churg-Strauss syndrome is not likely because she didn’t have history of asthma. SLE and Still’s disease are not highly likely.

Lymphoma is possible. IE and TB have to be ruled out.

Angiogram of celiac, mesenteric, and renal arteries and/or biopsy of sural nerve are needed to establish the diagnosis. I hope my hypothesis is correct. If it is correct, management of disease will be tough. Her cardiac and lung functions are not good. Opportunistic infection should be CAREFULLY monitored.

Professor Gerald Stein has also provided another excellent assessment below:

1. Problem List
# Fever
# Sweats
# Fatigue
# Weight Loss
# Numbness of her feet
# Dyspnoea
# Initial headache
# Leg Pain
# Shoulder Pain
# HT
# DM
# lymphadenopathy
# tachycardia(?AF)
# Quinke's sign(AR)
# ^JVP
# leg edema
# tachypnea
# dullness lung bases
# bibasilar crackles
# decreased light touch feet
# anemia
# ^ALP
# ^ESR large
# 2x3 cm mass arising from the hard palate
# chest xp bilat effusions ^ heart shadow
# EGD submucosal mass

1. Assessment 1.Temporal arteritis/GCA evolving from PMR, ? associated with CA S/O CA[gastric lesions CA, MALT]
2. Heart failure, ? IHD, D, AR[?HT related, R/O Lues]
3. DM sensory neuropathy
4. HT
5. Anemia, ? to GCA, R/O GI bleed
6. Gastric Mass, R/O CA, etc
7. Palate mass, R/O CA

2. Anemia studies-Fe, smear, ferritin, etc Biopsies as above+ Temporal Artery Bx, BS, HAIc, ECG, cardiac ECHO, Lues tests,

3. see assessment> Temporal Artery Bx Response to Prednisone 40 mg/d; Aspirin for AF with PPI; Tb eval before Prednisone

Professor Gurpreet Dhaliwal, University of San Francisco has kindly joined this month's opinion on the case. He has also raised some very important and interesting points. Thanks!

I have departed from the suggested format in order to share my general impressions and leading diagnoses:
This 80 year old woman has a subacute inflammatory illness of unknown etiology. Her age increases susceptibility to cancer and infection over other classes of disease (e.g., rheumatologic) and her lifelong smoking substantially increases her probability of cancer

Peripheral neuropathy (with an unusual migratory component) is described. Given her age, I wonder more about paraneoplastic neuropathy than autoimmune conditions, although intermittent arterial ischemia of the limb or the nerves of the limb caused by vasculitis, could mimic these symptoms. The transient leg pain (among other things) makes me wonder about this. Infections are infrequently implicated in peripheral neuropathy.

Generalized lymphadenopathy has a large differential diagnosis including infection (mycobacterial, fungal, viral), malignancy (lymphoma, metastatic carcinoma), and autoimmunity (sarcoid, lupus).

A hard palate mass could be a clue to a disease with a predilection for the hard palate (e.g., Wegeners, Behcets), but as described, it sounds like a torus palatinus

Many features point to new CHF (history of hypertension, new atrial fibrillation, dyspnea, hypoxia, crackles, effusions). I note that the JVP was normal, but this can be a challenging physical exam finding for even experienced practioners. Quinke’s sign is typically associated with chronic AI, but I suspect the specificity is not 100%. The murmur of AI was not detected, it is often quite soft and relies on proper patient positioning.

Her marked normocytic anemia is most likely anemia of chronic inflammatory disease. Bone marrow involvement must be considered with an elevated alkaline phosphatase and normal GGT (suggesting a bone source of alkaline phosphatase), but the other cell lines are not involved. If the alkaline phosphatase elevation was of the liver variety (with no other abnormal liver function tests), then an infiltrative disease of the liver, such as lymphoma or tuberculosis, would merit even stronger consideration.

Finally, there is a mention of a submucosal mass of OGD (EGD), but the location is not noted. Certainly a lymphoma or carcinoma may cause this, perhaps more likely than any infection (e.g., TB) or rheumatologic condition.

The ESR of > 100 must be noted, but it lacks specificity other than confirming the general impression of inflammation -- of unknown etiology in this case.

Here are my hypotheses:



INFECTION: In general, I do not suspect infection here. Other than her age, there is no reason to suspect a chronic indolent infection such as mycobacteria or fungus. Endocarditis would be a very reasonable explanation, although she failed to improve on broad spectrum antibiotics, so SBE seems less unlikely.



