random clinical snippets

have been away from posting clinical pearls received for the month because i was on surgery and the hours did not allow for even 45 minute blocks of time to write and copy, i will have to transpose those notes at a later date. lost ten lbs during that rotation, was sleep deprived, unshaven and had a constant facial/stress rash the whole time, had a great time though haha!

so to get caught up, now on last rotation, pediatrics, having a great time as well- totally different culture than surgery, medicine, ob/gyn, neuro. the hospital is more tolerable as well, art and paintings on the wall, and more windows with larger rooms. after this the clinical year will be over. it was

definitely fatiguing, but well worth the effort.

three bugs of neonatal meningitis

-E. coli

-GBS

-L. moncytogenes (need ampicillin to cover this)

meningitic doses are 100mg/kg - start w/cefotaxime until culture rules out.

dont want to use ceftriaxone in newborn because this drug can spike bilirubin.

axillary temp should be 1 degree higher than rectal

Glycogen storage disorder type 1 (von gierke's) here is some next level pimping courtesy of the liver fellow - whats the difference between von gierke's type 1a 1b and 1c?

1a - lack of the G-6-phosphatase

1b - lack of transporter - get IBD like symptoms

1c - lack of cofactor in the transporter

clinical significance? in 1b you get neutropenia, won't get that in other types

clinical presentation of von gierke's - obese, overfed, ^triglycerides, 60-70% hepatic adenoma, small percentage of this population goes onto HCC

indications for intestinal transplant

-tpn dependent (lifestyle issue)

-good post op care

-no social contraindication (sex drugs and rock'n'roll stuff)

-loss of vascular access

-intestinal failure associated w/liver disease

-recurrent sepsis

contraindications

-cant be immunosuppressed (cancer)

KVO abbreviation for keep vein open - run fluid at low rate so you don't have to hep lock the IV

when dealing with an oppositional teenager be concrete - "if you don't take your insulin, you will lose you limbs, go blind, then die"

methylmalonic aciduria - give metronidazole to decrease proprionic acid (made by enteric flora), proprionic acid is substrate used to make more methylmalonic acid

Serious bacterial infxn

-uti, bacteremia, menin

gitis

Oragel - not good for teething babies, can cause methemoglobinemia

baby physcial exam pointers:

increased fontanelle size associated with hypothyroid

posterior closes in 1st six months, anterior closes 1.5 yrs

nasal septal polyps think associated w/cystic fibrosis

ear pits (dimples anterior to tragus) associated w/sensorineural hearing loss -not associated w/renal anomalies

Heart exam: most babies have a systolic ejection murmur best ascultated at the left sternal border, its called peripheral pulmonic stenosis, it goes away in 6 months

Vaginal bleedi

ng from a neonate- everythings ok! the babies baby endometrium has responded to maternal hormones.

hip dysplasia increased risk in females because they are more sensitive to hormone relaxin, get sonograms upto 4-5 months then switch to x-ray b/c neonatal skeleton will have calcified to the point where it can be visualized.

now for my favorite thing ever! the asymmetric tonic reflex, this primitive reflex is elicited by turning the babies head to one side, and the baby will pose his arms just as seen in the picture below- its also aptly referred to as the fencer's reflex-

i could not get enough of this, its so cute. ok babies are cute.

primitive reflexes should be gone by 4 months.

medical metaphor-

open a book and read a page, how often do you know what it is about? you need to read the pages leading upto the current page to get any idea of the story. so it is with patients, you must get the history!

pelvic inflammatory disease can lead to tuboovarian abscess which can lead to fitz hugh curtis abscess.

3 things you can never miss in ER

1. ectopic pregnancy

2. ovarian torsion

3. appendectomy

lower abdominal pain w/vaginal bleeding is rule out ectopic until proven otherwise.

ovarian torsion - radiates to groin, intermittent and sudden

sti's - fevers, discharge, dyspareunia

kids can get abd pain in UTI's

doing an abdominal/intracavitary ultrasound to rule out ectopic pregnancy? need to document two things

1. +/- intrauterine pregnancy

2. if +, document fetal heart rate if possible

tip- aminoglycosides increase botulinum levels and can precipitate botulinum toxicosis

maternal lupus can have maternal antibodies that cause complete heart block in neonate, may also present w/cutaneous lesions

bowel viral gastroenteritis can lead to secondary lactose intolerance (transient), as well as strip the gut of disaccharidases therefore don't give fruit juices because just make it worse because of osmotic diarrhea, also don't give cold fluids (i don't know why i just wrote that down)

allergic eosinophilic gastroenteritis is non IgE mediated - its secondary to multiple food allergies, can have patient on inhaled steroid but swallow it!! don't inhale.

milk protein allergy: presents young and this one is IgE mediated, bloody stools

oral allergy - from eating raw fruits can get swelling tingling in mouth, allergic to skins/pollens etc and this is IgE mediated

an adverse reaction to MMR vaccine is usually an allergy to the gelatin in which it is carried.

egg allergy? no flu or yellow fever vaccine

UTI's

risk: boys >> girls for first 18months because of increased bladder pressures, then girls >> boys in risk from thereafter

patient was a 20 year old female w/neuropsychiatric lupus complicated by episodes of immune mediated thrombocytopenia, before giving IVIG you have to check... IgA levels, bone marrow biopsy before giving steroids to make sure not a hematological malignancy

3 stages of whooping cough - only worth treating if you catch it in the catarrhal phase - use a macrolide (not erythromycin because can lead to pyloric stenosis vis a vis its gastric activity)

1. catarrhal phase (low grade)

2. paroxysmal (whooping stage)

3. convalescent stage

viral gastroenteritis? BBRAT diet

bread banana rice apples toast - only good for 24 hours

asymptomatic carotid notes

Carotid atherosclerotic disease

Symptomatic or asymptomatic?

