Acute Otitis Media

Acute otitis media (AOM) is a frequent disease in childhood with over 90% of children over three years old having had at least one episode. It is a difficult diagnosis and the major cause of antibiotic misuse and abuse. (AOM is the most common indication for antibiotic prescription).

Definition:
Rapid onset of signs and symptoms of acute infection within the middle ear with evidence of effusion.
(recurrent OM: 3 or more episodes of AOM in the previous six months or 4 or more in the last 12 months)

Why so common:
It is to do with the eustachian tube in children being smaller and more horizontal than in adults (<10degrees, in the adult >60degrees angle). The nasopharnyx is a carrier site for many pathogens and their virulence is increased after a viral illness typical of the winter season such as influenza or rhinovirus. This explains why AOM rates are increased after the winter season and in children that attend daycare (lots of children mixing viruses).

Etiology:
the so called infernal trio is responsible for majority of AOM cases through all pediatric ages:
Streptococcus pneumonia
Haemophilius influenze (non typeable (NOT HiB!!))
Moraxella Catarrhalis
(could add Group A Beta Hemolytic Streptococcus as the fourth agent).

Complications and consequences:
Potential for developmental delays
Chronis effusion requiring tympanostomy tube insertion (30% will undergo repeat infection within 5years)
Mastoiditis! The rates are increasing now, this means admission to hospital with IV antibiotics and can result in severe CNS complications

Risk factors:
Daycare (six children appears to be the cutt off), tobacco smoke exposure (dont forget 3rd hand exposure parents!), seasonality (more in winter and spring), bottle feeding, use of push-pull top bottles (negative pressure in the middle ear draws bacteria up), pacifier use, obesity, cleft palate, Male more,
African americans more.
(exclusive breastfeeding upto 6months reduces AOM rates compared to formula fed)

Diagnosis:
Correct diagnosis is essential, do not treat unless the diagnosis is sure
Acute onset of symptoms
Inflammation of tympanic membrane (assess with penumatic otoscope)
Presence of effusion (will appear as bulging tympanic memebrane on otoscope)

Symptoms:
Classically earache, fever and irritability
The symptoms of AOM are often nonspecific and no one symptoms is present in more than 50% of cases, look at the ear!
Use the COMPLETES mnemonic in assessing the ear: Colour, Other, Mobility, Position, Lighting, Entire surface, Translucency, External ear, Seal.
About half the children will have obstructing cerumen which can be a problem.

Treatment:
Pain managment with paracetomol or ibruprofen
(Paracetomol 10mg/kg/does max 4grams)
Antibiotic therapy is based on Age, laterality and severity
give antibiotics to: all children under six months, all children between 6months and 24months unless unilateral and mild and to over 24months only for severe bilateral disease. in all other cases use the watch and wait approach.
Amoxicillin 80-90mg/kg/day divided in 2 doses max 3grams/day
Up to date with vaccinations, note: Pneuomcoccal vaccine has decreased AOM RATES

Complications of Measles

Nice easy rule to remember the complications of measles; the rule of tens.

10% Otitis media

1% Pneumonia 
(make sure you discriminate viral from bacterial pneumonia in this case. Viral pneumonia caused by measles itself will be concomitant with the rash. Bacterial pneumonia caused by co-infection will appear 1-2 days after the rash has gone.)

0.1% Meningoencephalitis 
(another nice little division here is in quarters; 50% will be cured and fine after measles meningoencephalitis, 25% will have some kind of neurologic sequele and 25% will die! this is the reason we vaccinate people with the MMR vaccine!)

0.00001% Panencephalitis
(this occurs many years (average 7 years) after measles infection and for most means death, another good reason to vaccinate with the live vaccine unless you are immuno-compromised of course)

Other complications: Diarrhoea (most common), Seizures (as rare as meningitis)

(Measles mickey, a reference to the measles outbreak in Disneyland)

Paediatric UTI's

Paediatric urinary tract infections, are the second most common type of paediatric infection after respiratory tract infection. And the second most common type of bacterial infection in children after acute otitis media. Early recognition and prompt treatment are important to prevent progression to pyelonephritis and renal scarring. 

Etiology:
In very young children and infants the origin of UTI is most likely from hematogenous spread, whilst older children and in like adults the origin is from an ascending infection originating from the perineal area.
More frequent in females except for the first few months of life where it is more frequent in males, due to the fact malformations are more frequent in males and tend to present early. Obstruction to renal flow is a major risk factor, as urinary stasis provides the perfect environment for bacteria to grow.  A short urethra is what predisposes girls to UTIs.
If a child is having recurrent UTI's suspect a urinary tract malformation.
E.coli causes 75%-90% of UTI episodes, other bacteria include klebsiella, proteus and enterococcus spp.