AUTOIMMUNITY: The unusual scalp sensation, marked anemia, and ESR > 100 are consistent with giant cell arteritis (temporal arteritis / polymyalgia rheumatica / takayasu’s). GCA is frequent cause of FUO in the elderly and is increasingly recognized as affecting the aorta (e.g., majority of patients with biopsy proven TA have aortic involvement on PET scan.) If so, perhaps this would explain both a sign of aortic insufficiency and limb ischemia. This would be determined by temporal artery biopsy. The lymphadenopathy and oesophageal/gastric mass would be unusual. The features of other vasculitides



MALIGNANCY: The submucosal EGD mass, lymphadenopathy, age, and smoking history make cancers a primary concern. This could represent disseminated lung cancer (hiding in the reported fibrotic area), gastric cancer (based on the EGD mass), or lymphoma. I am most concerned about malignancy, although it is not clear why she has developed atrial fibrillation / heart failure at the same time.

I would pursue the following tests:
Echo to assess for CHF and aortic valve integrity
Biopsy and culture of neck lymph node and EGD mass
If all of the above are unrevealing, I would consider temporal artery biopsy.

The above assessments were very similar to my own and in view of the extensive detail therein, I feel that I cannot surpass them. Hence, I will not go into raptures of my own assessment this month but simply explain what happened next :-)

As Prof Matsumura mentioned above, microscopic polyangiitis (MPA) is not so rare in Japan whereas PAN and Wegener's granulomatosis are rare. However, the MPO-ANCA was found to be slightly positive and hepatitis B & C viruses were negative thereby, in my own opinion, elevating the diagnosis for MPA despite the absence of renal impairment.

However, in MPA renal dysfunction is almost universal when there is the onset of vasculitis. These findings are dichotymous. Hence, the only way to get the diagnosis was to get tissue (that being the issue!) and ruling out infection from Tb and infective endocarditis and excluding malignancy such as a disseminated GI cancer and lymphoma.

In the end, the patient underwent biopsy of the sural nerve which showed a leukocytoclastic vasculitis. There were no granulomata present.

The histopathology final report was consistent with Polyarteritis Nodosum rather than microscopic polyangiitis.

This is in keeping with the opinion of Professor Matsumura but somewhat surprising in view of the elevated MPO-ANCA level.

Tests for endocarditis and tuberculosis were negative.

Repeat gastroscopy revealed ulceration with no malignancy present.

The lesion identified in the hard palate was indeed Torus Palatinus ; a benign lesion of no signficance.

The patient had confirmed heart failure and and aortic regurgitation was confirmed by cardiac echo. This was effectively controlled with standard therapy.

Steroid treatment was commenced (with PPI cover) and there was resolution of most symptoms. Particularly striking was the improvement in malaise, appetite and energy levels (all steroid effects). The patient started walking from being bed bound just a few days earlier and continues to improve on 40mg Prednisolone /day.

For the manifestations, investigations and treatment of PAN, please see UpToDate 16.3

I would like to take this opportunity to thank all of the doctors who took part in January's case responses. The case answer has been posted late for several reasons, but mainly that I have been too busy ! :-o

Stay tuned for more discussions and cases in the future!

Please accept my apologies for the errors in spacing in this article. This seems to be due to a recent error in the Blogger programme.

A Word Of Caution in Overdose

Dear Bloggers

Today I want to touch on the topic of drug overdose.

This is a common medical problem. Overdoses should always be taken seriously and investigated and treated vigorously in order to avoid morbidity and mortality.

Although the textbooks tell us about individual drug overdoses, the predicted symptoms, signs, investigations and treatments, they do little to tell us how to manage mixed overdoses. The reason is, patients can take several drugs in combination at various different doses and with drugs that have different rates of release, absorption, volume of distribution and elimination kinetics. This is a total minefield for the physician.

In terms of working out what you are dealing with and what to do, always use a toxicology reference or database. A very good one in the UK is called ToxBase, although Skyscape.com also has several toxicology titles available for PDAs which give standard and sound advice. Checking UpToDate is also advantageous in such circumstances and of course the standard textbooks.

Charcoal

Although charcoal therapy is commonly advised to be given if the overdose is within an hour of ingestion, it does not mean that charcoal should not be given if the OD it past one hour. Quite the contrary. As some drugs are in a slow-release formulation, it may take several hours for the full drug dose to be released and absorbed, thereby resulting in toxicity and delayed elimination. Hence, even if the OD is known to be past one hour or the time of ingestion is unknown, charcoal should still be given EXCEPT if there is evidence of bowel perforation or obstruction. Impaired consciousness is a contraindication to charcoal ONLY UNTIL the patient has had their airway secured with an endotracheal tube. Multiple doses of charcoal might need to be given rather than just the customary one dose.

