Depression in the elderly #GPEP1

We recently had a talk on depression in the elderly. I Thought I would try to compress it down into a couple of pages for those who are interested.

Forgive me the length and the clichéd photos.

First rates:

Old people have lots of friends who die, they are lonely, they can’t do the things they used to. Therefor they must be more depressed, right?

Yes and no:

Rates of depression are stable at around 3% of the more youthful and the older population. This is when using the DSMIV criteria.

But if you take 100 older folks and put them in front of a psychiatrist they will usually have 10 pts who they feel are depressed tho many wont meet the criteria. What is it the specialists are seeing that makes them feel this patient is depressed?

Most would argue they are seeing suffering, burden of disease. The illness effect upon them, chronic pain, reduction in function, social withdrawal often mimic depression. Will discuss this a little more later.

This is reflected in the statistics of depression in multiple settings: Those at home have the lowest rates, It increases across the spectrum from rest homes in independent units, to rest home inpatients to the final and highest risk group those in hospital.

In fact if you follow the elderly around a time of loss most do very well exactly the same as younger people with a period of grief and slow improvement. A patient was quoted as saying “I suffer aloneness, I am no depressed” Which is an interesting sentiment and worth thinking about when dealing with these patients.

 

So onto the diagnosis, this can be difficult as depression is a line on a spectrum.

As with any disease we need to decide where this is.

Most diseases we make the diagnosis on one major factor: Impairment of function does it cross this line.

We then add in some time factor : Duration or persistence.

Then we look at specific symptoms, we may count them (4-5 of 9)

We may look for special symptoms, psychosis, suicidal thoughts

We consider cognitive effects, slow thinking

physical effects, psychomotor retardation or agitation, sleep, weight gain/loss.

another common symptom is a spiritual one, those who are believers in a  certain faith often feel separated from god. those who are atheists or agnostic may explain they feel somehow disconnected from a greater purpose.

In short we are looking for Aaron Becks triad. (Nothing to do with JVPs and low BP) Of negative thoughts of self, others and the future. In short, Im miserable, other people are crap and its never going to get any better.

This gives us our diagnosis of depression from there we have some subtypes.

Bipolar: sometimes high, hypomanic/manic
Anxious: anxiety predominant symptoms
Agitated: irritable, psychomotor agitation, pacing, fidgeting.
Psychotic: psychotic symptoms.

In New Zealand we often hear about the high rates of suicide in our youth esp our maori and pacific youth. But the highest rates of all groups are white males over 80 years. There are not many of them but their numbers are growing rapidly. Sadly this is considered one of the harder groups to engage with. They have the highest rate of completed suicide, they chose lethal methods. 

Illness and depression: as i mentioned earlier in the elderly there is an interplay between physical illness and their depression.

This interplay is  bidirectional. We know diabetics BSLs go haywire if their mood is low.

Some very interesting studies have been done on mortality and morbidity post myocardial infarction and the patients mood. A diagnosis of depression at the time of MI increases your mortality 2-3 fold over the following year! This is provided you survive the first 3 days. Having low mood doesn’t seem to effect your massive aneurysmal wall rupturing but does increase your PVC rate.

Another illness that needs to be considered is the possibility that their mood disturbance is a first symptom of a neurodegenerative disease. In some studies upwards of 20% of patients who develop Parkinson’s disease are diagnosed the year before with depression. This is before any outward signs are present. It has been shown to proceed dementia and often complicates the diagnosis.

Another important discussion is around the patients alcohol intake. We know that alcohol is a depressant and the best treatment for low mood in the context of abuse is to reduce intake. The elderly are quiet drinkers, occult drinkers. Very different to teenagers who get pissed punch someone or crash a car. It’s a good thing to question each time you seen an older person with falls. But why do they hide it so much? Simply society is much more accepting of young idiots getting drunk than old folks who should know better. I wonder if the phrase “Dulce et decorum est pro-ethanol morti? ” is pretty close to the truth.