Presentation:
Varies with age of the patient. Neonates and infants are more likely to present with non specific symptoms such as; poor feeding, vomiting, failure to thrive, jaundice, hypothermia/fever, diarrhoea, strong smelling urine.
At around preschool age UTIs will present with more nephrogenic symptoms as well, such as dysuria, urgency and increased frequency.
Adolescents are more likely to have the classic adults symptoms. Important to note that adolescent girls are more likely to have vaginitis.

Diagnosis:
Diagnosis is classically difficult and based on urinalysis, urine culture, blood tests and imaging. bear in mind that urine test is not enough for diagnosis and culture is needed.
Urinalysis: typically leukocyte esterase and nitrites positive with presence of WBC sediment, the combination of these three has the highest sensitivity.
Urine culture: There are four ways in which urine can be sampled for culture in children.
-Suprapubic aspiration (sterile procedure, good for infants, obtains very good sample, bladder easily sampled with low complication rates)
-Bag collection (high chance of contamination thus, can be used to rule out infection is negative culture, but positive culture must be suspected to be a false positive), if you use a bag clean area well and bag must be changed every 20minutes to keep sterile, not recommended by CDC)
-Midstream collection (difficult in children, generally from only 3 years age in male children, make sure perineum area is cleaned well before hand)
-Catheter collection (performed as a sterile procedure, risks urethral trauma and introducing bacteria, used more for children with malformations in the urinary tract)
A clean catch urine sample with more than 100,000 CFUs (colony forming units) on culture of a single organism is classic criteria for UTI (>1000 CFUs for suprapubic aspiration). If there is growth of more than one organism consider that sample was contaminated.
Diagnosis in young children requires pyuria (>10 WBCs/mm3 in urine) and positive culture of a single pathogenic organism.
in older children and adults a single positive culture is enough.

Imaging:
Typically delayed by 3-6weeks unless urinary tract obstruction suspected or the child has an atypical UTI.
First line is Renal Ultrasound, it can spot many urinary tract abnormalities and is quick and cheap. However it poorly depicts the ureters and gives no functional information.
Micturating cystourethrogram (MCUG) shows anatomy well and can detect vescicoureteral reflux.
Nuclear cystography used when MCUG not possible and is great for serial follow up as radiation lower than in fluoroscopic studies.
Nuclear cortical scanning is best to see damage to kidney or presence of scarring. most frequently done with Tc11mDMSA. remember that it does not show the collecting system.

Treatment:
Initiate treatment immediately after culture drawn this reduces severity of damage to kidney (don't wait for culture results).
Antibiotics: 7-14 day course is standard (evidence that 2-4 days can be effective in lower urinary tract infections, if you can confirm no reflux). Oral treatment and parenteral treatment are equally efficacious as long as dosage correct. IV antibiotics recommended in children unable to tolerate oral therapy and infants less than one month until systemic infection ruled out.
In neonates: Ampicillin + Gentamicin/Cefotaxime
if you suspect an infected line or instrumentation cover for staph spp. with Vancomycin

Prevention:
Recurrent UTIs in 15% of children, quite often in children with malformations of the urinary tract (also without, 20% without any). Prophylactic antibiotic therapy is being debated and efficacy questioned.
Prophylaxis with Cotrimoxazole or Nitrofurantoin given at bedtime (to concentrate in bladder overnight). Nitrofurantoin is theoretically much better because it selects for the urinary tract however it commonly causes vomiting and hence is unpopular.
If recurrent UTI diagnosed then further imaging studies are recommended. 

Last notes:
-An atypical UTI is one where the child is seriously ill or has one or more of the following:
poor urine flow, abdominal mass, raised serum creatinine, septicemia, infection with a non E.coli bacteria, failure to respond to treatment with suitable antibiotics within 48hours.
-The term UTI includes Cystitis, pyelonephritis and renal abscess (actually difficult to determine is upper or lower tract infection in children.
-Uncircumcised males have higher incidence if UTIs than circumcised males.
-Failure to thrive, feeding problems and fever are the most consistent symptoms
-Positive leukocyte esterase and nitrites dipstick test has sn 70% and sp 99%
-Bacteremia in 5% of cases of pyelonephritis.

Children are not little adults

Starting Paediatrics today, its important to realize that the medical approach to children can be incredibly different than that to adults. Children differ from adults physiologically and in their exposure to the environment, here is a list of some important points to consider when dealing with a paediatric patient: 
(this post is based on the WHO document linked here, reference are included within that document)

• Minute ventilation per Kg bodyweight a day is higher in children. It is around 600l in <1year old  which is 3 times the value of an adult, 200l. Therefore environmental toxicants will be delivered to the airways of a child at a higher level than adults. for example: ozone, lead, particulates, nitrogen oxides, mercury, moulds, volatile organic compunds etc. 

