Simple approach to PAIN

Pain is ubiquitous in medicine and often overlooked. Despite a thorough definition, 'an unpleasant, sensory and emotional experience associated with actual or potential tissue damage', it is impossible to really understand someones pain unless you have felt it yourself. It is a highly diffuse symptom with a massive impact on patient well being and quality of life (it may even be much more diffuse than believed). It is an all encompassing entity which if you take Dame Cicely Saunders concept of 'total pain' concerns not only physical aspects but also social, spiritual and emotional aspects. 

If you take cancer pain, it is the most frequent presenting symptom and present overall in the majority of cancer patients. Shockingly pain is reported in a minority of cancer medical records, it would seem that many oncologists dont assess pain, probably fixating on battling the cancer itself (one of the toughest battles in medicine to add). Pain should be considered a disease entity itself and if it is properly assessed, addressed and treated, it could go a long way to enhance patient quality of life.

Here is a simple approach to pain you should consider whenever a patient says they are in pain:

First ASSESSMENT:

ABCDE 

A is for Ask: Ask about the pain: use the OPQRST approach:

• Onset
• Provoking factors 
• Quality of pain
• Region and Radiation of pain
• Severity 
• Timing and history 

When assessing severity use the NRS or VAS technique; "on a scale of zero to ten, where ten is the worst pain imaginable and zero is no pain, how would you describe your pain severity" (this is NRS, VAS is the application of a mark on a 10cm line to indicate pain severity in the same way).

score of 1-3 is mild  (VAS would be 1-3cm)

score of 4-6 is moderate pain (4-6cm mark)

score of 7-10 is severe pain (7-10cm mark)

One really important thing to think about after you have taken a thorough history is "what is causing the pain?"

B is for Believe the patient, don't dismiss them.

C is for Control: choose and appropriate pain control method, best way to apparoch pain treatment is with the WHO pain treatment ladder, which can be applied to all pain and not just cancer pain. move up the steps if pain is not well managed or still present.

• 1st step: PARACETOMOL (to treat mild pain)
• 2nd step: WEAK OPIOIDS (for example tramadol or codiene, these are opioids with a ceiling effect where inceasing drug dosgae will not improve effect from a certain point)
• 3rd step: STRONG OPIOIDS (consider for mod-severe pain). (for all opioids "start low and go slow"
• at any point you can add adjuvants to the ladder: NSAIDS, corticosteriods, antidepressants, anticonvulsants, benzodiazepines.

D is for Deliver pain control in a timely manner

E is for Empower the patient in pain control, patient education is so important. 

Second MANAGEMENT:

The four A's:

• Optimize ANALGESIA
• Optimize ACTIVITIES of daily living
• Minimize ADVERSE EFFECTS due to treatment
• AVOID unnecessary  drug taking

Third REASSESSMENT:

Simply, reassess often!

Summary: ABCDE OPGRST AAAA Reassess!

How do I study for this?

Studying in my final year of medicine, there is one question I get asked by the years below me all the time. "how do you study for this? what should I study from, the books, pubmed or the internet?"

Compared to twenty-thirty years ago and with the boom of the internet we have a huge amount of resources at our disposal. And its this huge variety in educational resources makes this question an increasingly common one. Here is my answer:

Disclaimer: First of all, everyone has their own best method, some people learn best from videos, others from quizzes and case studies, this is an important disclaimer when considering study methods.

What is there?:

• Fundamental textbooks
• Wikipedia
• Pubmed
• Uptodate
• Lectures and lecture notes
• Clinical case and question books/sites
• Revision books
• Senior and classmate notes
• Group sessions
• Youtube
• The ward
• medical blogs
• FOAMed/MEDed and twitter

(SKIP TO SUMMARY/ANSWER AT THE END IF YOU LIKE)

Textbooks:
The bread and butter of medical study. Often huge, boring and full of what some may consider unnecessary detail. Older doctors will swear by them and the younger doctors may completely avoid them. Use your textbooks as reference! No one has time to read the entire Goodman and Gilmans pharmacology or Kandels textbook of neuroscience. Textbooks are becoming increasingly thicker and thicker and the level of information can terrify first and second year students. When it comes to the fundamentals however, use them! but look for concise or targeted student versions:
Anatomy - Greys anatomy for students
Physiology- Berne and levys physiology
Pharmacology- Rang and Dales
These kind of books for the basic sciences are a must read in their entirety, try and find a smaller concise version for each core subject afterwards. Its in the clinical subjects where you should only use textbooks for reference, Harrison Cecils etc.

Read them, make brief notes, highlight important concepts, bookmark pages, the fundamental textbooks need to look like they have survived a train-wreck after the first couple years of medicine.
moving to the clinical years is where things get tricky...


Wikipedia:
Whenever you google a clinical condition the first post is most likely to be wikipedia post. Hugely informative and structured perfectly with sections for diagnosis, presentation, prognosis and related diseases etc. Take it with a grain of salt. Wikipedia is created by hardworking freelance contributors, many the posts are accurate and uptodate but you never know, they may not be! Until wikipedia has more efficient controls in place, its best used as a quick refresher and definition search tool 

Pubmed:
The centre of all that is EBM (eveidence based medicine), you can effectively answer any clinical question here for free. however, its hard work! often you have to search  hundreds of articles, and even if you find a nice review, it will probably contain many pages of information that you just arn't ready for yet as a medical student. which brings me to Uptodate

UptoDate:
Requiring a login or at least a registered institution, its not free! However this is the best place hands down to answer any clinical question you may have. The information is reviewed regularly and all the relevant clinical information that is interspersed through articles on pubmed is concentrated here. Again there is the issue of perhaps being a little too advanced for the average medical student. Best used a reference to clinical questions especially patient and disease management questions. 