Serum and Urine Drug Screening

Patients should be checked for several compounds either by serum or urine examination including NSAIDs, acetaminophen (paracetamol [UK]), benzodiazepines, lithium, neuroleptics, tricyclics, amphetamines, canabinoids, opiates/opioids, ethylene glycol, methanol, ethanol etc..

ABG

Arterial blood gas should also be taken to assess for acidosis or alkalosis - these may be clues indicating the type of overdose. A metabolic acidosis with a raised anion gap might suggest alcohol, methanol, ethylene glycol in the context of an overdose. A respiratory alkalosis might suggest early NSAID overdose which may later change to a metabolic acidosis.

Anion Gap and Osmolar Gap

Check the Anion Gap [Na -(Cl + HCO3)]; >16 is + but truly significant is >25.

Causes of Raised Anion Gap Acidosis remember KUSSMAL.

K etoacidosis
U remia
S alicylates
S epsis
M ethanol / ethylene glycol
A lcohol
L actic acidosis

Osmolar Gap = Measured Osmolality - Calculated Osmolality;
Calculated Osm = 2 x Na + Urea + Glucose

Normal mosm/kg. It is raised in poisoning from methanol, ethylene glycol etc.

ECG

Check an ECG -- look for the evidence of acquired Long QT. Patients are at risk of Torsade de Pointes if the QT is significantly prolonged and such patients need to be in an ICU monitored bed. Remember in such cases, magnesium, defibrillation and atrial/ventricular overdrive pacing are the treatment of choice for drug induced Torsade and NOT other antiarrhythmic agents that can make the situation worse!

Radiology

Check an Xray of the chest -- look for potential aspiration and pulmonary oedema. Sometimes tablets are aspirated and cause lung collapse and chemical damage. The CXR or a chest CT may show the tablet(s) and of course, emergency bronchoscopy for removal!

Abdominal Xray can be performed which may reveal radio-opaque drugs such as heavy metals, iodinated compounds, lithium, enteric coated tablets and NSAIDs etc..

CT head scanning should be performed in the unconscious patient to exclude cerebral oedema or another cause for the unconsciousness e.g. sub-dural haemorrhage.

Infection Screening

In those circumstances when the patient has a fever, unconsciousness and features of infection, a lumbar puncture should be performed to rule out meningitis (after CT head indicates no raised intracranial pressure).

Check blood, urine and sputum cultures as well.

Aide mèmoire and trial of treatment

In the unconscious patient, make sure to check pupillary size. Small 'pin-point' pupils and a low respiratory rate can signify opiate overdose. Be sure to proceed with a trial of naloxone to see if it rouses the unconscious patient. Don't wait for the toxicology report as the patient might have already stopped breathing. Naloxone is safe and it is rewarding to see a completely unconscious patient wake within seconds of the antidote only to complain to you 'Why did you wake me up!', and not thank you for saving their life :-(

Conversely, dilated pupils might signify an SSRI, Cocaine, Amphetamine OD etc...

50 of 50

Moreover, remember that NSAIDs, insulin and oral diabetes agents, to mention just a few, in overdose can commonly result in hypoglycaemia. Serum and CSF glucose concentrations DO NOT correlate well so remember to give the 50ml of 50% dextrose even if the capillary bedside glucose appears normal.

Acetaminophen OD and its treatment

Some hospitals are not able to do rapid acetaminophen levels -- they may take a week to come back from the reference lab! Hence, in those institutions, when it is not known what the patient has ingested and it is not possible to test for the drug or that it takes longer to get the result than would be clinically useful, the antidote to acetaminophen should be administered which can be oral methionine or N-acetylcystine (i.v.).

In view that it might take 48 hours for a significant acetaminophen OD to become clinically detectable with hepatic necrosis and fulminant liver failure, as physicians, we cannot take chances by ruling out that the patient has not taken an acetaminophen OD even if it is considered to be an uncommon occurrence. Remember, any prescribed drug or over the counter drug is a potential poison in overdose. However, the drugs commonly ingested in OD and which can be fatal, should be investigated and treated. If unable to be rapidly tested for, then consider to treat anyway! Remember that liver and renal function tests plus, particularly ABG and INR testing are important clinically and prognostically in liver failure from acetaminophen overdose. Prolongation of the INR, hypoglycaemia, renal failure and acidaemia portend a poor prognosis (King's Criteria).

Don't take risks. Don't take chances. Investigate and treat accordingly.