• Calorie and water needs are higher in children. Cal/kg/day and ml/kg/day have higher values in younger children, its pretty obvious considering their anabolic state and growth demands. Therefore oral exposures are likely to be higher in children, think of pesticides or mycotoxins that are common in food. I could mention here that a vegan diet may be harmful to children since their calorie demand is so much higher (even though I'm an avid supporter of plant based diets). 

• Gastrointestinal absorption is higher in children and dynamic. For example a child may absorb 70% of ingested lead while an adult around 5-20%. There are microbiome changes throughout childhood, contributing to digestion and absorption. important considering pharmacokinetics, always prescribe drugs in mg/kg not by single doses. 

• Renal function: GFR (glomerular filtration rate) is low at birth (around 10-15ml/min/m2 for a normal full term newborn) and doubles in the first week of life (cirtical period). GFR reaches adult values by around 6-12 months, the general rule is 8 months. tubular function is impaired (secretion) at birth and is normal by 1 year of life. 

• Hepatic function: The activity of phase 1 enzymes are reduced and mature at different rates as child grows. in fact activity of these enzymes can then exceed adult rates between 6-12 years age. phase two enzymes are ready at birth for processes such as conjugation and acetylation. Therefore metabolites of xenobiotics may differ between adults and children, even if rates of metabolism are the same. 

• Transplacental exposures: Many chemicals and drugs cross the placenta, including mercury, lead, substances of abuse, alcohol etc. We all know the story of thalidomide. Also physical factors can affect the baby such as heat and ionizing radiation. important thing to point out here is that maternal exposures do matter!

• Breastfeeding: Breast milk is the safest and most complete nutrition for infants, so mothers should avoid toxic exposures. We use breast milk to spot environmental contaminants, its very likely that you reading this have DDT in your fat because your mother was exposed to it as a child. Lipophilic chemicals are especially good at transferring in breast milk, hence why we don't prescribe quinolones for breastfeeding mothers. 

• Size and surface area: The ratio between skin/surface area to body volume/mass is much higher in children, about 3x for a newborn compared to an adult and 2 times with an infant. therefore dermal exposures may be much higher in children, children also tend to have more skin abrasions/cuts and rashes which make it easier for germs/contaminants to cross the skin barrier. Very important to consider the surface area in children when dealing with burns.

• Organ and system development: the organs in a childs bodie grow and mature throughout childhood. Neuron growth and maturation (myelination and synpatogenesis) continues right the way through puberty, The respiratory system continues linear growth after birth so any exposures to toxic compunds (tobacco smoke! ozone etc.) can have very adverse consequences. The immune system is also actively maturing throughout childhood.

In summary, children have unique and differing-to-adults exposures and a highly dynamic developmental physiology. Combining this with a longer life expectancy and the insidious effects of environmental toxins, it is very important to consider the world/environment we leave behind for children to inherit. 
Children have a completely different pharmacokinetic profile and can be exposed in a variety of ways, so its also important for physicians to be vigiliant in paediatrics pharmo-prescribing. 


Bonus point: Introducing a food early to children does not increase their risk of allergies, NEJM editorial.

What is Prealbumin?

Prealbumin AKA transthyretin is a transport protein synthesized by the liver that binds thyroxine. It is used in hospital as a marker of a patients nutritional status, more specifically a measure of 'protein' nutritional status. (other markers for protein nurtional status include: albumin, retinol-binding protein, transferrin, creatinine, blood urea nitrogen). Serum prealbumin is often requested when patients are on parenteral nutrition or  other forms of nutritional support. Normal serum prealbumin concentrations range from 16 to 40 mg/dL; values of <16 mg/dL are associated with malnutrition. It has a half life of around two days, much shorter than albumin's which is around 20 days, making it a good marker to understand acute changes in nutritional status. There will also be changes in prealbumin with liver disease and chronic kidney disease. The problem is that prealbumin is related to acute phase reactants meaning that it is affected in inflammatory states, such as with injury or infections. It can help to look at C-reactive protein (CRP) when assessing prealbumin, CRP is also an acute phase protein (in fact many studies look at the prealbumin/CRP ratio). Another drawback is that the prealbumin test is more expensive than a simple serum albumin test and so in some institutions the test is not available. Some studies have been published recently that suggest that there is little relation between nutritional markers such as prealbumin and actual nutritional status probably because of too much interference by inflammatory states (source). 