Lectures:
Tedious, time consuming and highly dependant on the skill of the lecturer. We have all sat through a lecture so boring that you struggle to keep your eyes open, it can be a waste of time. On the contrary we have all been to that amazing lecture that kept us on the edge of our seat and full of curiosity at the end. Sometimes I feel I learn more from certain lectures than I ever could in a day reading through the relevant textbook. As much as we moan and and groan about them, lectures are important! attend them, drink coffee, and make notes! lectures will form the backbone of your study and are an important place to cement the core concepts you will need to study in revision. The medical exams are often about what you were lectured on remember.

Clincal cases and question books/sites:
Use these after you have studied, prior to exams. The best way to really test if you really know a subject is to test yourself. Often through testing yourself you find the holes in your knowledge base. it really works! Clinical case books are excellent, a little tedious but are probably the best way to test yourself in a way that will prove to be useful when you start work as a doctor (that special way of thinking when you approach a patient). Multiple choice question books and similar quiz books have now been surpassed by websites with endless question banks. The BMJ on examination site (which I use regularly) is just fantastic. One of my colleagues swears by the Firecracker app, where he answers about 50 quick questions a day on the metro/underground on the way and back from university. Unfortunately there is a catch, these questions banks can be incredibly expensive, so maybe its best to use these resources only before the big exams such as finals or end of phases.

Senior and classmates notes:
Forget it, the source isnt always reliable and most of the learning is in producing the notes yourself. One of my colleagues makes a killing selling his anatomy notes to first years, perhaps a good buisness solution, dont fall for it. On the plus side, notes may be targeted to an exam well and help when you have missed lectures. My advice, avoid if possible.

Group sessions:
Moving a bit away from the topic of resources, group studying is a real preference for some people. I think I will address the debate 'group vs solo studying' in another post. It depends a lot of the group itself and the study method, tackling clinical cases together is a good method.

Youtube:
What a resource, there are hundreds of videos on youtube and many of them are fantastic. I mentioned in a previous post Paul Bolin lectures and how they are brilliant for students preparing for the USMLE. Youtube is probably the best place for people interested in surgery and procedural medicine. Intubation, inserting catheters, chest drains and surgical approaches its all there (although can take some searching to find decent videos and in the correct language). Its incredibly difficult to learn a procedure from reading a book or passage, they are best learnt visually in a step by step matter, or better yet on the ward!!

The ward:
A must for all students. Spending time on the wards presents potential learning opportunities in areas which are favoured by in examinations, particularly practical assessments. Remember that medical school is a precursor for life as a doctor and thus, adequate exposure is necessary to assimilate the abilities expected of new doctor when they start. Although tempting to spend less time on the wards, especially near exams, try not to skip these session. Take a pen and note pad, note down everything you learn or new drug/disease/concept you hear. Try and take at least one history every time you are on the ward.

Medical blogs (like me :)):
There are some incredible medical blogs out there, life in the fast lane and emergency anatomy to name a couple that I usually use. It can be difficult to keep track of the variety in posts and to stay on track when studying a particular subject. You have to be careful with the accuracy of the information and sometimes it best to use the references in the post and read the original material before even reading the main post. I kind of feel that blogs are actually best for gaining an insight into the world of medicine, for opinions on the latest research and methods and for all that humanitarian stuff that forms much more of medicine than most of us are aware about. Patient care and professionalism are fundamental to a great doctor, it can be hard to find a good understanding about some of these issues from textbooks, blogs are invaluable! (not many textbooks will have a part about how to study like this will they ha).

Twitter:
There is an amazing movement happening in medical education at the moment, the hashtag or FOAMed movement. Hashtags like #FOAMed and #MEDed are attached to various things from the internet (videos, blogs, websites) to form this huge collection of medical education resources. More specific hashtags can be used to focus on the subject at hand #FOAMcc for crtical care for example or even summarize the findings from important conferences like #AHA16. Its a wonderful movement and its keeping medicine uptodate almost instantaneously and completely for free. Watch this space!

Ok I have rambled on a bit now and my lunch break is ending. Here is my best answer to the question above:

Attend lectures, make notes and read through them briefly that same day. Use the lectures to form a kind of back bone of core topics. Use the text book to cover these core topics by subject. And use the entire textbooks when addressing core fundamentals like anatomy and physiology. 
When you start clinical modules, use smaller review books with a more concise approach (I'm thinking Kumar and clarks vs Harrisons for example or Surgical talks vs Sabistons surgery). Whenever you have a clinical question use Uptodate and Pubmed. If you feel you need to understand something better use the fundamental textbooks. Try and explore the topics with twitter and blogs. When you are close to exams use clinical case books and online question banks, referring to the textbooks when you find a hole in your knowledge. 

NOTEs:
_The Eisenhower box to time management, works for studying too:

Remember you don't have to study everything in order, spaced repetition is the better way of learning in the long term.

Any questions feel free to comment and Ill get back to you, gotta runn..

RE: Antibiotic sensitivity overview

Modified version of this great post by Dr Michael Shamoon on CORE-EM. I added the orange box for macrolides and includes Clarithromycin, Azithromycin and Erythromycin. (Telithrmycin also has the same sensitivties). 

Forensic Medicine: Death

As a doctor you will inevitably have to deal with death and dying. Its hard and emotionally testing but you have to know what to do. There is a chance that you will be called to certify a death and you may have to make a decision about whether an autopsy is needed. I hope to cover everything about death in this post. disclaimer: I attend an international medical school so the laws may be different in different countries, most of the laws described here fit English and Italian law, I have tried to be as general as possible so to cover most countries. 