Symptomatic -
-focal neurological symptoms
-refer to appropriate distribution
-1+ TIA/Stroke
-w/in last six months

*vertigo and syncope not generally caused by carotid stenosis


Asymptomatic
-trials have established CEA for asymptomatic men w/ ICA stenosis >60% w/life expectancy >5yrs with perioperative risk of death <3%.
Woman? medical management

aspirin recommended for all having CEA

Three trials VA, ACAS, ACST
1993 -VA - absolute risk reduction was 1% over 4 year follow up
444 men w/50-99% stenosis (assessed w/arteriogram)
randomized to aspirin or aspirin + CEA, mean 48 month follow-up
results
-decreased stroke/TIA
stroke or TIA decreased 8 vs 20.6%
pertinent negative: no difference in ipsilateral stroke
no different in combine stroke/death at 4 years (41 v 44%)

1995- ACAS - absolute risk reduction was 3% over 2.7yrs
1662 adults w/60-99% stenosis to ASA325 vs ASA+CEA
end point was ipsi infarction or death in perioperative period
results
-ipsi stroke/peri stroke or death 5 v 11 @ median f/u 2.7
Men had ARR of 8% women 1.4% 2/2 periop complications
-subgroup analysis - less effective in women (but not significant)

ACST - absolute risk reduction 3.1% over 3.4 yrs
3120 patients w/>60% asymptomatic, there was an immediate surgery and versus deferral group vs medical management.
-@3.4 yrs - CEA perioperative death/stroke was 3.1% w/in 30 days
-immediate > deferral @5yrs 6.4 v 11.8 for strokes and periop death
-ARR >men

Please take five minutes...

and follow along this gorgeous piece of music!! so beautifully written, every note is perfectly placed. perfectly timed

brain repair after stroke

Here is a very interesting grand rounds at UCSD about brain repair after stroke


principles of brain repair from grand rounds

1. brain repair is time sensitive - stroke physiology is a sequence of cellular events, have to time treatments accordingly (sequence growth factors, or if give NMDA blockers early kill recovery)
2. brain repair is experience dependent - need exposure to the lost function, task specific rehabilitation + repitition that leads to increase in behavioral recovery
3. have to optimize patient selection type, many therapies are $$, and there are many variables that modify outcome (age, handedness, genetics, medications, timing of events...)
4.value of domain specific endpoints - less global endpoints may be needed to understand repair issues because global recovery may be too broad to measure whats working

List of all neuro programs

This link was taken from student doctor network, it is a google map with every neurology program listed, nice to get a bird's eye view. Thanks to Dandelionwine for making it

original link

American Academy of Neurology practice bulletin regarding prescription of "neuroenhancement" in well adults

practice of medicine traditional goals or obligations

1. prevent and diagnose disease or injury

2. cure/treat the disease or injury

3. reduce suffering

4. educate

5. help patients die in peace and dignity

6. reassure the well

ethically more complicated behaviors

1. participating in executions

2. participating in interrogations

i add these

3. use of medicine as a direct coercive force

4. research and experimentation with complicated ethical questions

5. profit motivated medicine

role is divided into

core domain

-these are obligatory

secondary domain

-considered ethically permissible

AAN describes prescribing medication for the purpose of neuroenhancement at best to fall into the category of secondary domain and at worst ethically impermissible

reasons prescribing for enhancement may be considered permissible

-improves well being (similarly to plastic surgery)

-benefits > risks

issues worth considering before prescribing-

-prescriptions will be "off-label" until medications are specifically designed and approved for the purpose of enhancement

-"off label" use should be based on

1. plausible rationale

2. based on available evidence

3. consistent w/standard of care (unfortunately very little clinical evidence to inform this use)

-before prescribing must inform patient

1. not FDA approved for this use

2. side effects

3. risks (short term and long term)

4. alternatives to not taking the medication

Ethical considerations before prescribing

-Thorough assessment of patient

e.g. - just because a patient is requesting neuroenhancement does not mean they are well, have to do a full work up for existing pathology. the request itself may be evidence of existing condition or the patient's interpretation of their symptoms

thus the request for neuroenhancement is still a "chief complaint"

-Beneficence and nonmaleficence

the putative benefits of enhancement (increased competitiveness, intelligence etc) are difficult to quantify and thus difficult to compare to the risks of treatment. thus clearly stating treatment goals will help the physician

-Distributive justice

drugs unlikely to be covered by third party payers, will remain in the domain of the rich, so consider the effects of limited access on society.

-conflict of interest

"avoid financial arrangements that influence patient care", inform patients of conflict of interest (stock, financial incentives etc...)

