Monday, March 31, 2014

1.Outpatient care for DM: 
-ask about hypoglycemia
-ask about sugar control
-screen foot exam annually (inspection, foot pulses, 10-g monofilament plus testing any one of the following: vibration using 128-Hz tuning fork, pinprick sensation, ankle reflexes, or vibration perception threshold)
-protinuria screen yearly
-dilated eye yearly
-A1C every 3-6 mos dpending control
-lipids annually
-vaccinations
-Stress test if they have sx, anbl ekg, abnl exam.
-aspirin?
2. Inpatient management of DM
-Things affecting glucose control: NPO, loss appetite, acute stress
-Avoid hypoglycemia (death)
-Hyperglycemia will impair immune response and healing.
-Goal 110 fasting 180 postprandial
-Don't stop oral hypoglycemics if they can eat
-If they're really sick or will need studies, hold PO hypoglycemics
3. Inpatient management of DM-- insulin 
-Drop basal insulin by 1/2 to 2/3 if theyre going to be NPO
-Don't stop all their meds and replace with SSI: maintain home insulin regimen +SSI if needed.
-Total insulin 0.6 u/kg/day, or home dose, half if crcl<60
-Half of total dose basal, half prandial - if eating, divide prandial dose by # meals.
4. Sliding Scale:  
-Low schedule (<40 u/day)
BG 150-199: 1 unit bolus Insulin (regular or rapid-acting)
BG 200-249: 2 units bolus Insulin
BG 250-299: 3 units bolus Insulin
BG 300-349: 4 units bolus Insulin
BG Over 350: 5 units bolus Insulin
-Medium schedule (40-81 u/day)
BG 150-199: 1 unit bolus Insulin (regular or rapid-acting)
BG 200-249: 3 units bolus Insulin
BG 250-299: 5 units bolus Insulin
BG 300-349: 7 units bolus Insulin
BG Over 350: 8 units bolus Insulin
-High schedule (Insulin-resistant) (>81 u/day)
BG 150-199: 2 unit bolus Insulin (regular or rapid-acting)
BG 200-249: 4 units bolus Insulin
BG 250-299: 7 units bolus Insulin
BG 300-349: 10 units bolus Insulin
BG Over 350: 12 units bolus Insulin
5. DKA
-Gap acidosis
-+ketones (B-OH-butyrate)
-More common in DM1
-Usually stress trigger - look for it.
-Tx with fluid bolus (avg deficit 5-7 L). Give 0.9 NS
-Tx w insulin (start with insulin drip until the gap is corrected, then transition to SQ long acting insulin with an overlap of several hours)
6. HONC 
-More common in DM2
-Sugars > 600
-No ketones, no acidosis, serum osmolality > 320
-Tx with fluids (avg deficit 10L) 0.9 NS. Avoid LR because it has K and lots of people have renal failure
-Give insulin, but less than for DKA
7. Secondary DM
-Drug induced: steroids, tacrolimus, cyclosporine, thiazides, B-blockers
-Other disease: cushings, gestational, pancreas dx, CF, hemochromatosis
8. When to get EKG
-Baseline - people at risk for heart disease
-Maintenance - people with heart disease that you want to monitor
-Diagnosis - people with symptoms.
9. EKG
-large box 0.5 mV given normal scaling.
-small box 0.04s, large box 0.2 s
-Rhythm: if there is a p before every qrs, and qrs after every p = p:qrs ratio = 1
-P wave should be upright in 2, and down in AVR
10.

Sunday, March 30, 2014

1. Different types of hypertension
-Pseudohypertension, calcific atherosclerosis- old people its hard to get accurate bp measurements with the cuff.
-Accelerated hypertension -en dor gan damange wthout papilledema
-Malignant hypertension: one or more of the following: papilledema, pulmonary edema (sudden onset heart failure), neurologic findings, angina.
2. Medications/drugs causing hypertension:
-sympathomimetics (decongestants, anoretic agents). NSAIDs, steroids, cyclosporine/tacrolimus, OCPs (takes 3 cycles/3 months to normalize BP after stopping OCPs), TCAs, erythropoeitin. -more than 1-2 drinks, smoking, caffeine, amphetamines/cocaine
-licorice flavored foods
3. Exam findings:
-BP tends to rise on standing in essential hypertension, tends to fall in secondary
-Carotid bruits (think renal artery atherosclerotic narrowing), chest bruits (coarctation), abdominal bruits (renal a stenosis)
4. Baseline labs at diagnosis 
-BMP to look at renal function
-U/A (protein)
-EKG
-TSH to r/o thyroid disease
-Fasting lipids
5. JNC 8 nuances:
-Outcomes (mortality, CAD) correlate with home BP measurements much more strongly than office measurements
-Chlorthalidone protects against electrolyte swings better than hydrochlorothiazide
6. Comorbidities
-HTN and diabetes: ACE or ARB, or CCB/thiazide in black patients
-HTN and CKD: ACE/ARB
-HTN and CAD: B-blocker + ACE/ARB
-HTN and stroke: ACE/ARB
-HTN and heart failure: ACE/ARB + B-blocker
-HTN and LVH: ACE/ARB
7. Diuretics: 
-Absolute indications: heart failure, elderly (good evidence of stroke mortality reduction in this group with diuretics/CCB), systolic htn
-Use with caution: Diabetes
-Relative CI: gout/meds that cause hyperuricemia like cyclosporine, dyslipidemia
8. B-blockers
-Absolute Ind: angina, after MI, tachyrhythmias
-Relative Indication: heart failure (not crazy bad), pregnancy (IUGR), DM (suppresses sx of hypoglycemia)
-Absolute CI: asthma, COPD, heart block
-Relative CI; dyslipidemia, athletes, PAD (can worsen claudication)
9. CCB
-Absolute Ind: Angina, elderly patients, systolic hypertension
-Relative ind: PVD
-Absolute; heart block (amlodipine/nifedipine OK)
-Relative CI: heart failure (neg ino/chronotrope)
10. ACE-I
-Absolute Indication: heart failure, LV dysfunction, after MI, history of angioedema (ARB also CI-- try CCI, has some renal protective effects)
-Absolute CI: pregnancy (fetal renal agenesis), b/l RAS, hyperkalemia (esp if Cr > 2.5, K > 4.5, can increase K)
11. When to initiate medications
-Stage 1: one drug, stage 2: 2-drugs
-Any end organ damage (LVH, AV nicking) - start meds, don't wait for lifestyle modifications to take effect.
-Evidence of renal injury: start ACE even if their BP is normal. Titrate ACE up as high as you can without causing hypotension. Continue even if proteinuria resolves, because it will resume once you stop the meds.