First of all how does one certify a death and how can you be sure that someone is in fact dead?
The respiratory, cardiovascular and neurological systems are regarded to be essential for life. therefore most assessments of life will address these systems. 
When the authorities come to you for a death certification, what they need is a proof of death, they don't need you to determine the cause of death. Usually there will be an ECG at hand and you will certify death by verified lack of cardiac activity (20min continuous ECG). If there is no ECG, then you will have to determine death based on post-mortal phenoma and other physical signs. 
There is anyway a mandatory 24hour period of observation of the body (usually in the morgue) just to make sure the body is in fact dead. the observation is mandatory except for putrified bodies (rotting bodies) or with decapitated bodies. 

In the UK you can certify death by fulfiling the following criteria:

• No palpable pulses.
• No heart sounds on auscultation (or asystole on ECG).
• No reaction to painful stimuli
• No breath sounds on auscultation and no observed respiratory effort. 
• Pupils dilated and not reactive to light.

Its important to assess without any unnecessary delay and ensure accurate documentation in the patient notes with your assessment and the time of death. 

In order to bury a body the national mortuary regulation requires a complete MCCD (medical certificate of cause of death form) with a cause of death. This makes determining the cause of death more important than certifying death as the body cannot be buried without it. The form is used for statistical purposes. The form has three spaces for the cause of death; a final cause of death, an immediate cause of death and an initial cause of death. Its not easy to state what the actual causes and potential chain reaction to death is. Frequently the final cause of death is cardiac arrest or respiratory arrest, but what caused it? 
A couple of examples:
Stab wound - massive hemorrhage - cardiac arrest
Abdominal aortic aneurysm - anuerysm rupture - cardiac arrest
(dont use an abbreviations when filling out this form).

There is an area whee you state comorbidities that may have contributed to the death and a separate area to fill in regarding traumatic deaths (was the death a suicide, homicide or accident). after filing the in the form you simply sign it and state your registration number. 
The aim of the MCCD is to monitor deaths in the country, and still quite often we don't know what caused some deaths. For example a patient arrives in ER and dies shortly after or a patient with a history of heart disease dies at the GP practice. You have to pay attention when filling in this form, you should fill in the form with "scientific knowledge and good conscious" as the Italians put it. 
a physician should fill in this form only is he or she feels relatively confident about the cause of death (you can never be 100% sure). Any cause of death can be put on the form, if the cause of death is not filled in or the form not submitted then an autopsy will be requested by the national health system (NHS) (hospitals themselves can also request an autopsy). Never feel forced to fill in the form. With autopsies the system feels safer. 

If a normal national health autopsy is conducted and suspicious lesions are found for example a neck hematoma, then the autopsy is automatically stopped and referred over to the judicial system. Before a judicial autopsy no one can touch the body (no tampering). There is sometimes are threats to pathologists dealing with a body from gang members.

Its important to note that the families have no say in what happens to the dead body, dead bodies do not belong to the family. Although ethical and morally its good to inform the family about what is happening to the body of course.

Just to highlight, if you are not sure about the cause of death do not sign the form!

There are two laws that protect the dead a first law protecting the dead against maiming and a second law basically saying that family's have no say in what happens to the body. Many religions don’t want the body tampered with and this clashes with the law, the law needs to be respected.

Judicially speaking, a dead body is not a person and therefore loses the rights of a person. There are many controversies and questions related to privacy, however the answer usually swings to the fact that dead bodies have no rights like living people. 

Every year in Milan 2-3 bodies and in Italy over 1000 unidentified bodies are discovered and buried without a name. Some places tried to provide a facility where you could put a picture online of the cadaver in hope of an identity such as the  UK missing persons bureau. Although these can clash with some authorities over privacy issues. 

When a person dies the family will need more support than ever. 60-70% complaints to doctors regarding life-death issues are due to the family not  being given enough attention and feeling like they were not appropriately listened to. After a death, sit down and talk to the relatives. There usually is a bereavement team at the hospital you can contact, who will liaise with the family. 

Pathological phenoma following death

These phenoma can be used to identify a person, the time of death and sometimes even the cause.

After immediate death there is an early post mortum period, then after the decomposition period and finally after that taphonomic factors.

The early post mortum period is what forensic pathologists and doctors certifying death will mostly be dealing with. You may even get a call to certify death when the body is already full of worms, but a doctor is still needed to certify death even in this case.

Three phenoma are seen during the early postmortum period

• Algor mortis (cooling)
• Rigor mortis (rigidity)
• Livor mortis (a hydrostatic phenoma)

Algor mortis (not Al Gore mortis)

Algor mortis starts as soon as the vital activity of the body stops. We cannot see with the naked eye the metabolic changes on a cellular level but you can feel and measure the temperature. The body will start at around 37 degrees on death and will slowly reach the temperature of the surrounding environment. Never trust if a body just feels cold, always use an objective measured reading.  Depending on the reference textbook you use, Below 34 degrees is considered not compatible with life. Use an internal measure of temperature, for example the mouth or rectum (or even tympanic temperature, see below). The time from death is linked to the temperature but depends on many variables.

You may be asked if the death was recent or not. You can try and correlate the environment with the temperature you record, there are in fact many equations that can be used to estimate the time of death but even the best of these will give you a result with plus or minus 2 hours minimum from time of death (plus or minus 4 hours is probably a better considerate). Many of these equations insist on rectal temperature and hence the error because the rectal temperature ha a large plateau in which it does not alter, it takes a while to change.

Ear temperature is much more representative of cooling, the speed and for how long for. This is because the variables change less in the head (no difference in body fat surrounding for example). Often many doctors with take the temperature with the back of the hand, never do that! use a thermometer!