-Liability

courts will probably analyze injury claims for neuroenhancement similarly as they do other cosmetic procedures - courts may or may not be more aggressive

case: Zalazar v Vercimack - expert witness testimony is not needed to prove causation for cases involving informed consent elective medical procedures because "there is no medical issue that requires explanation for the jury".

refrain from guaranteeing an outcome

The following are a couple of selected key practice guidelines put forth by the AAN

1. prescriptions of meds for "neuroenhancement" are not legally obligatory, not prohibited and legally permissible in the US

2. prescriptions of meds for "neuroenhancment" are not ethically obligatory or prohibited and therefore are permissible

3. there is limited evidence of efficacy and safety info for these agents

4. liability is uncertain and may favor the plaintiff

5. refusal to prescribe is both ethically and legally permissible

6. informed consent applies for the prescription of "neuroenhancing" meds

7. ending prescriptions for "neuroenhancement" after they have been initiated is both legally and ethically permissible

Reference:

Larriviere D, Williams M, Rizzo M, Bonnie R. "Responding to requests from adult patients for neuroenhancments, Guidance of the Ethics, Law and Humanities Committee" 2009. American Academy of Neurology. www.neurology.org

The macula speaks softly but carries a big stick.

In the OR today I saw a vitrectomy- the removal of the vitreous fluid from the posterior chamber of the eye, a surgical treatment for retinal detachment. As I observed this surgery and saw the macula live and very clearly for the first time something hit me (not a scalpel). It is surprising how humble a structure the macula is, especially considering how powerful it is. It is a square centimeter or so (no bigger than your pinky nail) but it receives all the light from the world that will eventually be processed into "sight". Without the macula one is essentially blind (peripheral vision will be spared, but try crossing the street using only your peripheral vision). It is really so small and so simple appearing, at least grossly, it almost looks indistinguishable any square centimeter of tissue, but it is oh so much more talented! As I was looking at this through the ophthalmologist lens, I found it amazing to consider that this little bit of mild mannered tissue catches light! Not only that it transforms it into a patterned electrical signal. How marvelous! This little bit, this tiny tiny bit of tissue can even sort wavelengths of light, weigh and average the intensity of the inputs and send it off in a ordered pattern that will eventually be critical for survival. Think about what that means in the most basic sense, electromagnetic fields can be sensed by carbon based tissues. How gorgeous! Even more so to consider that this little piece tissue came about organically, spontaneously. It is fun to speculate how this came about, why should sensing light matter to ocean life (where photoreceptors have been presumed to originate)? Theories abound, but the truth remains unknown. So it is that a structure appearing so small to the naked eye makes it possible to view the ends of the cosmos. There is lesson in there somewhere...

ophtho notes last day

glaucoma (cannot be prevented, but goal is to prevent losing eyesight within their lifetime)

epi

2nd most common cause of blindness in world (cataract #1)

asymptomatic!! like htn

glaucoma - no longer just increased intraocular pressure, need nerve damage now for definition

look for donut hole in optic nerve

sensitivity of IOP w/pressure of >21mmHg is 50%!!!!

narrow angle

pressure lowering drug - acetazolamide, timolol

laser iridotomy - putting a hole in the iris to assist in aqueous flow

open angle treatment

-prostaglandins, beta blocker, alpha agonist.

-drainage shunts can be placed

exfoliative glaucoma is when the iris sheds cells and pigment (during pupillary constriction/dilation) and blockes aqueous outflow.

family history

sibling odds ration 3.7

parents odds ratio 2.2

nasal field defect can clue you in to glaucoma because very rare to find neurological cause of nasal field defect

keratoconus - look up

pc haze post cataract surgery (develop membrane)

central retinal artery embolus
-tpa to ophthalmic artery not a good choice for because no benefit + increased mortality
tx - drop pressure - ocular massage, put a needle in eye drain pressure.

rule of hemiretina -half the retina (inferior or superior) w/pathology on funduscopy most likely vascular

vein occlusion



BRVO - hypertension - creates sclerotic arteries and AV nicking decreasing venous return and perturbing flow

CRVO (central retinal vein occlusion) - most commonly associated w/glaucoma, can also get w/coagulopathy, notice both hemiretinas are involved

wet macular degeneration gives you choroidal neovascularization

retinal neovascularization: diabetes, CRVO, BRVO, carotid disease
tx antiVEGF and PRP- panretinal photocoagulation
new vessel growth is bad because can cause - hemorrhage, traction retinal detachment, and neovascular glaucoma (anterior chamber)

"infections/inflammation in retina tend to look white"

papilledema has by definition increased ICP

ophtho notes

ophtho exam

LLL - lids, lashes, lacrimal system

CS - conjunctiva, sclera

K -cornea (~1mm thick, mostly collagen)

HPI: common chief complaint: eye pain

is it surface, ciliary, or deep orbit?

corneal abrasion, ulcers, lacerations exquisitely painful - goes away with drop of anesthetic (lasts for 20 minutes)

ciliary - iritis, acute angle closure, deep more boring pain, photophobia, light causes ciliary body spasm - narrow angle closure, relieved w/cycloplegics (dilators)

deep orbit -retrobulbar, myositis, optic neuritis multiple sclerosis

?'s - whats symptoms, tearing? time of day? recurrent symptoms? contacts? allergy, seasonal, dry eyes, topical meds? in one eye? suggests recurrent erosion

contact lens history - wearing habits, soft vs rigid vs gas permeable vs hard, cleaning habits?