Saturday, March 29, 2014

1. Opioids 
-Conjugated in liver and are excreted via kidney (90-95%). Worry at CrCl<30
-Dilaudid and fentanyl do NOT have toxic metabolites so they're better for ESRD patients. Most other opiates do.
-Need bowel regimen.
2. Fentanyl Patch
-Fentanyl patch takes 12-24 hours to reach full effect
-Lasts 24-72 hours
-Put on an area without a lot of adiposity (i.e. back)
2. Fentanyl Patch Conversion
-Simple rule: 1mg PO morphine is approx 1/2 mcg fentanyl
-25mcg/hr q 72 hours fentanyl patch is equivalent to the following
-Morphine 15mg IV or 50mg PO q 24 hours
-Dilaudid 3mg IV or 12 mg PO q 24 hours
-Oxycodone 30mg PO q 24 hrs
-Vicodin/tylenol 3 - 9 tables a day
-Norco 4-5 tabs q 24 hours
3. Methadone conversion rate depends on daily morphine equivalency dose. 
-Morphine <100mg/day (1:3)
100-300mg/day (1:5)
300-600 mg/day (1:10)
600-800mg/day (1:12)
800-1000mg/day (1:15)
>1000mg/day (1:20)
-Long and variable t-1/2 (12-120 hours).
-Drug drug interaction
-QT prolongation/torsades.
4. Basic IV to PO morphine conversion- 1:3 
5. Opioid equivalency chart 
6. Morphine peak effects + dosing
-IV peak effect 10 minutes, lasts 1-2 hours.
-SQ peak effect 20 minutes
-PO peak effect 30-60 minutes, lasts 3-4 hours.
-Dose at peak - so IV, dose, wait 10-15 mins, if they are still in pain, give more.
-Breakthrough pain - give 10% of total daily dose at once. Dose at peak.
7. Management of opioid side effects
-Constipation: softener + stimulant (colace + senna aka pericolase), miralax, sorbitol, bisacodyl. If no BM in 4 days consider enema
-Sedation: tolerance usually develops. Avoid sedatives/anxiolytics, consider adding CNS stimulants (caffeine, methylphenidate), reduce teh dose.
-Nausea/vomiting: reduce the dose or pick another drug. Antimotility agents (metoclopromide, prochlorperazine), scopolamine patch, haldol (potent dopaminergic antagonism at the CTZ). Haldol works after spinal anesthesia with local or morphine
-Pruritis: reduce the dose or pick another drug. Antihistamines, H2
-Delirium: reduce the dose or pick another drug. Antipsychotics (haldol, risperidone)
-Respiratory depression: sedation always precedes respiratory depression. Stop opiate, low dose naloxone to avoid withdrawal crisis. Dilute 0.4mg (1mL of 0.4mg/mL amp) in 9cc saline. Use 1cc q5 minutes until respirations improve. Also, bag-mask while you do this.
8. Short vs long acting
- Titrate inpatient meds until they are OK to go
- Take 24 hour total dose, convert to PO
- 80% long acting, 20% for breakthrough
9. Opiates for renal dysfunction
- Fenanyl is better
- Morphine is worse- glucuronidated to M6G, which is more potent and more emetic than morphine.
10. Benzos & opiates
- esp those who are glucuronidation (like lorazepam) compete with morphine for excretion, and can synergize the toxicities.

Friday, March 28, 2014

1. Initiate insulin- 
-start with weight based basal dose of lantus, or start with 10 units.
-0.2units/kg
-If Cr clearance <60, divide insulin by half since its renally cleared.
-Titrate until their fasting sugars are at goal (typically fasting 80 to 120-125, 2 hour post prandial 150-180)
-If fasting sugars are good but A1C is high, consider adding mealtime coverage
-Once you're at over 50 Units, divide into 2 doses for better absorption.
2. A1C goals
-Based on ACCORD trial : randomized older, sicker people to either go to A1C of 6.5 or 7.5; mortality was higher in more aggressively managed group 2/2 more hypoglycemic episodes.
-6.5 - if young, not a lot of comorbidities, and not having hypoglycemic episodes
-7 - most people. Evidence shows it reduces microvascular complications of DM, and will reduce microvascular disease if reached soon after diagnosis.
-7-8 - old, lots of comorbidities, history of severe hypoglycemia, risk of falls, longstanding DM, bad micro/macrovascular disease.
3. Glucose monitoring - home glucose monitoring has not been shown to improve sugar control.
4. Hypoglycemia
-Take 15-20 g glucose dose
-Wait 15 mins, then given another dose
-Have a snack/meal once you're back to normal.
-If its really bad, can have glucagon at home to give for rescue
5. Retinopathy
-Most frequent cause of new blindness between 20-75 years of age.
-Sx: blurry, spots, floaters.
6. Neuropathy
-stocking glove
-risk factors: dm duration/control, htn, cholesterol
-exam: monofilament (6 sites on each foot; loss of any 1 indicates neuropathy)
-tx: gabapentin, TCAs (ami/nor), lyrica, duloxetine, NSAIDs do not work.
7. Charcot joint
-microtrauma leading to joint destruction, fracture, dislocation
-15% of diabetics.
-sx: swelling, stiffness, instablility
-tx with braces, joint replacement
8. Nephropathy 
-Microalbuminuria -> Cr rise.
-Screen: annual albumin/cr ratio.
9. CV goals:
-BP <140/90
-Statins for everyone; high (atorv 40-80, rosu 20-40) if high risk CVD, or mod-low dose if mod-low risk.
-Aspirin if CV risk > 10% (generally all diabetic men > 50, women >60 who have 1 more major risk factor- (fam history early CAD, htn, smoking, microalbuinuria, dyslipidemia)
10. Prevention
-Pneumovax once before 65 and again after 65
-Hep B vaccination 20-60

Thursday, March 27, 2014

1. Type 1 DM:
-7.5-10% adults with presumed DMII will have +Antibodies
-Antibodies: GAD65, IA2, ZnT8
2. Things that cause
3. Pre-Diabetes
-A1C 5.7-6.4
-Fasting glucose 100-125
-10% progression to DM2 every year
4. Diabetes Prevention Program trial (NEJM)
-3 arms:
-Standard lifestyle recommendations + placebo twice daily
-Standard lifestyle recommendations + metformin titrated to 850 mg twice daily
-Intensive lifestyle modification (low-calorie/low-fat diet, moderate physical activity 150 min/wk)
-Mean of 2.8 years of follow up.
-Intensive supervised lifestyle decreased risk of developing DM by 58%, metformin by 31%
5. Meformin
-drops hepatic gluconeogenesis
-typically lowers A1C 1-2% @ max dose.
-Titrate to 1000 BID to lower GI symptoms.
-CI if there is a risk of renal problems-- if Cr >1.4 (F) >1.5 (M), or if they have acute heart failure, or if they need a dye study/cath - hold for 48 hours.
6. Sulfonyurea,
-drops A1C 1-2% @ max dose.
-Glipizide (10 mg qD XL, 10 mg BID if not XL release).
-Causes weight gain, hypoglycemia.
-Avoid in people with insulin, NPO.
-Cheap.
7. DPP4-I
-Enhances GLP-1 by stopping degredation
-Sitaglipitn (Januvia)
-Lowers A1C ~1 point
8. GLP agonists: 
-GLP-1 secreted from the gut after food: slows gastric emptying, stimulates insulin secretion, inhbits glucagon.
-byetta and victoza (injectibles),
-lowers A1C about 1%,
-slows gastric emptying,
-typically causes weight loss.
-But also causes pancreatitis, AKI
9. Thiazolidinediones
-Avandia
-PPARy inhibitors, Increases glucose uptake in skeletal muscles
-FDA black box
10. Insulin 
-Short acting: humolog, novolog used for SSI and mealtimes
-Long acting: Lantus for basal control (starts at 2, lasts 24, no peak)
-If their insurance won't cover lantus, do NPH, but that has to be dosed BID
-Can use combined long/short (70/30), dosed 2x a day.