Rigor mortis

The physiology of rigor mortis is well understood. The lack of ATP production after death causes ATP to eventually run out and the actin-myosin contractile unit of muscles to be locked in place (the myosin heads cannot detach without ATP). The onset takes a little while, while there is still ATP in the muscle. Eventually the muscle becomes locked in place and it is a very strong contraction. I read about pathologists forcing the joints (breaking the joints) in order to get arms or limbs straight.  It tends to start at the head and extend down to the feet and it devolves in the same way from head to feet. It can even take a few days to resolve in some cases.

Livor mortis

Livor mortis sets in after a few hours. It is quite simply the pooling blood in the body due to gravity. Slowly as time goes by, the endothelium collapses and the blood infiltrates the tissues. The pooling of blood will cause discoloration of the tissues, and you will see pink purple areas on the skin. If the cadaver was on it's back, the lower part of the body will be pink and the compressed areas of contact will be white. A handy test is if you compress the pink area with your finger, if the death was less than 6-10 hours ago then the blood will move away on finger compression (become white). If you were to roll the body  less than 6-10 hours after death then the pink areas would move, if the death was greater than 6-10 hours ago then the pink areas will stay pink .

Time frames

First considering algor mortis there are four stages after death with related time periods

Algor mortis:

0-3hours Plateau phase (no change in temp)

6-8hours Fast cooling stage (most accurate for determining time of death)

10-12hours Final plateau phase

11-30hours End of cooling.

Rigor mortis depending on the textbook tends to begin at around the 3hours-12hours mark, with the highest intensity of contractions between 12 and 48hours, resolution is around the 72hours mark.

Livor mortis has an onset around the 2hour mark with the highest intensity of discoloration at the 12hour mark, at 10hours-12hours the blood can still migrate at the 48-72hour mark it becomes fixed.

(Note that compression areas will be white and hanging limbs will be pink, consider gravity).

Transformative processes

When you are asked to certify a dead body you have to know what to expect. If the death happened a long time ago you will see the so called transformative processes. When these processes kick in you need to be aware that its impossible to determine the time of death. The onset and time frames are incredibly variable and depends on many variables and environmental factors.

Transformative processs can be either destructive or conservative.

Destructive:

Autolysis

Putrefaction

Maceration

Conservative:

Mummification

Adipocere

Corification

Mummification is caused by the loss of water from the soft tissues, and can preserve the tissues for a very long time. In theory if you rehydrate the tissue you will see the same tissue as before. True mummification is very rare. 

Adipocere usually occurs when the body is left in water, the tissue becomes a weird creamy soft texture and then sets after a while to an incredibly rock hard shell. 

Damp bodies may not putrefy and can undergo so called wet mummification where all the cells are lost and just the fibrous collagen based skeleton of the tissues remains, it appears very similar to mummification with brown appearance.

Criminal cases look at the exterior limits of these processes. It can be hard to not lose body parts when these processes kick in when you are collecting the body. 

Putrefaction is the main transformative process for dead bodies at our latitude. Putrefaction is decomposition of the body and causes a marble like green discoloration to the body (green due to hemoglobin catabolism), usually the processes start in the lower right quadrant of the body (this is because the cecum contains the highest concentration of bacteria in the GI tract). There is also bloating due to the gases produced. Eventually everything breaks down and turns to water. When you come across a putrefied decomposed body this is one of the rare scenarios where on the MCCD you can write the cause of death as indeterminate.

Many factors affect these processes: temperature, wind, season, soil pH, moisture content of soil, morphological characteristics, patient age, cause of death, laceration or discontinuations of the skin.

Forensic Pathology

Forensic pathology regards the diagnosis of when a lesion occurred and how it occurred. All physicians will have to deal with violence and trauma at some point. It is important you can describe a lesion well and accurately as your report may be used as evidence in a court case. You should be able to diagnose a lesion, age it, describe it and know what to do to preserve evidence.

There is a branch called humanitarian forensic medicine, for example proving migrants underwent torture in their home country. For these migrants, the evidence you present may determine whether they will be allowed political exile or not. Your report is the only piece of paper that will be able to support the evidence of ill treatment or torture when presented to regional councils and police.

In humanitarian forensic medicine you may also be needed to age unaccompanied minors of undetermined age. For example migrants  without any documents, is the migrant above 18 years age? it could make all the difference. Police can refuse territory to migrants over 18yrs. You need to know what to do to verify age.

Forensic pathology starts with a physical exam. You need to assess the whole body (you also need to listen to the patient, don’t forget!). If you don’t document a lesion or ‘crime’ and the victim doesn’t talk, then any evidence of the ‘crime’ will disappear. No sign of a crime can remain if there is no documentation. You need to have a keen eye to spot scars or bruises on darker skin.

Description of lesions needs to be metric and repeatable, there is no reason to not take a photo of a difficult to describe lesion. (although now there are issues with tampering of photos with programmes such as photoshop). If you take a picture, place a ruler in the periphery of the lesion at the same level of the lesion and consider putting a coin in the photo to help spot distortion or modification of the image later. Lastly make sure you take the picture perpendicular to the skin surface.   

How do you describe a lesion?

Need to address:

•   area of body affected
•   type of lesion
•   colour
•   edges/limits
•   shape
•  orientation
•  size

Types of lesions:

Blunt force trauma

Sharp force trauma

Gun shot wounds

Asphyxia

Thermal injuries

Poisoning

Blunt force trauma

• Excoriations
• Bruising
• Lacerations

Cause by any force against the body surface by a blunt object. You can tell on a cadaver if the blunt force was performed when the cadaver was alive or dead by looking at histology. On histology, live tissue injury will show an inflammatory reaction with extravasation of red blood cells into the tissue. On dead tissue there is no inflammatory reaction, you can also use immunohistochemistry to spot the presence of cytokines and see if there are inflammatory cells present.