Further Care

Remember that when the patient gets better you should keep them under close supervision to avoid repeated intentional harm within the hospital. High risk patients are especially vulnerable. This means 24 hour supervision and no less.

Psychiatrists

Psychiatric input is necessary as soon as they are over the acute phase of the attempted suicide. DO NOT JUST SEND THEM HOME. Psychiatric assessment and / or further treatment may be necessary. Not all suicidal patients need to be admitted for psychiatric assessment. This can be done as an outpatient if the patient is deemed low risk for further suicide attempts.

For a fuller explanations on the various drug overdoses please see the references mentioned above or any major text on the subject.

Please consider :-)

January's Case

Dear Bloggers

Here is an anonymised case for January. Please have a go! Drop me your opinions on the case and we can see if your are right!

This 80 year old female presented with a two month history of the following symptoms:

• Fever
• Sweats
• Fatigue
• Weight Loss
• Numbness of her feet
• Dyspnoea
  

The symptoms started abruptly two months before with onset of fever. The patient took her own temperature which was about 38 degrees Celsius. She was unable to say if there was day-night variation in the fever. There were no associated chills or rigors.

The patient noticed sweating, albeit intermittently, and only when she had the fever. She denied drenching night sweats.

The fatigue was apparent from the outset and continued throughout the two months prior to and during the admission to hospital. There was associated weight loss noticed by the patient with her clothes feeling larger on her and her wedding ring becoming loose.

The numbness occurred initially in both her hands and feet and became constant in the latter and disappeared in the former after several weeks. On admission, she complained of only foot numbness up to the ankle area.

The patient also noticed worsening dyspnoea especially on exertion. She denied orthopnea, cough, sputum, wheeze, haemoptysis.

On further questioning she admitted to further symptoms of

• Initial headache: this headache occurred at the beginning of the symptom complex. She was unable to denote the severity on the pain scale. There was no throbbing nature to the pain but she did admit to an unusual feeling on her scalp. There was no visual disturbance, no jaw or tongue claudication.
• Leg Pain: she admitted to initial upper leg pain which soon disappeared. There was no complaint of this on admission. The patient did not complain of weakness.
• Shoulder Pain: this was apparently a long standing problem going back several years and had not worsened prior to or during the admission.

The patient had initially been admitted to a local clinic for investigation and treatment. It was suspected that the patient had an "infection" and she was commenced on piperacillin and sulbactam without improvement of symptoms or resolution of the fever. She was referred to another hospital for further investigation.

Previous Medical History

• Hypertension
• Impaired Glucose Tolerance
• Insomnia
  

Medication

• Rampiril 10mg/day
• Diazepam 5mg once nocte

Family History

Nothing relevant

Social History & Habits

She lived with her family. Her husband was deceased. She was an ex-smoker although only recently having given up.
She did not consume alcohol and had never received a blood transfusion, tattoos or needle stick injury.

She had no pets and had never travelled abroad.

Review of Body Systems (questions to patient only; no physical exam at this stage)

CVS: No palpitations, chest pain, leg pain on walking
RESP: as above. No sinus pain, no epistaxis,
ABDO: No abdominal pain or swelling. No nausea, vomiting, diarrhoea, constipation, malena, haematochezia or jaundice.
MUSC-SKEL: No muscle or bone pain. No joint swelling or morning stiffness.
URO-GEN: No urinary symptoms or vaginal discharge. No post-menopausal bleeding. No change in the colour of her urine.
CNS-PNS: No visual disturbance, no hearing disturbance, no speech disturbance. No weakness or other new sensory disturbances. No seizures in the past.
ENDO: No polyuria, polydipsia. No alteration in hot or cold tolerance. No history of renal stones.
SKIN: No complaints.

On Examination

General: She appeared chronically unwell. She was alert, conversant although unclear with precise history. She appeared sweaty. Conjunctivae appeared pale. No cyanosis.

Lymph Nodes: Non-tender lymphadenopathy was present at both jugulodigastric nodes and small, fixed 'shotty' nodes in the groins.

Mouth: large, 2x3 cm mass arising from the hard palate. Pink colour, smooth, no ulceration or bleeding. Patient denied trauma to the identified area.

CVS: Pulse 140 per minute, irregulary irregular with low volume quality. It was not possible to ascertain collapse or slow rising nature. BP 120/70mmHg in the right arm in the supine position. Sitting BP was not performed. JVP was 5cm and with an irregular peak in keeping with the irregular pulse. Quinke's sign was positive.
Heart sounds 1 & 2 were present with no obvious 3rd or 4th sound. No murmur evident. There were no carotid bruits.
Legs revealed pitting oedema >40 seconds in the posterior ankle region. There was no clinical evidence of DVT.