trauma

sharp vs blunt

establish the force involved - size of object - fist is bigger than orbit, usually bones break globe is preserved. more worried about smaller objects (pencils, golf balls, paint balls etc)

foreign body?

chemical?

infraorbital hypothesia? orbital floor fracture disrupts nerve.

pain and loss of vision may not correlate w/severity of injury

topical anesthetic is epithelial toxic, can cause ulceration over time (no prolonged use)

hypopion - white blood cells in anterior changes

drops:

antibiotics - drop or ointment

corticosteroids - milky white (risk of cataract and increased intraocular pressure)

combo antibiotics and steroids

cycloplegics (red-top)

anti-glaucoma

beta blocker

check airway hypersensitivity

carbonic anhydrase inhbitors

alpha2 blockers - cause depression

prostaglandins

Orals

diamox (acetazolamide) lowers intraocular pressure fast (used in narrow angle and pseudotumor cerebri)- sulfa allergy

oral prednisone

anti-inflammatory - indomethacin

dendrites on the cornea under fluorescein dye- herpes

angular artery will anastomose w/internal circulation (retinal arter)

random clinical notes:

neurofibromatosis1 - can have sphenoid wing dysplasi

scleral show- see sclera above and below the iris secondary to sympathetic tone (muller's muscle, tarsal), seen with exophthalmopathy in grave's

iris becomes pigmented secondary to sympathetic tone (during development and birth). if you have horner's at birth can get anisochromia (different eye colors).

sarcoid - increases size of lacrimal glands bilaterally

iritis - seen in automimmune disease

pseudomonas/gonococcus can eat through the cornea and as fast as 24-48hours

dry macular degeneration progresses to wet

wet - edematous ischemic choroidal neovascularization and retinopathy.

risk factors for macular degeneration

age, white people, fam hx/genetics, smoking, diet (AREDs vitamin help), cardiovascular

AREDs vitamins (vit A,C,E and Zinc shown to decrease relative risk of macular degeneration by 25% (trial AREDs II)

Lutein may help although no RCT's have been conducted

treatment for wet macular degeneration- antiVEGF (intravitreal injection) qmonthly, side effects- may increase risk of CVA

Diabetic retinopathy - 2 signs

macular edema - most common cause of blindness in working age adults

neovascularization - bleed, heal fibrose, cause traction bleeding detachment, tx - laser antiVEGF

neovacular glaucoma - vessels grow near canal of schlemm, membranes form crowding area can cause acute narrow angle closure

radiation therapy can cause a retinopathy results in lipid exudates (hard exudates) that look indistinguishable from diabetic retinopathy

cherry red spot in adult? (without tay sachs!) - central or branch retinal artery occlusion

syphillis - interstitial keratitis (salmon patch)

sudden loss of vision in one eye - check red reflex - if not there can be retinal hemorrhage

External Disease, Review of Common Disorders and Treatment

blepharitis - itchy burning tearing or inflammation of meibomian glands in eyelid (oil layer stabilizes the tear layer from evaporation)

hordeolum or chalazion?

chalazion - lipogranuloma occurs in leibomian gland, can last for months, warm compress helps

hordeolum - occurs anterior in the eyelid in sweat and sebaceous glands (normally staph infxn)

basal cell - crusting in one area only (most commonly on lower lid), if in medial canthus no lashes where tumor is!

viral papilloma - sessile of pedunculated (normally caused by HSV) tx cut it off +cryotherapy

molluscum contagiosum - pox virus, common in kids, round waxy umbilicated, tx excision and cryotherapy

contact dermatitis - can get from eye drops, can involve entire face!

dacrocystitis - infection of lacrimal sac (tear draining) tx - don't drain external if can help it - use systemic antibx and warm compress, if doesn't get better will need laser surgery.

dry eye -

red painful eye impaired- vision or no? (first question) - no vision? need to be seen now. angle closure glaucoma (pain and blindness)

uveitis, trauma

have you had eye surgery recently? painful red eye after surgery - must be seen immediately. rule out endophthalmitis (most dreaded complication) need to be seen and tapped, intravitreal anti-bx

gonococcal keratoconjunctivitis - hyperacute conjunctivitis (<24hours), ask about urethral discharge, can penetrate and bind to healthy corneal epithelium - seen daily by ophthalmologist daily irrigation, anti-bx

conjunctivits- itch?, allergy?

EKC - epidemic keratoconjunctivitis - exposure to symptoms - 5-12 days. systemic symptoms, virus moves to cornea and inflammation subepithelial infiltrates and drop your vision, lesions in cornea can last months or years

hsv dendritic keratitis - active viral replication in epithelial cells, stains w/rose bengal and fluoroscein, can deinnervate the cornea (making painless neurotrophic ulcer), deinnervation decreases healing of cornea. add oral tx, or trifluridine q2 (9 times a day)

sleeping in contact lenses increases risk of bacterial keratitis 20x because of hypoxia under lense tx corneal ulcers w/fortified antibiotics q30minutes! acanthamoeba keratitis - amoeba that gets in during swimming or hot tub w/contacts lenses, ring ulcer

anesthesiology notes

Oxygen:

Not oxygenating:

look at color of skin: cyanosis,

temperature: don't want cold, clammy

stridor - upper airway (inspiratory)

wheezing - lower partial small airway obstruction (starts expiratory can be both)

pO2 <60 begin to get tissue ischemia

CO poisoning - sat will be 100% - have to look at pH!!! pH will be acidotic

people with a history or current treatment with bleomycin should not be given 100% O2 because this can accelerate the development of pulmonary fibrosis

02 tank - E is the size of tank (basic transport tank). all tanks filled to 3000psi - full tank lasts 1000L!!

so for example 750 psi - is a quarter full, which means 250L, at a flow rate of 5L/min you have (250/5) 50 minutes of O2.

say you're in preop and patient has cardiac history, how can you assess the risk of post-op cardiac complications?

you would use the revised cardiac risk index (RCRI).

does the patient have:

1 undergoing a high risk surgery

2. ischemic heart disease

3. chf

4. history of cva

5. insulin dependent diabetes

6. creatinine >2

a point for every yes answer, then how many points?

Risk of post op cardiac complications

0 0.4%

1 0.9%

2 7%

3 or > 11%

a wide pulse pressure in patients w/hypertension has been associated w/increased perioperative adverse events

here's a little advice from an ENT attending:

"save 20% of your income every year starting from residency, you will be a wealthy man"

and more from the ENT

...at some point in your life you realize you have a determinate end, you have to start being real with people, lose the intimidation factor and talk to people irrespective of their station because we all have to meet god someday, talk to the powerful in the same way that you talk to the low.

back to anesthesiology

here are some contraindications to using succinylcholine as a muscle relaxant:

if a person has had a stroke, the death of the upper motor neuron increases the expression of extrajunctional nicotinic acetylecholine receptors at the neuromuscular junction (lower motor neuron) and because succinylcholine is a depolarizing NMJ blocker, the depolarization can cause a hyperkalemia. This hyperkalemia can be severe enough to cause cardiac arrest. If you are using succinylcholine expect the patients K to jump 0.5mEq/L. Succinylcholine also contraindicated in persons w/history of burns, trauma, malignant hyperthermia (succinylcholine is a trigger for this, as is the volatile halothane).

An observation I had about anesthesia:

Anesthesia is interesting in that there is differentiation between sedation, amnesia, anesthesia, analgesia, and paralysis. The definitions being:

Sedation: a general lack of awareness, but not necessarily loss of consciousness or loss of explicit or episodic memory memory

Amnesia: the loss of memory

Anesthesia: the loss of consciousness or feeling or awareness but NOT the loss of pain

Analgesia: the loss of pain.

Paralysis: loss of voluntary (and sometimes involuntary) muscle function

So now this is where it gets interesting, if you are brought under general anesthesia with an intravenous drug, propofol, you will loss consciousness and possibly your memory of any new stimulus the occurs while under the influence of this agent. And then if you are cut with a scalpel blade while under propofol anesthesia, although you are unconscious, your sympathetic nervous system will be greatly activated. Your heart rate and blood pressure will go up in response the destruction of your tissues. And although you are not aware of it, you body will be experiencing the pain of the scalpel. That is why in addition to anesthesia a patient is given opioids (pain-killers).

Once pain-killers are in the system the sympathetic response to the scalpel is blunted, and even though the body is subjected to the trauma, it can be said the patient feels no pain. My question is, how does the experience of pain differ if one has no episodic memory of the pain or at the very least did not consciously experience the pain? Its an interesting distinction that anesthesiologists make between anesthesia and analgesia. What complicates matters is that there exists evidence that although one is under general anesthesia there is some baseline awareness. Evidence for this conclusion comes from experiments where patients are read material while under anesthesia and then given free association exams post-operatively. The central finding is that those who were read to under under anesthesia free associate with content from the literature they were read, in one example when prompted with "Friday" the the free association was Robinson Crusoe for several patients to whom this work was read none for controls. So what is going on here with general anesthesia? Loss of consciousness does not completely erase an experience and that learning does take place. An interesting (and probably unethical) study would be to see if Pavlovian classical conditioning exist in unconscious humans. Essentially you attempt Pavlovian conditioning while under general anesthesia (probably using nociception) and then see if this effect persists when the stimulus is applied to the same person now conscious, it would provide evidence for the idea that conscious awareness is just the "tip of the iceberg" from the perspective of cognitive functioning.

Now, my own suspicion is that the universe is not only queerer than we suppose, but queerer than we can suppose. I have read and heard many attempts at a systematic account of it, from materialism and theosophy to the Christian system or that of Kant, and I have always felt that they were much too simple. I suspect that there are more things in heaven and earth than are dreamed of, or can be dreamed of, in any philosophy. That is the reason why I have no philosophy myself, and must be my excuse for dreaming.

-John Burden Sanderson Haldane

Primary care prevention project idea: PP4P

Novel Strategies for the prevention of type 2 diabetes: Pay the patient for performance (PP4P)


Eugene Scharf –MS3
3/9/11
Primary care rotation: Scarsdale medical group


Case:

Patient DM is a 36 year-old man with a past medical history of hypertension and obesity. He was last seen in the office two years ago for a check up. The interval history between now and his last visit is remarkable for an increase in bodyweight of 20lbs. He now presents to the clinic for an annual physical.