So what should we do with the elderly who can’t stop drinking? we accept that younger alcoholics cant and work on harm minimization. They get their vitamins and thiamine. Which leads to how much to give via what route? Oral thiamine is so poorly absorbed I believe the correct molar dosage is a shitload. You need to give it IM. We happily give B12 to patients and other meds but need to make this change.

Ok after that sidetrack

We have made our diagnosis what tests should we order?

Tests fall into two groups, those that we can treat and hope their depression improves and those for ongoing treatment.

The treatable ones, B12 and Folate go together often low in the elderly good to check and be sure. Thyroid function (TSH) might see the odd hypothroid and depression presentation in your career. Calcium, we all remember the, stones, groans and psychic moans.

then some for the future: ECG, you need a baseline for comparison, most of our drugs are going to have some QT concerns. LFTs not a bad test for the future again can be changed by our meds.

Treatment:

First agent: This is really a bit of a toss-up. Tricyclic antidepressants are better in a trial setting but SSRIs do better in the real world. This really comes down to compliance which is most effected by side effects.

SSRI win out for me, As I havent had a trip to Hawaii for a conference im still using citalopram over escitalopram but some would argue the decreased risk of QT mischief is worth the increased cost.

Second line I would use TCA and specifically Nortiptyline, reasonable in regard to H/L does take a some fiddling to get the dosage up but has milder withdrawal than others

Third option in NZ is Venlafaxine, you can have it funded if you have trialed both SSRI and TCA. worth reminding people of the withdrawal and the need for a washout period before starting this.

Other therapies.

Something for anxiety and or sleep?

New Zealand has seen a massive surge in the use of Quetiapine. Many call it Vitamin Q with tongue firmly in cheek. It is good for ruminant thoughts and is sedating. But its no better than Benzos for falls risk, No antipsychotic ever made anyone smarter and many dont tolerate its side effects.

“Grandmas little helper” Benzos have gone well out of fashion in the elderly, people are concerned about dependence and risks of well just about everything being increased. Our psychogeriatricain was arguing that they are very well known drugs, we know the side effects, we know most people dont become dependant and that using them for a short period they are very effective for sleep/sedation.

 

Finally we discussed when to refer to tertiary services.

We came up with 3 reasons:

1. Assessment, you just aint sure of the diagnosis, would like a second opinion.

2. Treatment knowledge/Actual therapy, do you not know what to do next or can you not access it.

3. Access to rehab, one of the most common referrals, the loss of function from their illness is enough to require inpatient or outpatient rehabilitation and increased services.

So there is my wall of text on depression in the elderly if you made it to here well done, will try make the format more digestible in the future.

 

References:

Depression post myocardial infarction: http://circ.ahajournals.org/content/91/4/999.short and http://www.psychosomaticmedicine.org/content/66/6/814.short

 

The Unofficial Bone Shop House Surgeons Survival Guide

During my time in Christchurch I worked in the bone shop,

There was a book/PDF that was distributed which helped many of us early on and serves as a great refresher.  In the interests of #FOAMed I thought I should share a couple of links.

Before doing this I checked with Chris Cresswell ( @emtutor ) who wrote the original! which has since been edited. Its full of practical advice and worth a read. The word doc is good to have on your smart device of choice. As with all of these sorta things, doesn’t replace your local advice/protocols, If it seems odd check something else!

I decided I should put the first page up so you can get the flavour and practical nature of it.

viva la #FOAMed

  • The Unofficial Bone Shop House Surgeons Survival Guide
  • Welcome to The Bone Shop
  • Don’t try and read the whole of this guide.  Read the introductory paragraphs, then before you see each patient look at the X-rays, read any previous notes, referral, consultant film reading, look the injury up in this guide, talk to the nurse, look up McCrae and decide what you’re going to do before the patient comes in.
  • Everyone expects you to know nothing.  The nurses know everything and will give you lots of help.
  •  For the first few weeks you will feel you are superfluous and are slowing things down.