RESP: Resp Rate 26 per minute and regular. SpO2 93% on ambient room air. Trachea central with two-fingers appliable to the suprasternal notch. The chest was mildly hyper-expanded, dull to percussion bilaterally at the bases with 'wet' early crackles.

ABDO: Soft, flat, non-tender. No hepatosplenomegaly, no ascites. Bowel sounds normal. Renal angles revealed no tenderness. Rectal exam - no masses and blood was absent.

MUSC-SKEL: No joint pain or swelling on passive movement in any of the large or small joints. Muscles revealed no tenderness.

PNS:
Tone: Normal throughout in upper and lower limbs.
Power: Normal 5/5 throughout
Reflexes: Normal throughout in upper and lower limbs.
Coordination: Within normal limits
Sensation: Indeterminate change in hands for light touch; loss of light touch in soles and dorsum of both feet. Temperature, nociception, vibration not measured.
Babinski: negative bilaterally (flexor plantar)

CNS:
II: bilateral cataracts, normal constriction to light and accommodation. Visual fields difficult to accurately determine but grossly within normal limits for age.
III / IV / VI: Within normal limits
V: Motor and Sensory within normal limits
VII / VIII / IX / X / XI / XII: Within normal limits

No cerebellar signs.

Lab Studies

Hb 8.6, WBC 6.6, MCV 92, Plts 24.6 (normal). AST / ALT / gamma-GT / Bilirubin within normal limits. ALP 432 (ALP 1 iso-enzyme elevated). BUN and Creatinine within normal limits. Creatinine Kinase (CK) within normal limits.

Serum electrophoresis normal. Bence Jones protein not tested.

Coagulation normal. Urinalysis normal except for trace of protein.

ESR >100mm/hr.

HBV and HCV negative.

Chest Xray: Bilateral small effusions. Hyper-expansion. Cardiac silhouette slightly enlarged. No mass lesions or bone erosions.

CT of Chest and Abdomen: Bilateral effusions. A small area of fibrotic change in the right anterior lung. Normal amount of pericardial fluid. No mass lesion identified. Liver normal looking. Spleen normal size. Kidneys - normal texture, no hydronephrosis. Pancreas appeared normal.

Oesophagogastroduodenoscopy (OGD): revealed a submucosal mass; no biopsy had been taken on initial inspection.

Questions

1) Please make a full list of ALL the patient's problems and make assessments according to diagnostic grouping.

2) What other laboratory study or studies would you consider performing in this patient?

3) What is your top suspected diagnosis for the MAIN problem in this patient and how would you establish the definitive diagnosis?

The answer to this case will be available in the near future. Please send in your responses and get published online. Anonymous replies are welcome too!

Ever Heard of Evernote?

Dear Bloggers

Today, I thought I would introduce you to something truly unique and ultra-portable!

It is the new internet and phone based application called Evernote.

This application is superb for keeping notes wherever you are. You can type your notes on your PC/Mac, iPhone or PocketPC (Windows Mobile) which then automatically get uploaded to your account in the web-cloud. These notes can then be viewed or edited on any of the above communication platforms.

What actually sets this application far apart from the others e.g. Google notes or MobileMe, is that the application is able to search your entire documents for words, and that includes words within pictures!!! Say for example, you have written information within a picture, Evernote will find it! Even photographs can be searched for words. Great!

You can also upload voice notes as an additional feature.

This is great for physicians who want to look up some information from their notes on the go or take a quick note in a lecture or just to upload their thoughts on conditions or for reminders.

Having tried this application, I can highly recommend it. It is easy to use, has the same features across various platforms, is quick to find information and immediately backs up information. Perfect!

The application is FREE! Yes, FREE! Upload information per month is 40 megabytes but for those with more gelt, $45 per year gets you a monthly 500 megabyte upload quantity. You decide.

If you are interested in checking this out, click on the following link.

A Different Way To Perform Male Urinary Catheterisation

Dear Bloggers

Welcome to 2009 !!

Today I would like to discuss about, what I regard as the most appropriate technique for male urinary catheterisation.

Catheterisation of the male bladder is in my opinion a difficult technique to get right. Why you may ask [with a smirk and a frown]? Because it is not taken seriously enough by medical personnel. The disregard of proper aseptic technique can lead to hospital acquired infections with its attendant morbidity and potential mortality. If it were a central venous line insertion, the patient would have their skin sterilised with alcohol / iodine and draped before entering the vascular space. With the bladder however, there seems to be a more relaxed, less serious approach to the appropriate use of aseptic technique. This is clearly not ideal and needs attention.