PMH:
Hypertension – diagnosed 2004, controlled with medication
Obesity –5’10” 223lbs BMI = 32
PSH:
Inguinal hernia repair 1997
Ankle fracture ORIF 1999

Family history:
CAD in father (MI age 55)
Stroke in grandfather (mother’s side)

Social history:
Born in Mumbai, India. Moved to US in 1995, employed as a computer programmer. Single, sexually active, uses protection. Some exercise on weekends. No tobacco, no caffeine, social drinker, occasional marijuana use.

Medications:
HCTZ 25mg
Ayurvedic herb tea
Multivitamin daily

Allergies: NKDA
ROS: +decreased appetite +fatigue +thirst
Physical Exam:

PE:
Gen: obese man in NAD
Vital signs:
T: 36.8 BP 136/80 P 78 RR 14
+central obesity, waist: 43”

Laboratory studies:

BMP: 140 | 110 | 18 / 175 Ca: 9.0 Mg: 2.3 Phos: 3.3
4.0| 25 | 1.3\

CBC: 7.8\ 40 | 14.0 / 350
Liver chemistry: 7.9/4.5/1.3/0.1/50/45/80
Lipids:
Total cholesterol: 250
HDL: 39
LDL: 160
Triglycerides: 185
A1c: 6.0%
TSH: 5.05
Total T4: 7.6
HIV: negative
Hepatitis panel: negative

How should we think about DM’s case? Does the combination of his increased waist circumference, high blood pressure, abnormal lipid panel, high random glucose, and elevated A1c indicate that he is at risk for developing type 2 diabetes? His social history is also remarkable for a sedentary lifestyle (employed as a computer programmer) and too little exercise (weekends only). Finally, DM is also relatively young (age 46) so it is important to know whether there are any interventions that could possibly have long lasting positive consequences on his life quality and mortality. However, what is certain is that DM’s metabolic and physiological health information indicate that he has come to a critical juncture in his life, and his behavioral decisions will now have lasting implications. In this paper I will argue that preventing his and others progression to type 2 diabetes can be significantly reduced by creating cost-saving patient performance financial incentives. Let us first create the context for this discussion.

In 2001, Boyle et al. published an estimate of the prevalence and incidence of type 2 diabetes in America. Based on data from both National Health Information Survey (NHIS) and National Health and Nutrition Examination Survey (NHANES) his group estimated that the prevalence of diagnosed diabetes in America in 2000 was 4.0% or approximately 11 million. His group then went on to predict that by the year 2050, there would be approximately 29 million diagnosed cases of diabetes, with a prevalence of 7.2%1. However, the American Diabetes Association (ADA) reported in 2010 that the current number of diagnosed cases of diabetes was 18.8 million, as well as 7 million cases of diabetes undiagnosed2. This report also indicated that the annual incidence of diabetes was 1.9 million cases/year. Holding that incidence constant and taking only diagnosed cases into consideration, this means that our nation would arrive at Boyle’s et al. 2001 estimate of 29 million cases by 2020, or thirty years ahead of his groups’ original prediction. This 2010 report by the American Diabetes Association also estimated that there are approximately 79,000,000 cases of pre-diabetes in America. Boyle et al followed up with a 2010 report3 that adjusted their prior predictions and re-stated the prevalence of diabetes in America by 2050 based on estimates of incidence and mortality to be between 21 and 33%, with a “middle of the road” estimate of 25%. Combining this estimate with a 2008 Pew Research Group report4 US population estimate of 438 million the result indicates that an estimated 109,000,000 Americans will have diabetes by 2050, up from 11 million at the beginning of the century.

I next sought to investigate the cost burden of diabetes. To this end the ADA published a cost analysis in 20075. This analysis reported the annual national burden of diabetes to be at least $174 billion in 2007 dollars (a figure >5.5 times the 2010 NIH total budget). This cost was broken down into medical expenditures ($116 billion or roughly 2/3 of the cost) and lost productivity ($58 billion, 1/3 of the cost). This analysis concluded that half of all annual medical expenditures in diabetes related to inpatient medical care. Also, considering lost productivity, 82% of the total $58 billion of this cost came from reduced work productivity (35% or $20 billion) and early mortality (47% or $27 billion). The report concludes that persons diagnosed with diabetes on average incur healthcare costs of $11,744/person year, of which $6,649 are costs strictly related to diabetes. Also this cost analysis did not estimate lost productivity of disease burden on well persons (e.g. – well person missing work to care for relative with diabetes), the annual burden of Medicare diabetes administration costs, and assumed the annual cost of persons with pre-diabetes to be $0. Thus the actual costs were determined to be higher than the calculated estimate of $174 billion. Therefore, given the predicted incidence and high future prevalence of diabetes combined with the high annual financial burden of the disease I next sought to investigate whether preventive data exist, and if so what measures are either cost effective or cost saving.