Excoriations

Excoriations are loss of the superficial layers of skin due to blunt force trauma (not an abrasion, an abrasion is loss of the superficial layers of the skin caused by an object with a sharp margin like a knife). Excoriations often reproduce the shape of the object that cause it. 

Often the excoriation will heal with a scab and at this point it will become impossible to age the lesion. ED physicians may be the only people able to preserve material evidence of assault from the lesion. It’s easy, you simply swab the lesion for 30 seconds before cleaning  the lesion (moisten the swab with sterile water or saline before), store the swab in a tamper proof container and dry or freeze it (you can later give it to the police if necessary). Often under the nails of victim there is often attacker DNA (there can even be attacker DNA on the surface of a bruise from punches etc).

With excoriations you can often tell in which direction the blunt injury was caused and this can help reconstruct the event. (yet another reason for a good description and often there is some material left on the lesion from whatever object was used to create the lesion).

Scratch marks are a very typical and specific form of excoriation. Triangular or droplike in shape. They contain a lot of information about the author of the lesion and genetic information. A tyre mark may be another kind of distinct lesion (often the actual lesion is caused by the negative pressure by the treads in the tyre not the actual tyre surface).

Bruising

A bruise means the trauma was in that place, a hematoma is a collection of blood and the trauma causing the hematoma may be elsewhere on the body. When in doubt it is best to describe the lesion as a cutaneous discoloration. 

Great example; black eye can be caused by a direct trauma (punch to the face) forming a BRUISE or may be caused by a basilar fracture of the cranium creating the so called racoon eyes this is a HEMATOMA. They will look almost identical.

Note that MRI can be used to age and discover origin of a bruise/hematoma. Not that bruising may be difficult to spot for example of North African darker skin.

A bruise is different to a hematoma!

Bruises are closed lesions that show a distinct discoloration. The colour relates to the age of the lesion but also the size is important. You may have different colours at the edge compared to  the centre of the lesion due to difference in breakdown. You need to assess them carefully. For example a patient with multiple small bruises of same colour you can hypothesise were all caused at the same time. One large bruise may be purple while a neighbouring small bruise caused at the same time may be yellow.

Colour therefore depends on physiology, depth of injury and size.

Remember not to confuse a bruise with a hematoma.

Hematoma = filling of blood into a virtual space

Bruise = forcing of blood into a tissue

Note that old people bruise very easily and may even bruise spontaneously.

Lacerations

Third kind of blunt injury is a laceration. A laceration is simply a discontinuation of the skin, you can put the two skin edges together as normal and reconstruct the skin as there is no loss of substance. Bear in mind that a skin discontinuation may also be cause by a sharp force trauma. You have to describe the margins well.  Big clues that the laceration was caused by a blunt force trauma is irregular skin edges or frayed edges and bridges of tissue. You can look at the subcutaneous tissue and it will be irregular and not smooth with a blunt force trauma.

Sharp force trauma

• Penetrating injury
• Cut marks
• Stab wounds and mixed injuries

Penetrating injury

Depending on the book you use, pointed objects may or not be included in this category. A very distinct lesion to look for is needle tracks or syringe wounds. Always look for syringe marks in any unconscious patient, observe the whole skin surface, needles may be injected behind the ear or even on the genitals.

The shape of penetrating object lesions can tell you the shape of the object tip used to cause the lesion. The flaps of the skin lesions will match the penetrating object tip for example a squared end will cause an X shaped flap, a triangular tip will cause a Mercedes sign skin flap and a circular point a circular lesion.

An example is a penetrating injury to the cranium, surgeons keep the piece of cranial bone with the penetrating injury, the shape of the hole in the bone can tell you what kind of object caused the injury.

Cut marks

Cut marks are caused by a sharp edge weapon and cause a neat discontinuation of the skin edge and tissue. The cut mark usually has a tail at the edge of the skin discontinuation and this can give you a lot of information about where pressure was least and hence in what direction the cut was performed (obviously this depends on the curvature of the skin area and the object used, its still difficult to tell entry and exit point).

Stab wounds

Mixed weapons can give you stab wounds. These are weapons that can stab and can also cut. The cut mark is the result of passing the sharp edge and the penetrating injury the result of the pointed edge. Stab wounds contain a lot of information and will often reproduce the cross section of the blade. For example a double edged blade will produce a wound with two acute ends, a single edged blade will produce a wound with a single acute angled corner and an obtuse angled corner.  Sometimes the going in wound will not match well the going out wound and stab wounds may crossover each other making the lesion more complex and difficult to describe.

Remember that on skin and bones you may have residues of the instruments used to cause the lesions and you should always keep any debrided material.

Gun shot wounds (GSWs)

See future post on gun shot wounds...

Asphyxia

Asphyxia is a manner of death or disease that has distinct signs left depending on the method of asphyxia, the main types of asphyxia are:

•         Smothering
•         Choking
•         Manual strangulation
•         Ligature strangulation
•         Hanging
•         Drowning
•      Traumatic (compression) asphyxia
•         Plastic bag suffication

Unfortunately due to frequency of plastic bag suffocations in forensic pathology it has managed to deserve its own type of asphyxia.

With asphyxia there are many different types lesions that can be seen on the cadaver such as liver mortis, early rigor, delayed cooling etc. however, only one type of lesion is found on living bodies, petechiae! 