I have seen one worrisome technique which involves using long sterile forceps to introduce the catheter into the urethra without using full aseptic procedures. This has the inherent risk of introducing infection and is prone to technical failure.

I would therefore like to introduce you to a different technique which uses full aseptic technique and is easier to perform and is used as the norm in the UK system.

Step 1: Explain to the patient what you are going to do. You should never start any technique without obtaining informed consent from the patient. Do not take it for granted that the patient will say yes to any procedure. In an unconscious patient, catheterisation should be considered in the context of it being in their best interest for purposes of monitoring urine output and relieving retention.

Step 2: In a private examination area, fully expose the penis. NOW WASH YOUR HANDS USING STERILISING DETERGENT. Set up a sterile procedure pack on your bedside trolley. On the sterile procedure area, ensure you have a kidney-dish, a fluid receptacle, cotton wool, sterile gel, one or two 10ml syringes, saline and / or antiseptic fluid, an appropriately sized male urinary catheter and sterile gloves of appropriate size. A 10 or 12 French size Foley catheter is usually appropriate for most males. Put on the sterile gloves and then drape the inguinal area with a sterile paper sheet with a hole made in the centre to allow the penis to be placed through it. Some kits come with the hole already made.

Ensure a catheter bag is prepared in advance for collecting the urine.

Step 3: Prepare sterile saline or antiseptic liquid in the small container on your sterile procedure pack. Open the tip of the catheter pack with only the tip of the catheter allowed to protrude and replace it on the sterile tray. Open a new sterile gel used only for catheterisation. Do not use one previously opened as there is a risk of contamination.

UK hospitals have sealed Lignocaine gel specially prepared for catheterisation. This type of gel reduces the pain associated with the procedure. Load 10ml of sterile water or saline into a disposable 10ml syringe for eventual injection into the balloon port of the catheter.

Step 4: With your non-dominant hand, in this example the left hand, retract the foreskin of the patient (this is now a dirty hand and should never be used to handle aseptic utensils after this). With the clean dominant (right) hand pick up a cotton wool ball soaked in saline/disinfectant and wipe the tip of the penis to remove any debris. Repeat this with a clean cotton wall ball. Remember to throw your dirty disposables in a bin and never put them back on your sterile tray! Some doctors double glove the clean hand in advance and remove the top glove to ensure the remaining glove is definitely sterile.

Step 5: Now pull the penis vertically until straight and squeeze the gel down the external os into the urethra via the syringe. Aim to instill approximately 10ml of gel. Gently squeeze the outer corona of the penis to close the external os for about 2 minutes to stop the gel coming out and to give time for the lignocaine to anaesthetise the urethra. If the plain gel comes in a tube, use the additional 10ml syringe and pre-load it with the gel before instilling it down the male urethra.

Step 6: Now the tricky bit. Pick up the opened catheter with your aseptic dominant (right) hand and place the tip into the external os of the penis and release the external pressure on the corona whilst still holding the penis straight and vertical. Extend the catheter slowly down the urethra by pushing forwards and withdrawing the catheter from its protective sheath.

The catheter may need to be moved backwards and forwards as the gel does not always coat the entire urethra.

When the prostate is reached there will be some resistance. Push slightly more on the catheter until the resistance is overcome. Sometimes the catheter needs to be twisted in a corkscrew motion to achieve entry past the prostate.

NEVER FORCE THE CATHETER as it can create a false track inside the prostate. If in trouble call your senior doctor or the on-call urologist for assistance as soon as possible.

Sometimes using a larger French size catheter can achieve entry where smaller diameter catheters have failed.

Another technique is to use a stiffer catheter made from silicon and plastic polymer to achieve entry.

Step 7: Advance the catheter to its full length and place the open end in the disposable kidney-shaped dish to collect any escaping urine. Inject 10ml slowly into the balloon port. If the patient experiences pain then STOP as the tip of he catheter may still be in the distal urethra. Advance the catheter further forwards and then retry.

All being well, the balloon should inflate without resistance. Now pull the catheter gently until you feel mild resistance (the balloon should be at the neck of the bladder). The urine should now be flowing out of the catheter's open end and attach it to the prepared catheter bag.

Step 8: Remember to retract the foreskin to avoid acute paraphimosis. Wipe up any excess gel and remove the drapes and re-gown the patient's lower region.