Summary:

• synthesized by liver and bind thyroid hormone
• short half life, normal value between 16-40mg/dL
• marker of acute changes in protein-nutritional status
• best assessed with a complete nutritional panel and with CRP index
• nutritional markers are not a replacement for a good physical exam and history

sources: http://www.medscape.com/viewarticle/474066_6, http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/9005, http://emedicine.medscape.com/article/985140-overview, https://www.urmc.rochester.edu/encyclopedia/content.aspx?contentTypeID=167&ContentID=prealbumin, https://labtestsonline.org/understanding/analytes/prealbumin/tab/test/, http://pen.sagepub.com/content/39/7/870.long, http://www.ncbi.nlm.nih.gov/pubmed/25912205

Haematemesis

Haematemesis (vomiting blood) can present as either bright red in appearance (a medical emergency, suggesting an acute bleed) or a dark granular so called 'coffee grounds' (suggesting the bleeding is modest or has already ceased).

Causes of Haematemesis:

• Peptic ulcer disease: most common cause, often epigastric pain a well. Most often due to Helicobacter infection or NSAID use. 
• Upper GI malignancy: patient will often have fatigue, weight loss, anorexia and early satiety accompanying symptoms. 
• Varices: formed with portal hypertension when blood is trying to find routes to avoid the liver, most commonly with hepatic cirrhosis.
• Mallory-Weiss tear: characteristic history of forceful vomiting with haematemesis following (intial vomiting clear of blood). 90% of these will heal spontaneously.
• Gastritis/Duodenitis: consequence of Alcohol abuse or NSAID overuse. nausea and epigastric pain common.
• Oesophagitis: consequence of GERD. History of heartburn typically. 
• Dieulafoy’s lesion: developmental lesion, an unusually large (5-10mm) submucosal artery in the stomach wall. The pulsatility of which causes it to eventually erode through the stomach wall and perforate into the stomach. 
• Aorto-duodenal fistula: history of recent aortic surgery. 

Management, what to do:

The priority is resuscitation, patients with haematemesis may present in shock. So ABCDEs first. If a patient does present with shock or bright red haematemesis then after they are stabilised they need urgent upper GI endoscopy.
Get urgent CBC, U+E, coag screen, cross match and LFTs 
Varices have a high mortality rate and may be suggested by known chronic liver disease or characteristic signs if liver disease.
If patient has characteristic history of a Mallory-Weiss tear then endoscopy is not needed.
If active bleeding is not suspected and patient is stable, then take a full clinical history and exam. Suspect first gastritis, duodenitis or oesophagitis and pay attention to signs of malignancy.
If the diagnosis is not obvious consider inpatient endoscopy.

February round-up (Medical student gems)

Youtube Channel: DocMikeEvans

Dr Mike Evans whiteboard videos are incredibly simple and informative. They are incredibly good at explaining the key points of disease in a way that patients can understand easily. Already posted my favorite video of his. 

Book: Why Zebras Dont Get Ulcers by Robert Sapolsky

This guy is a world expert on the matter of stress. In his book he explains clearly the different mechanisms of stress and their various manifestations. The detailed content means its not a light read but its super interesting and well worth the effort.

Twitter accounts: @StudentBMJ @CaulfieldTim

There are so many twitter accounts to choose from, I am following so many these days. The student BMJ is a great resource for medical students especially those in the UK.Tim caulfield posts some really interesting studies quite regularly

Webpage: Which textbook to use, Cambridge recommends

The Cambridge University medical school reading list, I refer to this whenever I'm not sure which textbook to use for a certain subject. 

Film: A Beautiful Mind (2001)

This film is about famous mathematician, nobel prize winner and schizophrenia sufferer John Nash. Gives great insight into the condition of schizophrenia, also a bloody great film. 

Mania and Hypomania Mnemonic

DIG FAST 

Is a mnemonic for the symptoms of mania. Diagnosis of mania requires 3 or more of these symptoms over a period of at least one week, with impairment of daily life. If there is no impairment  or disturbance of daily life (mood isn't severe enough) the diagnosis is hypomania.

• Distractability and easy frustration
• Irresponsibility and erratic uninhibited behaviour
• Grandiosity
• Flight of ideas or subjective experience that thoughts are racing
• Activity increased with weight loss and increased libido
• Sleep reduced (e.g. 3-4hrs) but still feel restored
• Talkativeness 

Rheumatology: Fibromyalgia

Fibromyalgia AKA fibromyalgic syndrome (FMS) is one of the most common causes of chronic pain. It is characterised by allodynia, hyperalgesia and a wide range of other symptoms.
On average a FMS patient will have seen three or four different doctors before being diagnosed (taking an average of 2-3 years)!