Petechiae is a very distinct sign of asphyxia and is caused by high pressure in the capillaries causing them to burst. Not always seen, it can be subtle, for example on the conjunctiva it is a common sign with strangulation.

Smothering is a good way to get away with murder there is often no sign apart from petechiae. There may be scratch marks, compression marks from teeth inside the lips or fibres from the object (usually a pillow).

Choking is usually accidental often people with neurologic or psychiatric disease or issues with the swallowing reflex.

Strangulation is a mechanism of death and not necessarily the lack of air. The death can be caused by nervous factors such as compression of the glomus body of the carotid artery and reflexive cardiac arrest. There are many anecdotal deaths where an aggressive attacker grabs an old man by the neck and he just drops dead almost instantly (the attacker will be mentioning in court how he hardly touched him). You usually see bruising with compression of the airways. Fracture of the hyoid or cricothyroid cartilage can have a distinct pattern with strangulation too. A ligature strangulation will often have a linear bruise of uniform depth sometimes with fibres still around the area (eg. rope burn).

With hanging there are often distinct fractures and ligature signs. You can tell easily if the person was hung before or after death by again looking at the haemorrhaging in the neck and the presence of an inflammatory response which is lacking with a dead body.

Traumatic asphyxia is caused by a heavy object compressing the rib cage restricting breathing.

Drowning is an awful way to die, often taking longer than 6 minutes as you alternate between periods of consciousness and unconsciousness. An important note is that water in the lungs is not proof of drowning! There is often water in the lungs in cadavers and it may have many origins (although sometimes it can be obvious with the post autopsy lung able to stand by itself it’s so full of water). Often the only proof of drowning is the presence of diatoms (microscopic algae) in the blood and organs (the diatoms being distinct to the body of water where the drowning occurred). When you drown the alveoli burst and water mixes with the blood providing an entry point for diatoms to enter the blood.  A long period after drowning there may be characteristic skin wrinkling and pink discoloration but this is more for shipwreck victims for example.

Thermal injuries, a common form of abuse. (see post on burns)

Poisoning

History is so important! Diagnosis of poisoning will require; anecdotal evidence, autopsy and clinical toxicology. If suspected keep a sample of blood/urine for a specific toxicology test that may be needed later. Many poisons are not included in the general toxicology screen performed in most ER’s. Also consider keeping a small lock of hair (from the roots), with this you can prove that the drug was not present in the victims system at time zero. 

There were far too many gruesome images that were associated to this post so here is a raccoon reacting to them

Pulse pressure and atherosclerosis

The pulse pressure is the difference between the systolic blood pressure and the diastolic blood pressure.

PP = SBP -DBP

It is determined by the stroke volume (amount of blood ejected by the heart) and compliance of vessels (the vessels reaction to this bolus of blood).

A higher pulse pressure will be measured in the smaller arteries further from the heart, as the pressure drops and the compliance increases.

Elderly patients that have stiffer vessels with a lower compliance will have a higher pulse pressure, but this isn't the whole story. The pressure wave reflects along the vessels and is reflected more easily by a very stiff vessel (harder vessel has less give, so wave travels faster, less delay, a high pulse wave velocity). Usually the wave reflects and returns during the diastolic phase but when the wave returns earlier it can increase the measured systolic pressure and lower the measured diastolic pressure, overall increasing the pulse pressure. (picture below describes this much better graphically).

PP can be considered an independent prognostic factor for cardiovascular morbidity (and it makes sense as a sort of crude marker of atherosclerosis and arterial stiffness).
Higher PP is proven to be related to smoking, diabetes, dyslipidemia, obesity and power sports activity.
Every 10mmHg increase in PP is associated with an increase in cardiovascular death risk of around 10%. However, also a low PP (below 45mmHg in patients with already advanced heart disease is linked with increased mortaility).
Wide PP for example >80mmHg is almost diagnostic in the case of severe aortic regurgitation.

The value to look for is a peripheral PP over 55-60 mmHg, this should alert you to likelihood of arterial stiffness and increased cardiovascular risk.

Pericardiocentesis, you stick a needle where?!

Some brief notes of pericardial effusion

Presentation:

The most common presentation is Dyspnea and Tachypnea

In the later stages the patient may even end up arresting with PEA (pulseless electrical activity)

Signs:

Classical becks triad:

Jugular venous distension

Distant heart sounds

Hypotension

Other signs include: Pulsus paradoxus (drop of SBP of greater than 10mmhg on inspiration), low voltages on ECG, electrical alterans, cardiomegaly on CXR.

Risk factors:

Metastatic cancer, mediastinal radiation, end stage renal disease, recent surgery, tuberculosis

This list is very similar to the list of etiologies:

Malignancy, radiation, uremia, dialysis, infection, idiopathic, iatrogenic, post AMI.

Diagnosis:

Clinical diagnosis, best with ultrasound.

On ultrasound you may see; a dilated IVC without changein size on respiration, right ventricle collapse (in fact you may see collapse of any of the chambers).

Treatment:

Pericardiocentesis, depending on ultrasound findings and the expertise of operator, most often performed in the subxiphoid position, with a spinal needle aimed at 45 degrees towards to the left shoulder. Ultrasound is used to guide a spinal needle (keep the needle lateral to the probe so it is always in view, the same plane) into the pericardial sac, avoiding the myocardium. A guidewire and catheter can be positioned to facilitate the drainage. In an emergency setting the procedure can be performed blind or with the help of ECG lead attached to the needle (if you see ST segment elevation then you have gone too far). 