Step 9: Remember to measure the residual volume of urine, which will then allow you to ascertain the initial output in one hour. [After 1 hour, output equals total volume minus the residual volume; this needs to be followed hourly if clinically desirable]. Aim to attach the catheter bag to a dedicated stand or bedside structure so that the lower tip of the bag avoids touching the floor as it is otherwise a risk for contamination and hospital acquired infection. Ensure the bag lies at a level lower than the patient's bladder so that urine can actively drain away.

You're done! Once well practised, this technique should take 5-10 minutes to do (without complication) but has inherent measures in place to try and prevent infection through avoiding unnecessary contamination and uses a sterile gloved hand to do the manoeuvres rather than forceps.

Please consider this as an alternative technique for your patients.

As additional advice, in those patients with haematuria or heavy urine contamination, catheters can become blocked and if this does occur, you will hopefully get a call from the friendly ward nurse informing you that the patient's urine output has dropped or stopped. Please see my last blog about the assessment of reduced urine output. Any patient with a Foley catheter in situ who has a significant drop in urine output and who has no obvious reason for this should have catheter occlusion considered as a potential cause.

One way to tell is to instill 50ml of sterile water down the free end of the catheter and then to suck back on the plunger to see if fluid comes back out. If you get free flow of urine back then the catheter is unblocked. If nothing comes back then a new catheter should be placed instead. If only the water comes back then there may be a problem occurring higher up in the urinary system to account for the lack of draining urine or there may be an intra-renal or pre-renal cause that will need further assessment.

This set of instructions is only but a guide. At all times clinical judgment should be used when performing any invasive technique and the ultimate responsibility is yours. If in doubt, always discuss matters with your senior doctors before performing any invasive technique with which you have suboptimal experience and / or confidence. If you are in doubt, it is better to defer performing the technique yourself to someone who can do it (and preferably they can teach you how to do it at the same time). I do not subscribe to the adage of 'see one, do one, teach one' as it is prone to failure and teaching of poor technique. As a friend once said to me 'it is not practise that makes perfect but it is perfect practise that makes perfect'. Now I do subscribe to that !

Please consider....

The Knee Jerk Response To Urine Output

Dear Bloggers

Today I want to have a final rant for 2008!

The rant is about the sometimes observed 'knee jerk reaction' that one sees by inexperienced physicians when the patient's urine output is low and furosemide is given to 'make the patient pee'.

Low urine output means assessment of the cause rather than just pumping diuretic into the patient which may makes matters far worse.

For example, low urine output might mean the patient has a urinary tract obstruction (post-renal), hypoperfusion from hypovolaemia (pre-renal) or intrinsic renal failure from an insult (e.g. ATN).

When one assesses this problem, take further history from the patient. They may tell you that they have trouble passing urine and / or a painful lower abdomen or distension suggestive of urinary tract outflow obstruction. On the other hand, it may be more clear whereby bleeding may have already been diagnosed e.g. upper GI haemorrhage. The patient might be taking nephrotoxic drugs, have sepsis or a local glomerulonephritis. The causes of pre -, intra-, and post-renal impairment are too many to discuss on this blog.

However, in patients who have low urine output, suffice it to say that the physical examination is of prime importance in addition to looking at the sequential laboratory studies, to identify the cause and follow the progression or improvement respectively.

When one examines the patient, start generally and then focus on the individual systems.

• Does the patient look ill? Confused? Sweaty?
• Then look at the hands! Check for those splinter haemorrhages as endocarditis can cause renal failure. Assess for encephalopathy by checking for flap (asterixis) -renal failure can cause flap the same as for liver failure and CO2 retention.
• Check the pulse - is there a tachycardia?
• Assess the fingers. Are they cold suggestive of vasoconstriction?
• Check the blood pressure - is there hypotension?
• Check the skin turgor on the dorsum of the hand / arm / inner thigh? Think to yourself, could this be dehydration?
• Feel for axillary sweaty - this is lost in dehydration
• Look at the conjunctivae to assess for anaemia - patient could be in a hypovolaemic state from bleeding
  
• Check the tongue & mucosa for dryness - a sign of possible dehydration
• Check the JVP - is it raised ? (could be a sign of CHF) or is there guttering (sign of hypovolaemia).
• Check the respiratory rate and rhythm - Is there Kussmul respiration / Air hunger -- can be seen in metabolic acidosis (renal failure), bleeding etc
• Listen to the chest - is there a focus of infection? Are there effusions / crepitations of heart failure?
• Listen to the heart for murmurs, added sounds
• Inspect the abdomen - is there a focus of infection? Are there signs of liver disease ? (liver failure can result in renal failure - hepatorenal syndrome)
• Are the renal angles tender ? (pyelonephritis / pyonephrosis)
  