Wednesday, March 26, 2014

1. CT Contrast nephrotoxicity
-Cr elevation 25% or 0.5-1 within 72 hours
-Due to renal vascular effects, direct tox to tubular cells
-Third most common cause of hospital caused renal failure, after hypotension and surgery.
Tx with hydration: 100ml/hr at least 4 hrs before and 12 after.
-Mannitol/lasix/dopamine/others: disappointing.
2. Meformin interaction 
-Contrast competes with excretion of metformin
-Rare but 50% mortality from lactic acidosis,
-Manage by d/c metformin 48 hours after contrast. Check Cr before resuming.
-Metformin is often mixed with other drugs, be wary in diabetics.
3. Lung cancer patients undergoing treatment
-CT q3-6 months
-Include upper abd (liver, adrenals) bc mets are common
4. CT & mets
-Get a CT chest with colorectal, renal, sarcoma, melanoma
-Colorectal tends to have cavitary mets (septic emboli can also cause cavitary lesions)
-Renal/sarc/melanoma tends to have round solitary lesions.
5. Esophageal CA
-Poor for esophageal masses, endoscopy better
-Little serosa, spread common
-CT look at nodes/regional spread
6. GIST/sarcoma: liver mets look cystic with mural nodule.
7. Colorectal CA
-CT bad for finding primary lesion
-Hepatic mets (72% sensitivity in meta-analyses; newer CT scans ~low 90s)
8. Hepatocellular CA
-As the liver regenerates (after cirrhosis), and HCC develops it tends to prefer blood from hepatic artery instead of portal vein.
-Thus HCC will highlight brigher than liver in arterial phase.
-In delayed phase, washout of HCC relative to liver
-Enhancement + washout very characteristic of HCC.
9. SBO 
-CT is excellent for detection (>95% sensitivity), KUB ~70% sensitive
-Dilated loops proximally, collapsed loops distally
10. CT-interventions
-Drain large abscess: aspirate, leave in catheter
-Drain small abscess: aspirate
-RFA, cryoablation
-Biopsy.

Tuesday, March 25, 2014

1. Radiation
-Absorbed dose in grays, biological effects in sieverts
-PA CXR: 0.04-0.06 mSv
-Standard thoracic CT: 4-6 mSv
-Low dose thoracic CT: 1-2 mSv
-CT Abd/pelvis: 10 mSv
-Natural background rad: 2.5-3.5 mSv/year - higher in high altitude locations like Denver.
-Risk of mortality from radiation is inversely related to age-- highest in infants, drops over time; higher in women than men. Kids' cells are more actively dividing, more have replicating DNA, vs old people with quiescent cells.
2. Pneumoperitoneum 
-May be 2/2 g-tube placement
-hard to see on portable, especially if they are not sitting up straight
3. Pneumothorax
-in young people, edges of lungs are hard to see-- not fibrosed at all.
-Can be hairline. Always check for this in young people with chest pain.
4. Multi detector CTs:
-320 slice Ct can get through 32 cm length of tissue (small child) in less than 1 second at sub-1mm resolution
-Less motion artifact
-Better temporal resolution if you want to say track a bolus.
5. Hounsfield Units
-every AM, the technologist puts water in the CT to zero it
-bigger electron cloud, more white (i.e. calcium)
+1000 : metal
+400 : bone
+40-60: liver
+46 White matter
+43: grey matter
+40: blood
+10-50: soft tissue (kidneys, muscles)
+15: CSF
0: water
-50-100 Fat
6. Uses of Hounsfield Units 
-1000 air
-Can use HU to do emphysema mapping-- separate different densities of lungs
-Can filter out bone, program to remove everything over HU of a certain number.
-Can subtract soft tissues from CTA
-Can segment liver, calculate total volumes, estimate residual volume (ie after resection, donation) to ensure there's enough liver left.
7. Contrast
-PO: drink 60-90 mins prior to exam.
Positive agent (barium, iodine) lights everything up
Negative agent: milk, water, volumen: good for seeing the mucosal (ie crohns dx, panc cancer to see duodenum) because the white whites out the walls of the bowell
-IV
Shellfish allergy not a CI
Power injector, good flush, 75-120cc
-IA
-Intrathecal
-Bladder
8. Phases of contrast
-Non contrast
-Arterial
-Portovenous (contrast goes through mesentery, portal v, light up liver)
-Delayed (collecting system)
9. Basic Body CT protocol
-PO + IV contrast: (inflammation/cancer) bowel obstruction, perforation (pain), hernia, abd abscess/infections (fever), appendicitis, diverticulitis (pain + white count)
-Non contrast: (stones, blood) kidney stones (flank pain), retropertioneal bleed (anticoagulated, recent cath), abd bleed (AAA rupture)
10. Allergy to contrast
-Anaphylactoid: 1-2/10,000: low osmolarity contrast; Tx: 1:1000 epi, 0.3 mL IM (epi pen)
-Other: n/v, pulmonary edema, seizure, renal failure
-Delayed: fever, chills, rash, pruritis, arthralgia, n/v, headache.
-For other and delayed reactions, pre-medicate with steroids/benadryl (everything from mild bronchospasm and milder).
-For serious circulatory collapse

Monday, March 24, 2014

1. BIRADS 0: need additional imaging
-Spot compression- put small paddle over spot to spread it out. Good for questionable areas, margin evaulation. Normal tissue spreads out, abnormal masses don't spread out.
-Mag views- good for calcification,
-U/s (if someone is young)
-MRI
-If you think it's category 3+, get a diagnostic mammogram
2. Category 1: negative
3. Category 2: benign finding. 
-Calcified fibroadenomas,
4. Category 3: probably benign- get short interval follow up
-Only can be diagnosed from diagnostic mammogram
-<2% risk of malignancy
-Circumscribed solid mass, round calcifications (NOT spiculated)
-Cannot be this if its a palpable abnormality. 
5. Category 4: suspicious, consider bx
-5-95% risk of cancer
-4A: low risk
-4B: intermediate risk
-4C: high risk
6. Category 5: highly suspicious of cancer, go to bx
->95% risk
-spiculated margins -- BAD sign.
7. Category 6: biopsy proven malignancy 
-Used after diagnosis but before treatment
8. Mammography 
In the US, the recall rates of screening mammography should be 5-12%. In Europe, its usually <2%. In Europe, you have to read 5000 mammograms a year to qualify as a center; in the US, 240.
-No difference in mortality here vs europe.
-In a woman <30 with a palpable mass, start with an ultrasound first, then go to mammogram.
->30 with palpable mass, go to mammography first
9. U/s
-Screening for high risk women with dense breast parenchma
-In someone <30 with a palpable mass, go to u/s
-Palpable mass, if mammogram is (-), always get an u/s sometimes they can be missed
-Bad sign: angulated edges, hypoechoic, acoustic shadowing
-Use same 7 birads categories
10. MRI
-Recommended for mutation carrier or first deg relative of mutation carrier
-Lifetime risk > 20-25%
-Radiation to chest (ie for hodgkins)
-Start age age 30