Modern diabetes prevention studies began in 1986 with the China Da Qing study, where 577 Chinese men with impaired fasting glucose were randomized to control, diet, exercise and diet & exercise experimental wings. At a 6 year follow-up, the proportion of individuals with diabetes was significantly lower in the diet & exercise group compared to the control arm (mean 44% vs 66%). The first large scale trial to support the benefit of glycemic control was published 1998, the United Kingdom Prospective Diabetes Study (UKPDS) showed that tight glycemic control in patients with newly diagnosed type 2 diabetes prevented microvascular endpoints (nephropathy, retinopathy, neuropathy) by 25%7. In short 3,867 newly diagnosed type 2 diabetics were randomized either a control group of conventional therapy with the aim of keeping blood glucose levels <270mg/dL versus experimental arms of insulin or sulfonylureas with the aim to keep blood glucose levels <110mg/dL. The UKPDS had a confounding variable worth reporting; in the experimental group sufficient glycemic separation (<110mg/dL) could not be achieved by just one agent thus metformin was added to the experimental group. As well the conventional group (control) had difficulty maintaining consistent blood glucoses of <270mg/dL, thus 80% of the control group received metformin as well. In fact 58% of the total control group patient*years of UKPDS were confounded by metformin use. Mean A1c’s were 7.0% vs 7.9% in experimental versus control, and at 15 year follow up there were no differences in myocardial infarction, stroke, or diabetes related mortality. A trial published in the New England Journal of Medicine (NEJM) 20018, approximately 85,000 female nurses taken from the nurses health study begun in 1976 were followed for 16 years for incident cases of diabetes (of which there were 3300). The study’s finding showed that the RR of diabetes increased sharply depending on BMI at the time of enrollment. BMI’s of >30 had a relative risk of 20.1 (16.6 -24.4), and BMI’s of >35 had RR of 38.8 for acquiring diabetes. This study clearly demonstrated that BMI and bodyweight greatly predicted disease risk. Another NEJM trial published in 20039, by the Diabetes Prevention Program Research Group demonstrated the superiority of diet and exercise compared to metformin or placebo in preventing diabetes. In this trial (DPP), the experimental group consisted of diet and exercise and was formally defined as losing 7% of bodyweight, physical activity >150 minutes per week, and dietary fat constituting <25% of total caloric intake. Both the metformin and placebo group were given information on the importance of exercise, but no requirements. Interestingly, on 50% of those in the diet and exercise group made the weight goal, average follow up was 2.8 years. The trial results clearly showed that diet and exercise prevented new cases of diabetes significantly better than either metformin or placebo. Cumulative incidence rates over follow up were for this study 14% vs. 22% vs. 29% at 3 years. It was shown that the number needed to treat (NNT) to prevent one incident case of diabetes in the diet and lifestyle group was 6.9. Finally, consider that diet, exercise, and weight loss interventions have been shown to persist past the treatment duration. For example, 20-year follow-up of China da Qing study published in the Lancet10 showed that the relative risk of acquiring diabetes of those members of the diet & exercise treatment arm compared to the control arm was 0.57 at 20 years follow up. This finding supports the notion that early diet and exercise interventions have protective effects that outlast their treatment periods. This finding has enormous implications for diabetes prevention. My next step in understanding current methods for diabetes prevention was learning whether or not models exist for predicting absolute risk of acquiring diabetes. One such model from the Framingham Offspring Study11 attempted to assess this risk and created a model for a person’s 8-year risk of acquiring diabetes. This predictor model includes the clinical measurements fasting glucose, BMI, HDL-C, triglycerides, family history, and blood pressure together to create a weighted score with which to predict a person’s risk of diabetes. If patient DM’s clinical data are entered into this model, we arrive at a score of 10 or 20, depending on whether or not his fasting glucose is more or less than 100mg/dL. The uncertainty about this metric creates uncertainty about his true 8-year risk; as it is either <3% or 18%. However, the advent of hemoglobin A1c as a point of care diagnostic tool for diabetes helps to remove doubt regarding risk of diabetes when fasting glucose measurements are not available. I assumed that the risk of diabetes could be reasonably predicted and the diagnosis accurately made by using clinical metrics. Thus, in proposing novel diabetes prevention strategies, I next sought to learn whether or not existing diabetes prevention strategies were cost-effective. A 2010 systematic review by Li12 et al of twenty years of cost effectiveness analyses of diabetes prevention strategies indicated that several cost effective strategies exist, and many are cost saving. This review defined an intervention as cost-effective if it resulted in an inflation adjusted cost-effectiveness ratio of less than or equal to $50,000/QALY. One important prevention strategy that was found to be extremely cost effective (<1,200/QALY) in one analysis and cost saving in all others was the use of angiotensin receptor blockers (ARBs) for type 2 diabetes to prevent hypertension and progression to macrobalbuminuria and renal failure versus either placebo or standard therapy. Thus I propose as a first step toward preventing the morbidity of long term diabetes resulting from hypertension and renal failure is the subsidized provision of ARB’s or ACEi to all diagnosed diabetics. However this idea would only help prevent morbidity after a diagnosis and thus not fully address primary prevention. Given that several of the aforementioned diabetes trials have indicated that diet, exercise and reducing bodyweight is superior to all other primary prevention strategies for preventing type 2 diabetes, I next sought to understand if these interventions are cost effective. To this end the same Li et al. review addressed the cost utility of strict glycemic control (with insulin, sulfonylurea, or metfomin), diet, education, or behavioral modifications. In all other healthcare systems outside the U.S. these measures were highly cost-effective or cost-saving. In the US, strict glycemic control as a prevention strategy costs ~41,384/QALY. However in the CDC cost sensitivity analysis that provided this figure13, cost effectiveness for strict glycemic control depends on age. For example; in age groups 25-34 it was 9,600/QALY, and 35-44 was 18,309/QALY, much less than the average for all age groups. But if one refers back to the DPP trial, strict glycemic control was also achieved in a much more cost-effective manner: diet and exercise. Thus we arrive at the central question in diabetes prevention. If diet, exercise and bodyweight reduction have been shown to be superior to all other preventive strategies for type 2 diabetes, why can’t we achieve this goal? People at risk for type 2 diabetes may not control their diet or exercise because there is no incentive to. The morbidity associated with type 2 diabetes is oftentimes decades away, and thus incentive for good behavior now does not exist. However I believe that positive incentives can create cost-saving behavioral modifications resulting in significant prevention type 2 diabetes. Thus I propose that we can reduce the cost burden of diabetes by providing cash incentives to high-risk individuals between the ages of 25-44. Given that Hemoglobin A1c is a reliable marker of blood glucose control for the previous three months, and that glycemic control (fasting glucose <100mg/dL) is associated with reduced risk of diabetes, I propose cash incentives for hemoglobin A1c’s under 6.0% for high risk individuals (impaired fasting glucose, BMI >32, or diagnosed diabetes). For example as stated earlier, in 2007 the economic cost of diabetes was ~6,649/person. If a patient previously diagnosed with type 2 diabetes can show through lifestyle modifications that his/her A1c is now below 6.0% they are eligible for four quarterly payments of $250 (for the quaterly A1c’s) or $1,000 annually. In this scenario, the economic burden of $6,649 is reduced to $1,000, and the patient benefits directly and tangibly from his/her actions with a cash reward. The payments are made from either Medicaid or insurance. Paying patients for outcomes may at first seem counter-intuitive, however the measure would likely be cost saving in light of cost analysis data suggesting the decreased costs related to A1c’s <6.5% (i.e. reduced diabetes incidence). And if a patient is not able to lower his/her A1c to goal, no payments are made and the system absorbs the cost as would have without the program. A patient (similar to our patient DM) with pre-diabetes would be eligible for “Pay for A1c” program thus averting the cost to the system for each year of prevention (as indicated through A1c). One critical component to the program lies in establishing a correlation between A1c and BMI because although A1c defines diabetes, lowering BMI is what can prevent diabetes. To that end I propose a final step, cash incentive for BMI reduction. Thus for every type 2 diabetic patient whose BMI becomes less than 30kg/m2, a one time payment of $1,000 (the patient cannot go back and forth through the set point of 30 to collect multiple payments). As our century progresses the prevalence of diabetes is projected to grow rapidly, such that the annual cost burden of the disease may become unmanageable. In order to prevent this impending liability to say nothing of the human cost, stronger incentives must be created to modify human behaviors to ways congruent with clinical trial proven lifestyle interventions. First, hypertension medications such as ACEi and ARBs have been shown to be cost saving for preventing morbidity associated with hypertension and diabetic nephropathy (the leading cause of renal failure in the US). Thus subsidized provision of these medications for diabetic patients must be policy. Second, proper diet, exercise, and bodyweight control could be attained with financial rewards to those individuals between the ages of 25 – 44, and defined as high risk (impaired fasting glucose, A1c greater than 6.0%, BMI >30, diagnosed diabetic). Two proposals for achieving these measures are “Pay for A1c” cash incentive and a one time cash outlay for diabetics whose BMI’s are lowered to <30 through their efforts of diet and exercise.