• Can you feel a distended bladder in the lower abdomen? It is dull to percussion and when pressed and the patient may say they want to pass urine.
• Are there any abdominal bruits? Might suggest renal artery stenosis or a dissection if there is a compatible history
• Is there pitting oedema of the lower limbs? Might suggest liver disease, nephrotic syndrome, cardiac failure, venous obstruction, lymphatic obstruction or a low protein state.
• Look at the urine in the catheter bag (if one has been placed already) - measure the total amount since it was last checked. Look at the colour - is it dark suggestive of concentrated urine (hypovolaemia) or straw coloured in the euvolaemic state. Is it orange - bilirubin or red - bloody?
• Consider a rectal examination to look for GI bleeding and / or an enlarged prostate gland and / or malignancy.
  

The above features can help you to understand whether the patient is hypovolaemic, euvolaemic or hypervolaemic and a clue of the potential cause.

A patient with a hypovolaemic state (cold hands/feet, tachycardia, decreased skin turgor, hypotension, no axillary sweating, low JVP, dry tongue, dark small volume urine) should be given fluid to replenish the circulation and NOT diuretics! The reason for the decreased urine output is a result of ADH release and upregulation of the renin-angiotensin-aldosterone (RAS) system to retain water to maintain the circulation. Using a diuretic can result in worsening renal failure at the detriment of the patient. Yes, the frusemide splurge may make the doctor and nurses feel better that the patient is passing some more urine but the worst will be yet to come with the incipient renal failure.

A patient with an hypervolaemic state e.g. CHF, can have a low urine output as a result of vasoconstriction because of low cardiac output. Frank Starling forces denote that when the myocardium is overstretched (as in systolic heart failure), the muscles contracts less. Hence, to maintain blood pressure, the peripheral resistance increases which can reduce kidney perfusion and cause reduced urine output. Moreover, such patients also can have a high RAS activity worsening matters. In this situation, blocking angiotensin 2 production or activity (ACE-I / ARB) and aldosterone (with spironolactone) plus off-loading the circulation with a loop diuretic are the mainstay of conservative therapy. In this situation, it can improve the urine output quite appropriately.
A hypervolaemic state is demonstrated by symptoms and / or signs of CHF, liver disease, nephrosis etc. One might see a raised JVP, normal skin turgor, oedema around the eyes (nephrosis usually), pitting oedema of the extremities, abdominal ascites etc.

In a euvolaemic state, none of the adverse features seen in either the hypovolaemic or hypervolaemic states should be seen. One should also consider other causes such as:

• Drugs: e.g. morphine (causes release of ADH and direct urinary retention)
• Endocrine: SIADH
• Metabolic: hypoxaemia (increases ADH secretion)
• Misc: Pain and nausea (both increase ADH secretion)
• Urological: outflow obstruction e.g. prostatic hypertrophy with acute retention, bilateral ureteric obstruction from malignancy

Please refer to a standard textbook for the extensive list of causes. The above are merely examples to consider.

Hence, when assessing a basic thing such as urine output, we come back to basics. History and physical examination.

Looking at the laboratory studies can tell us further information e.g. worsening BUN and creatinine levels. Such lab results with an examination consistent with hypovolaemia tells us that the patient needs more fluid and not diuretics.

Normal laboratory studies but an examination consistent with hypovolaemia and low urine output should still prompt us to give more fluid.

On the other hand, a hypervolaemic patient may have laboratory studies indicating liver disease, cardiac failure (raised BNP) etc. These can guide us to a more precise diagnosis. Sometimes, such patients have existing renal dysfunction and so the cautious and judicious use of loop diuretics can be considered.

Remember that in acute renal failure, a meta-analysis of 9 studies in adults with ensuing or actual acute renal failure showed no benefit with the use of frusemide and in fact, caused ototoxicity (BMJ 2006;333:420-3)

If you are concerned about causing heart failure (a topic I have touched upon several times in the past) a fluid challenge of 250ml 5% dextrose can be given stat. One can then reassess the circulation for blood pressure, rise in the JVP (or CVP), pulmonary crepitations and improvement of urine output.

If urinary retention is considered, a renal tract ultrasound is quick, non-invasive and provides valuable information. Please don't jump for the contrast CT as contrast nephropathy can ensue.

Examination of the urine may reveal white cells, red cells, casts etc, that can point you towards an intrinsic renal problem rather than pre- or post- renal cause.

So, in summary, please fully assess your patients. Don't go for the easy option of giving frusemide to increase the urine output as you may just end up with a worse problem ! Get out of the habit of knee jerk frusemide and use the grey matter you have been given instead.

Please consider.....