Thursday, March 20, 2014

1. Free flap: SGAR (superior gluteal artery perforators)
-Take fat/skin over gluteus
-If you take the gluteus muscles, that's very morbid
-Vessels in the gluteal region tend to be flimsy and bleed frequently, and the fat quality is more fibrotic and harder to contour in comparison with abdominal fat.
2. Free flap: TUG/VUG (transverse upper gracilis/vertical upper gracilis) 
-Take gracilis muscle (leads to little functional defect)
-TUG vs VUG only differ by orientation of skin paddle
-The donor site isn't usually the best, unless they need a medial thigh lift anyways
-Good for small defects/small breasts.
3. Great article describing an algorithm for flap selection after breast reconstruction by the chief of plastics.
4. Recipient vessels in the breast: Internal mammary artery
-Advantages: reliably good vessel size, a good match for deep inf epigastric artery, reliable blood flow due to proximity to heart, medial flap placement leads to better cosmetic outcome.
-Disadvantages: you have to remove costal cartilage, the internal mammary vein is thin, she can never get a CABG with the internal mammary arteries.
-Article on using internal mammary perforators in order to spare the IMA for future cardiac surgery, but the perforators were really small (~0.5mm) and the success rate of anastomoses low (~30%)
5. Recipient vessels in the breast: Thoracodorsal. 
-Advantages: easy to find
-Disadvantages: they are in the field of radiation, also commonly cut during mastectomy. The arteries are smaller, you end up with a more lateral positioning of flap (worse cosmesis), you need a surgical assistant to complete the dissection, and if the flap goes down, you've lost the ability to do a latissimus flap because you've lost the thoracodorsal vessels.
6. Oncoplastic surgery:
-After a lumpectomy, rearranging the remaining breast tissue to fill the defect instead of using tissue transfers or implants.
-Difficult to spare the nipple in these cases.
7. How to restore anesthesia 
-if you think they are moving because they are too light (i.e. enough that they are being bothered by the ET tube) push propofol for fast sedation and increase gas %. You will need to increase your flow rate as well of carrier gas (i.e. O2) otherwise the gas will not enter. You can also add Desflurane as it is the fastest onset of the inhaled gases, and will work in 1-2 minutes.
-If you think they are moving because they are feeling some pain, propofol for fast sedation plus an opiate like fentanyl.
-Propofol will sedate someone fast (<30 seconds) but it has a tendency to drop people's blood pressure. If you give a small dose, the effect is small, but a big dose of propofol can drop someone's pressure by 20%, which may be dangerous in older, sicker people with little cardiopulmonary reserve.
8. Laparoscopic surgery & anaesthesia
-Young women tend to become bradycardic (ie to 30s) upon inflation (vasovagal?).
-The trendellenberg position makes it harder to ventilate, esp in overweight people; the fact that the gas being inflated is CO2 is worse, makes it even more important to ventilate well.
9. Crazy article in the NEJM about replicating CCR5 mutations in people already infected with HIV. They harvested CD4+ cells from the 12 patients, applied a zinc finger nuclease (zinc finger DNA binding domain selective for CCR5 + nuclease = gene-specific restriction enzyme). They infused back the autologous t-cells (only 11-28% of which were CCR5 deficient), and half were randomized to discontinue HAART. Safety was excellent. At 4 weeks, 13% of the patients' CD4+ cells were CCR5-. The mean half life of the modified T-cells was 48 weeks (!) which was actually longer than non-modified T-cells. For 1 out of the 4 patients that went off HAART, viral loads dropped to undetectable levels.
10. Ablation vs antiarrhythmics for initial management of a-fib {multicenter RCT, n=127, JAMA
Treatment group: treatment-naive a-fib patients
Outcome: (primary) time to the first documented atrial tachyarrhythmia of more than 30 seconds (symptomatic or asymptomatic AF, atrial flutter, or atrial tachycardia), (secondary) symptomatic a-fib, quality of life survey.
Results: 72% achieved outcome in antiarrhythmic meds group, 55% in ablation group. Recurrence of symptomatic a-fib at 2 years was 47% for ablation, 59% for drugs. No statistical difference for quality of life. 9% incidence of severe complications in ablation group- perforation leading to tamponade, stenosis of pulmonary veins, disrupted rhythm requiring pacemaker implantation. No strokes or deaths in either group.
Conclusion: Take the meds

Wednesday, March 19, 2014

1. Options for reconstruction after mastectomy: Silicone implants
-Advantages: feels more natural, looks better
-Disadvantages: costs more, holds its shape when it ruptures so ruptures can be silent, ruptures can also cause a significant inflammatory reaction,
2. Options for reconstruction after mastectomy: Saline implants
-Advantages: cheaper, deflatable (good for older/sicker women who wouldn't tolerate a removal surgery if something went wrong)
-Disadvantages: feels more plastic, more prone to visible skin wrinkling
3. Implants & Radiation
-Radiation damages the skin/muscle bed and makes it a worse recipient of both an expander and an implant, leading to worse medical and cosmetic outcomes.
-If you irradiate an implant, it damages both the tissue and the implant and increases risk of extrusion, contracture, and other complications.
-The best case scenario is if someone needs radiation, to avoid artificial implants altogether and got to an autologous tissue reconstruction. If you must use implants, wait for the skin to heal after radiation. Never irradiate an implant.
4. Implant general information:
-If you place it under muscle, the risk of extrusion is lower and the cosmetic appearance is often better.
-An expander may not be needed in everyone-- if the skin and muscle are in good quality, you might be able to put in an implant without an expander. But if someone is really skinny, or the tissue is really tight, you may need an expander.
5. Autologous tissue breast reconstruction: fat grafting +/- BRAVA
-Liposuction various parts of the body, inject into breast into various tissue planes
-BRAVA applies suction to breast, some people believe it opens up vascular spaces so that more of the fat grafts will take
-Some people think you can reconstruct an entire breast with fat grafting; however you will not get the same projection as with a flap or an implant.
5. Local flaps-- Classic latissimus flap
-Supplied by thoracodorsal artery
-usually does not have enough tissue to reconstruct a full breast, will likely still need an implant.
-You dissect out the entire muscle, swing it through the axilla to the front
-No functional loss unless the person is a rock climber or serious swimmer
6. Local flaps- TAP (Thoracodorsal artery flap)
-Like a classic latissimus, but instead of taking the pedicle and entire muscle, you take a much smaller segment by dissecting out only the perforators that go to the skin.
7. Local flaps- TRAM (transverse rectus abdominus myocutaenous)
-Based on the superior epigastric vessels (continuous with internal mammary vessels through "choke point")
-You take the skin and fat b/l, and then take the rectus muscle on the side that you take the pedicle. If you only take one pedicle and its a really big flap, you will almost certainly lose the far lateral contralateral portion of the flap to ischemia. If you take both rectus muscles, you will have much better perfusion of the flap, but this is extremely morbid...
-Because the TRAM is a pedicled flap, it's faster and easier, so good for people who are too sick to tolerate a long time under anesthesia.
-The risk of kinking a vessel (more likely vein, lower pressure) is present; you can prophylactically do another venous-venous anastomosis with one of the vessels to a vein in the axilla.
-If you cut the inferior epigastric vessels a few weeks before surgery, you will increase flow through the superior epigastrics.
8. Free flaps- free TRAM
-Blood comes from deep inferior epigastrics instead of the superior epigastrics
-Advantages over pedicled TRAM: all of the zones of the flap are better perfused, the vessels are usually bigger than superior epigastrics
9. Free flaps- DIEP (deep inferior epigastric perforators)
-Instead of taking the deep inferior epigastrics as a pedicle, you take the perforators. When you find them, trace them back to the origin off the DIEP to dissect them out.
-The smaller the perforators, the more you need, and the more likely you are to have to take out a cuff of muscle with them.
-Because you have to cut the fascia, you get complications (hernia, etc)
10. Free flaps- SIEA (superficial inferior epigastric perforators)
-You take the perforators of the superficial interior epigastric vessels, which enter above the fascia, in this way you avoid having to cut the fascia.
-Disadvantages is that these vessels are usually very small (<1.5mm, sometimes <1mm) and being superficial vessels, they are much more prone to spasm.
-You can do unilateral or bilateral SIEA

Tuesday, March 18, 2014

1. Patient controlled epidural provides better pain relief than patient controlled remifentanil for labor pain in randomized controlled trials. Remifentanil is fast on and off, which leads to less respiratory side effects in mom and baby (all opiates cross blood-placenta border), but is hard to time with contractions. Opiates have a history of insufficient pain relief for labor; they are better for visceral pain than somatic pain, so during the second stage of labor, which is mostly somatic pain, patients report significant pain with opiates. The benefit is that they are faster onset than epidurals.
2. For beautiful, less visible scars, approximate the epidermis with absorbable 7-0 suture spaced approx 1 mm apart. Injury that is confined to epidermis/papillary dermis will not scar, so if you make your sutures superficial enough, the sutures will not leave a scar (although obviously the incision will).
3. After an incision heals, the tissue will attain a maximum of 80% of its former strength; this will be attained at around 6 weeks. Someone should avoid stressing the wound for the first few weeks, but then should be encouraged to ramp up physical activity. The scar may take up to 1 year to mature; people should be advised to wear sunscreen to avoid darkening of the scar, and avoid tension/massage as that will worsen the scar as well.
4. Types of suture: chromic
-Absorbable
-Natural
-Half life 10-14 days
-Flimsy and sometimes hard to work with
-Primarily used on mucosa, particularly intraoral
-Apparently not supposed to be used on skin as it causes inflammation, although in many plastic surgeons' experiences, this is not necessarily the case
5. Types of suture: fast absorbing
-Absorbable
-Half life 3-5 days
-Very flimsy, breaks easily, hard to tie, especially 4-0 or less.
-Good for small skin openings where you just want a little help.
6. Type of suture: vicryl/polysorb 
-Absorbable
-Half life 21-28 days, 10% at ~35 days, complete absorption at 70
-Braided
-Strong
-Standard for deep closures.
7. Type of suture: maxon
-Absorbable
-Half life 28-26 days
-Monofilament
-Often used in larger caliber for abdominal fascia closures
8. Type of suture: biosyn/caprosyn
-Absorbable
-Synthetic monofilament
-Biosyn lasts a bit longer than caprosyn, half life 1-2 weeks.
9. Type of suture: nylon
-Non-absorbable monofilament
-Often used for superficial stitches (drain, superficial wound closures)
10. Type of suture: prolene
-Bright blue, non absorbable monofilament.
-Frequently used for abdominal closures.