 

  • It’s not your fault the waiting room is full: the head of department acknowledges there is a staff shortage and inadequate orientation.
  • What is acceptable angulation/displacement? A lot of the time we don’t know.  If you can get anyone to define “acceptable” for various injuries please add it to this guideline

 

  • Consider non accidental injuries.  Have a low threshold for discussing with paeds reg.
  • Consider bone strengthening medication for post menopausal women and men over 65 with #s.  We can prescribe calcium (eg calcium carbonate 1.5g bd) and vitamin D (eg calciferol 1.25mg daily for 7 days then once a month).  They need to see their GP to obtain bisphosphonates (eg alendronate).
  • Analgesia/sedation:Bier’s blocks may be performed by an anaesthetic SHO (or above) and are available in “working hours” (d/w duty anaesthetist), or you can do them yourselves provided there are 2 of you – one to do block and manage the cuff – and the other to do the manipulation.  You need to have attended a teaching session on Bier’s block by Anaesthetists prior to being able to perform the blocks yourselves.We do not currently use ketamine/propofol/etomidate in Bone Shop.

 

  • One alternative is using haematoma blocks (including selected ankles that need manipulating), regional nerve blocks, IV fentanyl eg 100µg, IV midazolam eg 1mg (or 0.5mg in the elderly) and Entonox.
  • For kids consider using 2µg/kg intranasal fentanyl as analgesia.
  • Consider using the 70% nitrous mixer from ED if you’ve been trained to use it. Remember to turn it off.

 

Links:

Text copy on EM tutorials:

http://www.emergency-medicine-tutorials.org/Home/surgical/orthopaedics-and-hands/ed-orthopaedic-fracture-clinic-guidelines

Dropbox for word download.

https://www.dropbox.com/s/t0igcoih2jbhjgz/The%20Unofficial%20Bone%20Shop%20House%20Surgeons%20Survival%20Guide.docx

 

 

#FOAMed

 

Thoughts on Poker and Medicine

While listening to Simon Carley on risk at #SMACC2013 I had one of those thoughts.

Medicine is more like poker than a lottery.

First I hope any serious poker players can forgive my over simplifications of a wonderful game. I also hope everyone can forgive my extreme stretching of this metaphor.

 

So why is medicine like a poker game?
It’s about prediction and probabilities, sometimes we are accurate and can be quite sure of ourselves but sometimes we get caught out by a surprise card or unlikely diagnosis.

In emergency medicine we often concern ourselves with the dangerous diagnoses, most poker players consider these options and likelihood their opponent will draw them. If you have played against a person/disease many times you can be more confident that you will be able to  judge their strength or recognise their tells.

In both luck plays a role that both doctors and card players are uncomfortable with. Everyone will have a “bad beat” where you are confident that you have the correct response or reaction but something unlikely/rare happens and you lose. This leads to both groups having superstitions and sayings which are similar.

“You play the man not his cards” sounds a lot like “It matters more which patient has the disease than which disease the patient has”

Like poker, medicine can be played at a number of stakes. Is it a life and death situation or just trying to rid someone of a minor irritation.

Texas Holdem

Medicine is most like Texas holdem (heads up).
I’ll explain why with an explanation of how it’s played and the similarities.

Heads up poker is played against one other person. You have your own cards and there are a number of communal cards which you make your best hand from. In this way a poker hand reflects a medical consultation information is slowly revealed and you attempt to gauge your position and certainty.

The rounds are as follows:

Pocket cards:

File:Pair of Aces.jpg

Firstly you are given two cards, an initial impression. You know from a glance if this patient is sick or not. Your system 1 is firing on all cylinders. You may get an instant diagnosis from the end of the bed, ?pocket Aces.

But you also know when you don’t have an idea. You know it will be hard or perhaps you just don’t want to play this hand.