Epidemiology
Prevalence 2-4%
Female (9:1)
35-60yrs (working age)
increased incidence in patients with autoimmune disorders

Symptoms/Signs
Widespread pain with tender points (pain elicited with palpation of these specific points)
Fatigue (doesn't improve with rest, number one complaint after pain)
Morning stiffness
Sleep disturbances (pt sleeps well but wakes up more tired)
variety of other disturbances; Headaches (tension-type and migraine), paresthesias, trouble concentrating, variable bowel habits, depression, mood and affective disorders, temporomandibular joint syndrome,  idiopathic back pain, non cardiac chest pain, vestibular complaints, ENT symptoms...

Diagnosis
Diagnosis is entirely clinical, by exclusion generally.
Rule out differentials, be vigilant of common co-existing conditions like irritable bowel syndrome
ACR 2010 diagnostic criteria
Reasonable diagnosis:
>Chronic widespread pain for greater than 3 months
>pain at 10 or more tender points (see image linked for specific locations, there are 18 defined areas)
(> also aiding in diagnosis; presence of Fatigue/stiffness and sleep disturbances)

Treatment
Centred towards the pain, but be aware that many FMS patients have concomitant psychiatric problems, so psychiatry referral suggested. Reassure patient its a physical diagnosis and warn them in some cases the symptoms will never resolve completely.

>Non pharmacological treatment
Exercise, CBT, homeopathy, physiotherapy, acupuncture, diet changes, relaxation techniques
all safe in the long term and may have potential benefits (small % of acupuncture pts had increased pain though)
Graded exercise showed benefits in many patients

>Pharmacological treatment
simple analgesics, tramadol,
tricyclic antidepressants
serotonin noradrenaline reuptake inhibitors (SNRIs)
alpha2 agonists (gabapentin, pregabalin)

Differential dx
Chronic fatigue syndrome (fatigue much more prevalent and severe, more an issue than pain)
Multiple bursitis/tendonitis (good response to local inection treatment, tender points absent)
Rheamatoid arthritis/Osteoarthritis (joint swelling, hands affected)
SLE (rash, systemic sx, ANA)
Ankylosing spondylitis (young male, lower back pain)
Polymyalgia rheumatica (older pt, acute onset, steroid responsive)
Hypothyroidism (weight gain, goitre)
Myositis (weakness more than pain)

Random pearls

• Although the etiology is unknown it is believed to be a central sensitization disorder, fitting in with the considerable overlap of IBS and dysmenorrhea with FM. A kind of abnormal response of the nervous system.
• RA and SLE often present as well. 
• FMS is increased in patients that have suffered a physical of psychiatric trauma (perhaps a starting point of the disease)
• increase in metabolic syndrome in FMS patients
• There are three subgroups to further classify FMS patients based on pain control, tenderness and associated symptoms
• In USMLE exam 'steroids' or 'NSAIDS' will not be the correct answer answer to treatment options
• 12th May is Fibromyalgia awareness day
• One third of FMS patients experience major depression or significant anxiety. 

Resources and Sources:
Medscape Fibromyalgia
Paul Bolin CRASH USMLE video on Fibromyalgia
ArthritisUK Great site for patients
More detailed look at diagnostic criteria

 #MEDed #FOAMed #Fibromyalgia #Rheumatology #Chronicpain #widespreadpain

Orthopedics: Fractures and Bone Healing

There is a lot of things to consider when a pt comes into the ER with a fracture. Do you know when you to treat with an OPEN or CLOSED reduction?

Bones can heal either by 'Healing Per Primam' or secondary healing with callus formation (much more common).
Healing per primam is direct healing of bone with tunneling of osteoclasts and migration/colonization of the tunnel with osteoblasts (no callus formation).

Secondary healing/callus formation stages:

1. Hematoma 
2. Granulation tissue 
3. (Soft callus) Cartilaginous callus formation 
4. (Hard Callus) Bony callus and cartilaginous remnants (lammellar bone deposition)
5. Remodelling to original bone contour 

Stephen Pearson strain theory, classification of fracture with regards to healing:

> Narrow simple line  > OPEN reduction

Requires absolute stability, usually a surgical fix with plates and screw so there is zero movement of bone fragments. healing per primam

e.g. this type of healing is ideal for fractures where we don't want a callus for example, joint fractures, fractures of the epiphysis (a callus would restrict movement). 

> Wide complex line  > CLOSED reduction

Requires relative stability, fix fracture with plaster cast or erfix etc. healing is by secondary bone healing with callus formation.

e.g. comminuted fractures, fractures with gaps and mutiple fragments.