Thursday, March 13, 2014

1. Types of urinary cath
Internal: foley, suprapubic
External: texas or condom catheters
2. Indications for use of urine catheters
-ICU/critically ill patients for close monitoring of UOP, Strict Is/Os.
-Surgical patients (all surg patients within 24 hours of surgery, surgery on contiguous/pelvic structure for a while, anyone with epidural who can't get up)
-Medical indications:
-acute retention/outlet obstruction
-hematuria + clots
-intravesicular delivery of drugs or irrigation
-neurogenic bladder
-prolonged immobilization  (sedation, parlysis, trauma)
-urinary incontinence in people with pelvic wounds/ulcers that youare trying to keep clean or heal
-end of life comfort care
3. NOT indications
-Incontinence, older people who have trouble getting up
-Specimen collection
-Provider convenience, patient request.
4. Catheter Associated UTIs 
-Bacteriuria occurs at 3-8% a day.
-10-25% of patients will develop clinically significant sx of UTI
-20% of hospital bacteremias are from foleys
-Usually MDR bugs.
-Prevent these by avoiding putting one in, pulling it out as soon as possible
5. Types of lines


Peripheral
Central
Catheters

Temporary:
-PICC (single or double lumen)
-Triple lumen
-Quintons (temporary dialysis): shorter, two lumens, often red and blue
-Cordis (introducers- usually shock/trauma/surgery)

Less temporary:
-hickman-- tunneled dialysis catheters start in the chest, insert into the IJ. Vs Quinton are in the neck.
-port a cath 
Vessel

-IJ: all central lines 
-Subclavian: portacath 
-femoral: all but portacath 
Location
IV access for 2-3days
Meds that require central lines (chemo, tpn, pressors)
Procedures (plasma exchange, dialysis)
Monitoring (CVP, swan-ganz_
Long term meds (home IV abx)
Complications
Extravasation, cellulitis, thrombophlebitis
Bleeding, arterial puncture, bacteriemai, pneumothorax, thrombosis, air embolism
6. Central line associated blood stream infection  
-8% of hosp patients get a central line
-Risk factors: ICU, chronic ill, immunocompromised, BM transplant, TPN administration (huge risk), how long its in, sterile insertion vs crash insertion, risk of infection from highest to lowest: nontunned > tunneled > implanted
7. The risk of catheter-related bloodstream infection with femoral venous catheters as compared to subclavian and internal jugular venous catheters: a systematic review of the literature and meta-analysis.
Marik et al, Crit Care Med. 2012 Aug
BACKGROUND:
Catheter-related bloodstream infections are an important cause of morbidity and mortality in hospitalized patients. Current guidelines recommend that femoral venous access should be avoided to reduce this complication (1A recommendation). However, the risk of catheter-related bloodstream infections from femoral as compared to subclavian and internal jugular venous catheterization has not been systematically reviewed.
OBJECTIVE:
A systematic review of the literature to determine the risk of catheter-related bloodstream infections related to nontunneled central venous catheters inserted at the femoral site as compared to subclavian and internal jugular placement.
DATA SOURCES:
MEDLINE, Embase, Cochrane Register of Controlled Trials, citation review of relevant primary and review articles, and an Internet search (Google).
STUDY SELECTION:
Randomized controlled trials and cohort studies that reported the frequency of catheter-related bloodstream infections (infections per 1,000 catheter days) in patients with nontunneled central venous catheters placed in the femoral site as compared to subclavian or internal jugular placement.
DATA EXTRACTION:
Data were abstracted on study design, study size, study setting, patient population, number of catheters at each insertion site, number of catheter-related bloodstream infections, and the prevalence of deep venous thrombosis. Studies were subgrouped according to study design (cohort and randomized controlled trials). Meta-analytic techniques were used to summarize the data.
DATA SYNTHESIS:
Two randomized controlled trials (1006 catheters) and 8 cohort (16,370 catheters) studies met the inclusion criteria for this systematic review. Three thousand two hundred thirty catheters were placed in the subclavian vein, 10,958 in the internal jugular and 3,188 in the femoral vein for a total of 113,652 catheter days. The average catheter-related bloodstream infections density was 2.5 per 1,000 catheter days (range 0.6-7.2). There was no significant difference in the risk of catheter-related bloodstream infections between the femoral and subclavian/internal jugular sites in the two randomized controlled trials (i.e., no level 1A evidence). There was no significant difference in the risk of catheter-related bloodstream infections between the femoral and subclavian sites. The internal jugular site was associated with a significantly lower risk of catheter-related bloodstream infections compared to the femoral site (risk ratio 1.90; 95% confidence interval 1.21-2.97, p=.005, I²=35%). This difference was explained by two of the studies that were statistical outliers. When these two studies were removed from the analysis there was no significant difference in the risk of catheter-related bloodstream infections between the femoral and internal jugular sites (risk ratio 1.35; 95% confidence interval 0.84-2.19, p=0.2, I=0%). Meta-regression demonstrated a significant interaction between the risk of infection and the year of publication (p=.01), with the femoral site demonstrating a higher risk of infection in the earlier studies. There was no significant difference in the risk of catheter-related bloodstream infection between the subclavian and internal jugular sites. The risk of deep venous thrombosis was assessed in the two randomized controlled trials. A meta-analysis of this data demonstrates that there was no difference in the risk of deep venous thrombosis when the femoral site was compared to the subclavian and internal jugular sites combined. There was, however, significant heterogeneity between studies.
CONCLUSIONS:
Although earlier studies showed a lower risk of catheter-related bloodstream infections when the internal jugular was compared to the femoral site, recent studies show no difference in the rate of catheter-related bloodstream infections between the three sites.
8. Don't use someone's tunneled dialysis catheter for anything but dialysis, because the more times you access it the higher the risk of infection and thrombosis.
9. Pressure ulcer risk & prevention
Braden skin index from 1-4 in 6 areas : sensory perception, moisture, activity, mobility, nutrition, friction, shear. High risk if score <=18. Sensitivity 70-90, specificity 60-80
-Pressure relief: turning in bed q2 hours, foam padding, air beds.
-Make them walk
-Treat incontinence
10. Pressure ulcer grades: 
-Category/Stage I: Non-blanchable erythema
-Category/Stage II: Partial thickness
-Category/Stage III: Full thickness skin loss
-Category/Stage IV: Full thickness tissue loss
-Unstageable/Unclassified: Full thickness skin or tissue loss – depth unknown
-Suspected Deep Tissue Injury – depth unknown