Everyone makes their bets, some times this is easy. The patient is dry start some fluids, pain relief/Raise. Other times you don’t want to initiate much treatment until you have more information/Check.
In medicine you can’t really fold. unless you take the next chart (don’t be this person).

 The flop:

Three cards are turned over. This equates well with the history, it’s where the money is. Based on what you know about the patient and you impression most times you can have a very good idea about how you are placed. But there is some difficulty. Many diseases are difficult to tease out, are you being bluffed by your opponent. Previous experience with the opponent/disease can help you here. Are they likely to play passively or do they often show their strength?

The Turn:

This is the physical exam. (might be giving too much credit here)

This adds to what has come before. The reaction to this, tells/focal signs often increase your confidence in your diagnosis. But again it can leave you feeling unsure. But often it makes minimal difference, your impression can remain unchanged based on presence or absence of some signs. This is also often when you take a little time to think of any other possibilities you may have forgotten, a few extra questions whilst examining.

 The River:

 The investigations. Everything is back, all the information you are going to get is there.

This confirms or refutes your previous thoughts. You often know where you stand are you “the nuts” ?

But everything can change and swing based on one investigation/the final card. Is the bloody D-dimer positive? 

Then the final rounds of betting, are you all in for one diagnosis or are you still unsure of yourself? Often you know your badly placed (Pt is sick) but you can’t be certain of why.

 Finally the hands are revealed; in medicine like in poker you may never find out if you were right. Your opponent may never reveal their cards.

The best you can hope for is to learn from your mistakes, minimise your losses and be ready to play again.

But remember, in the end the house always wins.

 

 

I digress. Blister Beetles!

Recently had a patient pitch up after an afternoon in the garden, she had been gardening when a bug fell down her top and she squished it and carried on gardening. After an hour or so she noticed the area stinging and checked to find a red area. She had a shower and noticed that the stinging was  a little less but when the area blistered she came to the acute clinic.

Pt was happy to share her story but as she had squished the bug on her “Décolletage” she wasnt so keen to have photos taken and shared with the word. So here is a nice US Marine with a blistering injury from a bug:

blister beetle

So Blisters from Beetles:

There are a few types of bugs that cause blistering eruptions and/or dermatitis.

The most widely know are the Meloidae family from which comes the Spanish Fly. The Meloidae are known as blister beetles in many parts of the world. They are so named because they cause a painful blistering eruption within 2-3hours of exposure.

A few blister beetles:

 

Black_blister_beetleLytta-vesicatoria spanish fly

 

 

Paederus beetles also cause a dermatosis and blistering but this generally occurs 24-72 hours after exposure. These have been having a recent resurgence in research as they are common in Iraq and have caused outbreaks in a number of American Army camps there. These lead to the 2007 report attached.

Paederus_rove_beetles,_showing_size

Depending where you are in the world these beetles have a variety of illnesses named after them. If you are in Africa and squish one and wipe you face you may contract “Nairobi eye or Kenya fly dermatitis” In India Paederus beetles also cause seasonal outbreaks. 

 In New Zealand Oedemeerida (the false blister beetles) are more common and famously caused an outbreak of blisters in soldiers near Auckland  in the 1980s. 74 Soldiers erupted with dermatitis after night exercises. An epidemiologists dream! Investigation lead them to the Thelyphassa lineata (Fabricius) after ruling out a number of other causes. Its ability to produce the reaction was tested on some willing participants (Medical Students)

So how do these little bugs cause such a wonderful bullous eruption and dermatitis. Both Melodiae and Oedemeerida produce Cantharidin which is a potent blistering agent. The male beetles produce all of the cantharidin and gift some to the females after mating. Male beetles secrete cantharidin from their joints so they dont need to be squashed to cause exposure and dermatitis. Wonderfully we dont know the exact biomechanical means of its production within the beetles. I also dont like to tell people where presents for my SO come from. Cantharidin is a very potent toxin with a LD50 of 0.5mg per Kg in humans. The most common animals poisoned by blister beetles are horses as the beetles commonly live in alfalfa and other green feed.