Complications of pericardiocentesis: pneumothorax, coronary artery injury, liver or stomach injury, dysrhythmias, 

Acute Renal Failure and Acute Kidney Injury (ARF vs AKI)

If you look up the definition of acute renal failure (ARF) you will probably find this; "an abrupt and sustained decrease in renal function". Thats all very well but what do any of these words mean?! how abrupt? how long is sustained? renal function measured how? Whats more, over 35 different definitions of ARF are used in the literature with varying mortality and incidence rates. This post should hopefully clear everything up about ARF and AKI and give some tips about how to manage ARF and AKI.

First of all, scrap the term ARF, the term AKI is used now and reflects much better the fact that small decrements in organ function not resulting in organ failure are still clinically important! ARF is used for the last stage of AKI where the kidney actually fails and RRT (renal replacement therapy, for example hemodialysis) is needed. 

Diagnosis:

How do you know if a patient has AKI? look at serum creatinine and urine output!

There are two main ways for classifying AKI, the RIFLE criteria and the AKIN criteria, both perform equally well in studies, but I will use AKIN criteria because it is used by the KDIGO guidelines which most of this post is based on.

Picture above shows the AKIN criteria in the red box, as you can see you can divide AKI into three stages depending on the level of serum creatinine (sCr) or urine output (UO) (or directly place them into stage 3 if they are on RRT or anuric for greater than 12 hours). Stage 3 AKI is synonymous with ARF. 

So you have assessed your patients sCr and UO and find that he/she has an AKI. what do you do next?

AKI Management:

• monitor diuresis (bladder catheterise if not already catheterised)
• careful physical exam (pay attention to whether the patient is 'wet or dry', you should be careful giving fluids in a 'wet' pt, see later notes on pulmonary edema)
• monitor fluid balance
• arterial blood gases
• order labs: sCr, Na+, K+, Ca2+, Cl-, CBC, urine dipstick, BUN, 
• renal US (you are looking for the easy dx of obstruction, see etiology below)
• CXR (pulmonary edema?)
• avoid contrast agents if at all possible
• consider ICU if stage 2 and up
• avoid hyperglycemia
• careful drug review: 

1. discontinue nephrotoxic drugs (eg. vancomycin, gentamycin)
2. discontinue drugs that impair GFR autoregulation (NSAIDs, ACEi, ARBS(angiotension receptor blockers))
3. adjust dosage of drugs undergoing renal excretion (many antibiotics)
4. withhold exogenous potassium (look for K+ containing infusions (such as isolyte) that the patient may be on) and stop potassium sparing diuretics like spironolactone and eplerenone. 

AKI treatment:

Treatment is mainly directed at the underlying causes, for example if the cause is dehydration give fluids, if the cause is haemorrhage consider giving blood transfusion etc. immunosuppressants for vasculitis, discontinue drugs, relieve urinary tract obstructions....

note: No specific treatment for AKI actually exists but we have to manage all the complications well. 

AKI causes:

The causes of AKI are best divided into three main catergories

• pre-renal
• intrinsic (parenchymal)
• post-renal

Pre-renal AKI:

Basically anything that causes a drop in blood pressure low enough that the kidneys own auto-regulation is unable to preserve renal function. consider:

Volume loss: hemorrhage, dehydration, diarhhea, polyuria, burns

Sequestration of fluids (3rd spacing): pancreatitis, peritonitis, rhabdomyolysis

Blood pressure drop: any form of Shock, hypotensive medications 

(note that not all patients have the same capacity to autoregulate their renal filtration)

Intrinsic AKI:

diseases that affect the kidney directly, consider:

Arteries: thrombosis, embolic events

Pre-glomerular arterioles: Vasculitis, malignant hypertension, atheroembolism, DIC, eclampsia

Glomeruli: glomerulonephritis, thrombotic microangiopathy

Tubulo-interstitium: Acute tubular necrosis (ATN), crystalluria, cast nephropathy, contrast agents

(note that anything that can cause a sustained hypotension can damage the renal epithelium and cause ATN)

Post-renal AKI:

This is caused by an obstruction to the urinary tract, consider:

Bladder outlet obstruction: BPH, urethra stenosis, neurologic bladder

Ureter obstruction in pts with 1 kidney: stones, cancer, papillary necrosis

AKI Complications:

AKI patients can die of four main causes:

• Hyperkalemia
• Metabolic acidosis
• Fluid accumulation (pulmonary edema)
• Uremic syndrome

Hyperkalemia occurs when serum K+ is >5 mmol/l

Symptoms of hyperkalemia include: intestinal colic, diarhee, weakness/paralysis, arthymias

Hyperkalemia has a distinct ECG: flattened P waves, wide QRS, peaked T waves

(peaked T waves is the first feature to appear)

Metabolic acidosis is caused by the failure of tubular interstutium to excrete normal daily acid load. symptoms include: nausea and vomiting, abdominal pain, hyperventilation, hypotension

(note that acidosis may worsen hyperkalemia)

Fluid accumulation is quite often iatrogenic! careful with hydration. 

Uremic syndrome has many presentations and may cause: pericardial effusion, nausea and vomiting, malaise, confusion, seizures, non specific diffuse abdominal pain, ileus, a tendency to bleed (so called 'lazy' platelets). 

Mean Arterial Pressure (MAP)

I'm currently studying shock, its a huge subject and incredibly important topic in medicine. It doesn't matter what kind of doctor you are, you need to be able to deal with shock. MAP is very relevant in the state of shock.

MAP a great indicator of the perfusion pressure of the organs. Its kind of like an average blood pressure, so if its low there isn't much blood reaching the vital organs. As we all know, blood pressure has two components a systolic and diastolic component. So its not so easy to work out MAP or 'average' blood pressure.