Wednesday, March 12, 2014

1. Hospital DVTs 
-Incidence 10-80%
-60% of DVT occur in hospitalized, recently d/c or nursing home patients
-PE most common preventable cause of hospital death
-5-10% in hosp deaths are 2/2 PE
-shown to reduce risk of DVT and risk of death in surgical patients
-not conclusively shown to reduce risk of death in medical patients
2. Risk factors for DVT
-Stasis - anything that causes immobility, either physical (paraplegia, stroke, leg pain, sedation) or medical (end stage heart/lung failure)
-Vessel injury - previous DVT, surgery, trauma, lines.
-Hypercoagulability - active cancer within last 6 mos, pregnancy,
3. Prevention of DVT 
-Early ambulation
-Heparin SubQ 5000 U TID - no adjustment for ESRD
-Lovenox 40, Lovenox 30 if CrCl < 30, CI in ESRD
-Fonda (factor Xa) 2.5mg
-Iffy evidence on whether SCDs really work.
4. Risk assessment tools. 
-IMPROVE trial: N>15,000, probabilty of symptomatic DVT within 90 days of d/c. Model (previous DVT, thrombophlilia, current cancer, age > 60)
-Padua N>1000
5. Bleeding risk 
-Absolute risk increase in bleeding overall for all patients is 0.5%.
-ACP 2011 guidelines lit review of last 60 years, found overall heparin prophylaxis will decrease PE events in 4/1000, but increases bleeding events in 9/1000 patients.
-IMPROVE trial model: strongest predictors of  active ulcer, bleeding within 3 mos prior to hopsitazliation, platelets < 50,000 age > 85
6. HIT occurs in up to 5% of people who get heparin.
7. Stress ulcers
-Cushings: CNS injury, usually devastating neurological event, single deep lesion in duodenum or stomach.
-Curlings: burn patients, esophagus, stomach small intestine, colon.
-Mortality can be up to 50% in ICU patients.
8. Which ICU patients needs stress ulcer prophylaxis? ASHP guidelines:
All ICU patients with a major risk factor:
-Intubation/mech vent > 48 hours
-Hx of GI ulcer/bleed within last year
-Platelets <50K, INR > 1.5
Or two minor risk factors:
-Steroids
-traumatic brain, spine, burn injury
-Sepsis
-ICU admission > 1 week
-Occult GI bleed > 6 days
-Routine stress ulcer prophylaxis is not recommended for non-ICU medical patients.
9. Which drugs
-famotidine 20
-nexium 40mg PO
-antacids and sucrafate also used
10. Problems with PPIs/etc. 
-drug interactions!
-increased risk of nosocomial infections like PNA with aspiration
-increase risk of C. diff

Tuesday, March 11, 2014

1. Decadron is good for vasogenic edema, such as that caused by an abscess or tumor, but not so great for edema associated with an acute hemorrhagic event
2. Antiepileptics and intracranial hemorrhage:
-Bleeds in the temporal lobe have the highest risk of leading to an epileptic event, although all lobar bleeds are relatively high risk and should probably get epilepsy prophylaxis.
-Bleeds in the cerebellum are extremely unlikely to cause seizures
-Dilantin used to be standard of care for seizure prophylaxis, but given its significant side effects, is now only given to people who have already seized to try to prevent future seizures
-In someone actively seizing, you would give Ativan to break the seizure and load them with dilantin to prevent future seizures.
-In people who have a risk of seizures but have never seized before, Keppra is a safe prophylactic agent.
3. MRI is indicated for evaluation of low back pain if the following are present 
-Neurological deficit
-Radiculopathy
-Progressive major motor weakness
-Cauda equina compression (sudden bowel/bladder disturbance)
-Suspected systemic disorder (metastatic or infectious disease)
-Failed six weeks of conservative care
4. MRI & low back pain: 
-75% of herniated discs improve with six weeks of conservative therapy.
-MRI testing is not associated with clinical benefit in randomized trials.
-Early MRI is not associated with improved outcomes in patients with acute back pain or radiculopathy (Level 2/mid-level evidence).
-If surgery is being considered, some physicians recommend, in the absence of red flags, to obtain an imaging study after one month of symptoms.
5. Reading AP spine plain films: 
-Count the lumbar vertebral bodies (non-rib bearing vertebra). 5 is normal. 
-Look to see that each vertebral body has 2 pedicles and 1 spinous process (eyes/nose) 
-Look for vertical alignment of the spinous processes.  Misalignment suggests a rotational injury such as unilateral facet dislocation.
-Look for smooth undulating borders.
-Look for uniformity among the disc spaces.
-Compare the pedicles with the spinous processes. Widening of the pedicles may represent a compression fracture. Comparison of these will also show rotation of the spine.
-Look at the lateral curvature, which may reveal scoliosis.
-Look at the sacroiliac joints to ensure the white margin is intact. Is the joint sclerotic, ankylosed (fused), or destroyed?
6. Reading latera; spine plain films: 
-Check for height loss in the vertebral bodies. This height loss may be due to trauma, metabolic disease, or metastatic disease.
-Look at the configuration of the end plates. Are the end plates crisp? Irregular endplates could reflect degeneration or infectious disease.
-Look at the disc space thickness. The disc space thickness should diminish as you go down the spine, but this should be subtly and uniformly.
-Check for alignment in the AP direction. Are the anterior and posterior spinal lines intact?
-Look to see if there any osteophytes projecting from the vertebral bodies. Are there any calcifications in discs?
-Check that the spinous processes are present. Did the patient have previous spine surgery?
-Last but not least, look for other abdomen and pelvic pathology. AP and lateral films can show calcifications in the kidney, vascular calcifications, or foreign bodies.
7. Algorithm for diagnostic testing in LBP
-LBP <3 months, no red flags = no testing, no imaging
-Suspected fracture: plain film. If its negative but pt still has multiple sites of pain or fracture is still suspected, bone scan before CT 
-Suspected infection: CBC, ESR, UA 
-Suspected cancer: CT, MRI 
-Suspected cauda equina: call neurosurgery
8. Pharmacologic management of LBP
-First line: NSAIDs, tylenol, muscle relaxants
-Evidence shows little difference between different NSAIDs and different muscle relaxants; choose less sedating ones. 
-Unclear whether NSAIDs are superior to tylenol. 
-Little evidence that opiates help; second or third line
-No evidence that PO steroids help
9. Prognosis of LBP: 
-90% resolve within one month
-5% remain disabled longer than three months
-Patients who are out of work >6 months = 50% chance of returning to work
-Out of work >2 years = almost 0 chance of returning to work. 
-Worse prognosis: older (>45), psychosocial stress. 


-35-75% recurrence rate. 
10. Succinylcholine can be given IM or IV. In IV form, the onset is 20-30 seconds, while in IM form the onset is 2-3 minutes. 