Paederus beetles have a more complex but better understood production of their toxin Pederin. The females in this case have  a symbiotic relationship with a Pseudomonas which produces the toxin. This is in turn deposited into the eggs and larvae. Further toxin is ingested when beetles eat the shell of their egg after hatching. Paederus dermatitis takes longer to reveal itself often 24 hours before discolouration which then goes on to blister.

Treatment: The best treatment is prevention, simple things such as removing beetles rather than squashing them. One prevention in Iraq was moving the night guards further from the light towers which attracted the beetles. With Cantharadin patient will usually have washed themselves as the burning is an early symptom. With Paederus they often only present well after the toxin has been spread and absorbed, these patients show classical Kissing signs where skin surfaces have touched eg: elbow flexures. Once the dermatitis is established the best treatment is topical steroids but if the case is severe oral antihistimines and even antibiotics have some benefit.

Blister beetles have been used for centuries and despite their toxicity people took them as an aphrodisiac. In roman times (wake up @eleytherius)  Livia Drusilla a great schemer of Rome attempted to poison visitors with cantharidin. Hoping they would act in a manner which they would later regret and allow her to blackmail them. (Its unclear if this was succesful) Cantarella which is the combination of Cantharidin and arsenic was reportedly the poison taken by Juliet to appear dead (We know how succesful that was)

References:

http://www.thefreelibrary.com/Outbreak+of+dermatitis+linearis+caused+by+Paederus+ilsae+and+Paederus…-a0242963583

http://www.ncbi.nlm.nih.gov/pubmed/2189910 Oedemerid blister beetle dermatosis: a review. Nicholls DS, Christmas TI, Greig DE.

Christmas TI, Nicholls D, Holloway BA, Greig D. Blister beetle dermatosis in New Zealand. N Z Med J. 1987;26:1515-1517 (paper copy)

When you think you see a dog but maybe it’s just spots.

Had this patient come in whilst on nights.

82 y/o female presented with chest pain.

Previously had CABG >15 years ago following presentation with “unstable angina”. which resolved her angina, nil since them.

Sudden onset chest and back pain and maybe between shoulders. not really a tearing quality but different to her pre CABG angina. pain wasn’t severe but enough to get her to come in. Felt her normal self otherwise.

Not on any medications.

Tachycardia 105. BP 108/64. (bilaterally)  Normal ECG sinus.

She looked pretty good TBH. sore but not “sick, sick”

Given GTN with no real change in pain. but settled with a push of morphine.

Istat troponin was negative.

Off for a CXR.

Was willing to say the mediastinum looked wide and the radiologist agreed that the aortic contour looked a bit funny.  We discussed presentation and decided that CT was indicated. I pushed for the scan as my gestalt was telling me there was something unusual about this patient.

Obviously there’s dissection from “top to bottom” as a colleague described it.

Formal report came back as extensive type A dissection extending from aortic root to abdominal aorta. There is no adjacent soft tissue reaction and no high density material on the unenhanced scan. These findings strongly suggest this is a chronic dissection.The false lumen is thrombosed in several locations and patent in others Major arch branches are patent.

Summary: extensive chronic aortic dissection with aneurysmal dilatation.

So my patient was now pain free, with an “old” dissection and lowish BP. Her tachycardia had settled after the CT. With discretion being the better part of valor I admitted her to the ward overnight. Repeat troponin in the morning was negative. She also had a D-Dimer added (no one confessed to this) which was negative. Discharged home.

I saw this patient recently in GP clinic and her BP remains low, no further episodes of pain. 

This was my first experience of when aortic dissection isn’t “aortic dissection” Anyone else had a similar case?

 Great discussion of Aortic dissection from LITFL: http://lifeinthefastlane.com/2010/09/die-like-a-king/