Reference:
1. Boyle JP, Honeycutt AA, Narayan KM, Hoerger TJ, Geiss LS, Chen H, Thompson TJ. Projection of diabetes burden through 2050: impact of changing demography and disease prevalence in the U.S. Diabetes Care. Nov;24(11):1936-40
2. American Diabetes Association
www.diabetes.org/diabetes-basics/diabetes-statistics/
3. Boyle JP, Thompson TJ, Gregg EW, Barker LE, Williamson DF. 2010. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence. Population Health Metrics. 8:29.
4. Pew Research Center 2008. US Population projections: 2005-2050.
5. Dall T, et al. 2008. Economic costs of diabetes in 2007. Diabetes Care Vol31:3, 596-615
6. Pan XR, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 1997;20(4)537-44.
7. UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. The Lancet, 1998. Vol. 352, 837-853
8. Hu FB et al. Diet Lifestyle, and the Risk of Type 2 Diabetes Mellitus in Women. NEJM 2001; 345;790-797
9. Tuomilehto J et al. Prevention of type 2 Diabetes Mellitus by Changes in Lifestyle among Subjects with impaired glucose tolerance. NEJM 2001 344:1343-1350
10. Li G et al. The long-term effect of lifestyle interventions to prevent diabetes in the China Da Qing Diabetes Prevention Study: a 20-year follow-up study. The Lancet, 371:1783-1789
11. Wilson P WF et al. Prediction of Incident Diabetes Mellitus in Middle-aged Adults: The Framingham Offspring Study. Arch Intern Med. 2007; 167:1068-1074
12. Li R, Zhang P, Barker L, Chowdhury F, Zhang X. Cost effectiveness of interventions to prevent and control diabetes mellitus: A systematic review. Diabetes Care 2010 33:8
13. The CDC Diabetes Cost Effectiveness Group. Cost-effectiveness of intensive glycemic control, intensified hypertension control, and serum cholesterol level reduction for type 2 diabetes. JAMA 2002; Vol.287:19