Monday, March 10, 2014

1. Hyperdensity on CT scan: blood - amyloid angiopathy 
-Amyloid builds up in blood vessels, weakening them.
-Most common in older people, and generally lobar. If the bleed is in the deep brain or cerebellum, this is much less likely
-Classic story is someone who comes in with recurrent lobar hemorrhages.
-Diagnosis of exclusion-- as you can only formally diagnose with a tissue sample.
2. Hyperdensity on CT scan: blood - hypertensive hemorrhage
-Most common places for hypertensive hemorrhage: (1) basal ganglia/putamen (2) thalamus (3) pons (4) cerebellum.
-Lenticulostriate
-Common in older people with a history of hypertension.
3. Hyperdensity on CT scan: blood - coagulopathy 
-Find out if the patient is on anticoagulation, check coag labs. Remember that some of the new direct thrombin inhibitors can't be monitored by blood tests, and that they were recently recommended as first-line treatment for a-fib by the american chest physicians guidelines.
4. Hyperdensity on CT scan: blood - hemorrhagic infarct
-About 20-30% are ischemic infarcts that converted to hemorrhagic
-Most of the rest are people who had a history of ischemic infarcts, that they then bled into as a result of starting anticoagulants.
-You will not see much mass effect with these.
5. Hyperdensity on CT scan: blood - vascular malformations
-Aneurysm: you will almost always see some subarachnoid blood with aneurysmal bleeds. If you look at the cisterns and they are all clear of blood, this is much less likely. Aneurysms at the MCA bifurcation may rupture into the brain and present as a temporal lobe hematoma due to the vessels being semi-embedded into the temporal lobe.
-AVM: you will not see much mass effect; the bleeding is usually within the AVM.
-Cavernoma/CCM: little mass effect, usually presents with microbleeds, rarely will you get clinically significant bleeds
-Other rarer entities: venous angioma, capillary teleangiectasias, hemangiomas; these are rarer and generally benign.
6. Hyperdensity on CT scan: blood - tumor
-Usually there is significant edema, and there will be noticeable mass effect from both the tumor mass and the surrounding edema.
-Benign tumors are less likely to have severe edema/mass effect than malignant.
7. Management of suspected intracranial hemorrhage: Step 1: stabilize
Airway, breathing, circulation
Airway, breathing, circulation
Airway, breathing, circulation
8. Management of suspected intracranial hemorrhage: Step 2: figure out if they need emergency surgery 
-Supratentorial bleeds rarely do, unless there is significant mass effect leading to herniation or threatened herniation.
-Posterior fossa bleeds- check for
(1) brainstem compression (look at cistern in front of the brainstem- cerebellopontine cistern, cerebellomedullary cistern). If present, this person will require an emergency decompressive posterior fossa craniectomy.
(2) signs of hydrocephalus from compression of 4th ventricle. Look at the 4th ventricle and the aqueduct to make sure they are open. If they have hydrocephalus, they will need an EVD soon but it's not quite as emergent.
9. Management of suspected intracranial hemorrhage: Step 3: Medical optimization 
-Blood pressure should be high enough to perfuse their brain (esp if there is an ischemia component to the stroke) but low enough that it won't worsen the hemorrhage. If the person has a long-standing history of hypertension, you will want to keep their pressures higher than in someone who doesn't to ensure adequate perfusion. Currently, keeping systolic <160 seems to be a good compromise between the increased ischemia at 140 and the increased hemorrhage at 180.
-Reverse anticoagulation: If they were on an antiplatelet agent, transfuse platelets. If they were on an anticoagulant, transfuse factors. It's important to know the reason for the anticoagulation, and to weigh the risk of an adverse cardiac event against an adverse neurological event. Fresh cardiac stents have a 10-15% risk of clotting off with a platelet transfusion, which may not be worth it with a small cerebral hemorrhage; while embolic events in patients with a-fib are rare, and will be outweighed by even a small cerebral hemorrhage.
10. Management of suspected intracranial hemorrhage: Step 4: imaging to determine etiology
-MRI +/- contrast to rule out tumor
-CT angio to rule out vascular malformation
-Coagulation workup
-If all your tests are negative, hypertensive hemorrhage or hemorrhagic infarct are the most likely. Teh management is the same (see step 3).
-It's important to get follow up imaging 2-3 weeks after the bleeding event (both MRI and CT angio) as a fresh bleed can hide a tumor or a vascular malformation (ex: aneurysms can thrombose in an acute setting, and be hidden on CT angio). This is especially important in younger, otherwise healthy people.
(from ricky)

Friday, March 7, 2014

1. Imaging of suspected SAH:
-If its fresh, CT without contrast
-If it's older (a few days), MRI- T2* or susceptibility weighted imaging is the most sensitive for blood; alternatively you can look for cortical surface edema on T2 FLAIR as a proxy for irritation from residual or past subarachnoid blood.
2. LP & SAH:
-LPs done in an ER setting are not-infrequently traumatic, and so the presence of blood therein may not be diagnostic.
-Xanthochromia testing on the LP sample to look for blood breakdown products may be helpful
3. Hypodensity on non-contrast CT scan: infarct 
-Generally non-expansile (vs edema)
-Within the first 4-6 hours of an infarction, a noncontrast CT is likely to show nothing.
-At approx 4-8 hours, you will start to see a developing hypodensity without significant edema; it will look very hypodense at this stage, almost black.
-At around 48-72 hours is the peak of edema, and you will see hypodensity with expansile effects on nearby ventricles/sulci. This is helpful for deciding management-- i.e. if you already see a midline shift within the first 24 hours, you know it will get worse, and you are more likely to put in an EVD.
-An old infarct will look hypodense on CT, but more greyish than black, and less homogenous. You may also see hydrocephalus ex-vacuo, where the loss of local brain tissue will lead to the enlargement of nearby ventricles.
4. Other causes of hypodensity on non-contrast CT scan
-Edema: Generally expansile- look at nearby ventricles/sulci to see effacement.
-Fluid collection (i.e. cyst or abscess): look for cystic-appearing shape, etc.
5. Hyperdensity on CT scan: calcifications {DIR} Age-related physiologic and neurodegenerative calcifications: 
"Intracranial physiologic calcifications are unaccompanied by any evidence of disease and have no demonstrable pathological cause. The most common sites include the pineal gland, habenula, choroid plexus, basal ganglia, falx, tentorium, petroclinoid ligaments and sagittal sinus. Calcification of the pineal gland is seen in two-thirds of the adult population and increases with age. Pineal calcification over 1 cm in diameter or under 9 years of age may be suggestive of a neoplasm. Habenula has a central role in the regulation of the limbic system and is often calcified with a curvilinear pattern a few millimeters anterior to the pineal body in 15% of the adult population. Choroid plexus calcification is very common finding, usually in the atrial portions of the lateral ventricles (Fig. 1). Calcification in the third or fourth ventricle or in patients less than 9 years of age is uncommon. Basal ganglia calcifications are usually idiopathic incidental findings that have a 0.3–1.5% incidence and increases with age. They usually demonstrate a faint punctuate or a coarse conglomerated symmetrical calcification pattern (1) (Fig. 2). Calcifications of the falx, dura mater or tentorium cerebelli occur in about 10% of elderly population"
6. Hyperdensity on CT scan: calcifications {DIR} congenital 
"This condition is frequently seen in Sturge-Weber syndrome (SWS), tuberous sclerosis (TS) and intracranial lipoma, but rarely in neurofibromatosis (NF), Cockayne (CS) and Gorlin syndromes (GS)."
7. Hyperdensity on CT scan: calcifications {DIR} infectious 
TORCH infections, viral encephalitis, intracranial TB or fungal infection
8. Hyperdensity on CT scan: calcifications {DIR} metabolic 
"Fahr disease is a rare degenerative neurological disorder characterized by extensive bilateral basal ganglia calcifications that can lead to progressive dystonia, parkinsonism and neuropsychiatric manifestations. It is associated with defective iron transport resulting in tissue damage with extensive calcification." 
Others: parathyroid disease
9. Hyperdensity on CT scan: calcifications {DIR} vascular 
"Calcification of the intracranial arteries associated with primary atherosclerosis is more frequent in elderly people. The highest prevalence of intracranial artery calcification is seen in the internal carotid artery (60%), followed by the vertebral artery (20%), middle cerebral artery (5%), and basilar artery (5%) (13) (Fig. 15).
Other causes of vascular calcifications include aneurysm, arteriovenous malformation (AVM) and cavernous malformation. Although patent aneurysms may contain mural calcification, partially or completely thrombosed aneurysms commonly have calcifications (14) (Fig. 16). AVMs may contain dystrophic calcifications along the serpentine vessels and within the adjacent parenchyma with a prevalence of 25–30% (13) (Fig. 17). Cavernous malformation is a benign vascular hamartoma that is frequently calcified in a ’’popcorn-ball’’ fashion (15) (Fig. 18)."
10. Hyperdensity on CT scan: calcifications {DIR} neoplastic 
"The most common intracranial neoplasms associated with calcifications (16) are oligodendroglioma (70–90%), craniopharyngioma (50–80%), germ cell neoplasms (dysgerminoma, seminoma, teratoma, choriocarcinoma; 60–80%), pineal neoplasms (pineoblastoma, pineocytoma; 60–80%), central neurocytoma (50–70%), primitive neuroectodermal tumor (PNET) (50–70%), ependymoma (50%), ganglioglioma (35–50%) (Fig. 19), dysembriyonic neuroectodermal tumor (DNET) (20–36%), meningioma (20–25%), choroid plexus papilloma (25%), medulloblastoma (20%), low grade astrocytoma (20%), and pilocytic astrocytoma (10%). Calcifications are rarely seen in schwannomas, and dermoid and epidermoid tumors."