There are some formulas that help (DBP = diastolic blood pressure, SBP = systolic blood pressure):

MAP = DBP + 1/3 (DBP-SBP)

MAP = 2/3 DBP + 1/3 SBP

There are many and quick search of wikipedia or on google will easily come up with many different formules, the two above are the simplest. (note: DBP - SBP is also called the Pulse Pressure).

A normal MAP in a healthy subject is around 90mmHg or in the range 70-110mmHg,
In the treatment of shock we are trying to get the MAP to around 65mmHg or maintaining it there.
(this is because a MAP above 60mmHg is considered enough to perfuse the organs. thus below 60mmHg you should start worrying about organ ischemia).

Tissue Factor and Thromboplastin

Tissue Factor (TF) (aka Factor 3 or CD142) is a protein with a key role in coagulation. TF is present in large concentrations in subendothelial tissue of vessels (so by smooth muscle cells and fibroblasts). The endothelium itself can also express TF but only in imflammatory states, same for circulating monocytes.
TF is responsible for triggering the so called extrinsic pathway of coagulation (or TF pathway as its also known). This path is triggered when the vessel is damaged and there is exposure of the underlying TF. It acts as a receptor for Factor 7 which leads to the cleavage of Factor 10 and the activation of the common pathway of coagulation and thrombin activation.

Thromboplastin is the name of a lab reagent and is actually the combination of TF and phospholipids. TF and phospholipids together can trigger coagulation. Partial thromboplastin is just the phospholipids by themselves and can trigger the intrinsic pathway of coagulation (TF not needed to activate intrinsic pathway). So when an 'activated partial thromboplastin time' APTT test is order it is a measure of the intrinsic path of coagulation.

Picture highlighting TF (yellow box), the extrinsic pathway (red box) and common pathway of coagulation (green box). #medicine #coagulation #labs #tissuefactor #bleeding #medicalschool #medicalblog #medED #FOAMed #study

Fever Of Unknown Origin (FUO)

I am sure you have all watched at least one episode of House, the series in which a witty Hugh Laurie is presented with difficult to solve cases almost every day. Obviously in reality these kind of cases are incredibly rare, but there is one kind of 'difficult to solve' problem in medicine which appears far more often than you think, the febrile illness without an obvious origin, FUO.

Definition and Diagnosis:

Fever greater than 38.3 degrees on several occasions, persisting without diagnosis for at least 3 weeks despite of at least 1 week investigation in hospital. (Later updated to 3days Inpatient investigation or 3days of Outpatient investigation).

Can be further classified into:

Classical (as defined above)

Nosocomial (the fever was absent on admission to the hospital)

Neutropenic (Patient is neutropenic as well, less than 500 neutrophils per mm3)

HIV associated (Patient has confirmed HIV infection)

You cannot conclude a patient has a FUO until you have performed the following basic investigations:

History, Physical exam, Complete blood count, Blood Cultures, Complete metabolic panel and Liver function tests, Urinanalysis and culture, Chest X-ray.

Etiology:

Three catergories of illness can cause FUO; 

infections, malignancies and connective tissue disorders.

There is a long list of the possible causes (See image) but don’t forget Drug Fevers in which a fever can be the sole feature of an adverse drug reaction (most commonly with antibiotics).

Age is very important when considering the etiology, for example in younger patients infections will be much more common (in children around one third of FUO are caused by self limited viral illnesses) and in the elderly (haematological malignancies and solid tumours will be much more common).

Also neutropenia associated FUO will be much more likely linked to a bacterial infection (although never forget genetic neutropenia exists such as cyclic neutropenia and benign familial neutropenia).

Malaria and respiratory infections are a common cause in returned travellers.

First steps:

Re do history and physical exam, a careful history is critical for diagnosis! 

Ask about: animal exposure, immunosupression, drugs and toxins, localising symptoms (for example, jaw claudication is consistent with giant cell arteritis, nocturia with prostatitis etc.). 

Note that the degree of fever, nature of fever curve and response to antipyretics has no specificity to guide the diagnosis. 

After a careful history the following exams will be useful (obviously performed in a targeted nature, guided by your suspiscions):

LEVEL 1 testing:

ESR, CRP, LDH, TST/IGRA, HIVab/RNA, 3 blood cultures for separate sites, Rheumatoid factor, creatine phosphokinase, heterophile antibody test, antinucleaur antibodies, serum protein electrophoresis, procalcitonin can be helpful

LEVEL 2 testing:

CT abdomen, CT chest (if these turn out to be negative move to FDG-PET, although be aware of its high false positive rate)

Level 3 testing: 

Biopsies and Endoscopies

Treatment:

Treatment should be withheld as long as possible until the cause of the fever is determined and empirical antibiotic treatment is not appropriate! However you must obviously consider the patients condition and febrile neutropenic patients have a much higher percentage of bacterial infections and so empiric treatment can be appropriate after cultures have been obtained.

Summary:

• Most cases of FUO are due to unusal represantations of common diseases rather than exotic diseases
• Reassess the patient frequently and the don’t underestimate the importance of a very careful history and physical exam (it is in fact critical).
• Almost any infective agent can be responsible for FUO
• Look out for Malignancy red flags in the history and physical exam such as symptoms (night sweats, weight loss, pruritus, rectal bleeding), radiation exposure, cigarette smoking, lymphadenopathy, hepatosplenomagaly, petechiae.

A long list of the possible causes of FUO #fever #medicine #fuo #medED #study #medicalschool

Study methods you should try

BLA BLA BLA BLA secret message hereIts time to go back to school or university (well for some of us). Its amazing how many people stick to their old study methods, Although these may work for some they can be terribly inefficient. This article has some great advice.