Thursday, March 6, 2014

1. Causes of sinus congestion
-Chronic sinusitis (mucosal thickening) 2/2 chronic infection or inflammation
-Allergic rhinitis
-Physical obstruction (polyps, inverted papilloma, severe deviated septum, large adenoids)
2. Copious, clear rhinorrhea-- if it drips like a faucet, is in an old person, tastes salty, and worsens when the person leans forward, worry about CSF leak. It can occur with pituitary lesion or spontaneously.
3. Gut microbiome can influence generation of toxic metabolites in people taking tylenol: Pharmacometabonomic identification of a significant host-microbiome metabolic interaction affecting human drug metabolism. {PNAS, 2009} "....in individuals with high bacterially mediated p-cresol generation, competitive O-sulfonation of p-cresol reduces the effective systemic capacity to sulfonate acetaminophen..."
4. Gut microbiome influences behavior; transfer of gut microbiome = transfer of behavioral preferences. "Commensal bacteria play a role in mating preference of Drosophila melanogaster" {PNAS 2010} "...In this study, mating preference was achieved by dividing a population of Drosophila melanogaster and rearing one part on a molasses medium and the other on a starch medium. When the isolated populations were mixed, “molasses flies” preferred to mate with other molasses flies and “starch flies” preferred to mate with other starch flies.... Antibiotic treatment abolished mating preference, suggesting that the fly microbiota was responsible for the phenomenon. This was confirmed by infection experiments with microbiota obtained from the fly media (before antibiotic treatment) as well as with a mixed culture of Lactobacillus species and a pure culture of Lactobacillus plantarum isolated from starch flies. Analytical data suggest that symbiotic bacteria can influence mating preference by changing the levels of cuticular hydrocarbon sex pheromones...."
5. Nosebleeds in...
-Children, are generally benign, as they are due to superficial vessel rupture in the anterior septum. Holding pressure makes them stop in a few minutes, they rarely lose enough to lead to anemia. Manage preventatively-- they are worse with dryness, so keep it locally moist by using topical vaseline and saline drops multiple times a day. Humidifier in the room is not super helpful, but can be used. If it's not able to be controlled this way, you can cauterize. If you're worried about a bleeding diathesis, ask them if they bled a lot when they lost their baby teeth, or if they've had surgery ask about bleeding during surgery; if that was normal, bleeding diathesis is unlikely.
-Teenagers, think angiofibromas
-Adults, are often quite serious. They are usually posterior nasal bleeds from the sphenopalatine artery, and are due to vascular pathology (arterioloscelerosis + hypertension -> rupture). They can lose a LOT of blood, and you can't hold pressure because they are posterior, under the nasal bones. Sometimes they will require IR embolization of the sphenopalatine artery.
6. Hearing test: Otoacoustic emissions
-This is the newborn hearing screen.
-"An otoacoustic emission (OAE) is a sound which is generated from within the inner ear....OAEs are considered to be related to the amplification function of the cochlea. In the absence of external stimulation, the activity of the cochlear amplifier increases, leading to the production of sound. Several lines of evidence suggest that, in mammals, outer hair cells are the elements that enhance cochlear sensitivity and frequency selectivity and hence act as the energy sources for amplification. One theory is that they act to increase the discriminability of signal variations in continuous noise by lowering the masking effect of its cochlear ampliļ¬cation.... Studies have shown that OAEs disappear after the inner ear has been damaged, so OAEs are often used in the laboratory and the clinic as a measure of inner ear health." (wikipedia)
-Evoked OAE: "Stimulus Frequency OAEs (SFOAEs) are measured during the application of a pure-tone stimulus, and are detected by the vectorial difference between the stimulus waveform and the recorded waveform (which consists of the sum of the stimulus and the OAE). Transient-evoked OAEs (TEOAEs or TrOAEs) are evoked using a click (broad frequency range) or toneburst (brief duration pure tone) stimulus. The evoked response from a click covers the frequency range up to around 4 kHz, while a toneburst will elicit a response from the region that has the same frequency as the pure tone." (wikipedia)
-Put a probe in the ear, play a sound, the probe records a response
-Benefits: fast, doesn't require sedation, only that they sit still/quiet for a few minutes, doesn't depend on behavioral response from child,
-Cons: you only get a yes/no response, no quantitative outcomes, any pathology in the ear (fluid in drum, eustachian tube pathology) will throw off the readings as you will not be able to record the OAE.
7. Hearing test: Auditory brainstem response (ABR)
"The ABR is an auditory evoked potential extracted from ongoing electrical activity in the brain and recorded via electrodes placed on the scalp. The resulting recording is a series of vertex positive waves of which I through V are evaluated.... The following are believed to be the sources of the waves:
Wave I – generated by cranial nerve VIII
Wave II – generated by the cochlear nucleus
Wave III – generated by the superior olivary complex
Wave IV – generated by the lateral lemniscus
Wave V – generated by the inferior colliculus"
(from wikipedia)
-You play a sound (start at 90 dB, gradually lower to see when the responses stop coming-- if you still see wave V at 20 dB that's a normal test) and then record the response with electrodes over the scalp. You can play clicks at different frequencies to find out about hearing loss at different frequencies.
-Pros: you get quantitative results, you can check responses at different frequencies, it's detailed data
-Cons: Child needs to be sedated for ~30-40 minutes
8. Hearing test: sound field
-Put the kid in a box, play sounds, look at their behavior/response to see if they hear the sound.
-Pros: non invasive, no sedation, fast, cheap
-Cons: not ear-specific (if one ear is bad, the other can obviously compensate), requires cooperation of child-- usually the child needs to be older than 6-9 mos for this test, any younger and you can't get good data from it.
-This is not really meant to stand alone, it's usually a clinical correlate to the ABR
9. Hearing/ear test: tympanometry 
-Apply pressure (from -200 to +200 mmH20) in ear, and then measure the compliance of the ear drum by emitting a pure tone and measuring how much is reflected.
-Normally the peak of mobility will be in the center of pressure (at 0 mmH20, neutral)
-If the ear is heavily retracted (usu eustachian tube dysfunctio) the peak of mobility will be at negative intracanal pressure-- as pulling the TM closer to neutral makes it work better.
-A flat tympanogram means the drum is not moving and something is wrong
10. Thyroglossal duct cyst: 
-A midline neck mass in a child is a thyroglossal duct cyst (TDC) until otherwise proven (off to the side usually lymph nodes, but rarely TDC can appear off midline.
-Before you surgically remove it, get an ultrasound to make sure they have a normal thyroid gland, as some people's only thyroid tissues is in the TDC. The u/s also looks at the anatomy of the TDC.
-Usually infrahyoid
-Treatment is surgical removal, and you don't just want to scoop out the cyst as the rate of recurrence is 25%. You want to remove the entire tract of the thyroglossal duct up to tongue, including removing the central part of the hyoid bone. The recurrence after this surgery is much lower

Wednesday, March 5, 2014

1.DDx Vertigo in descending order of commonality:
-BPPV
-Menieres
-Viral neuritis (recovers spontaneously in younger people, may takes months in older adults)
2. Menieres disease= idiopathic endolymphatic hydrops 
-Increased pressure in endolymph, stretching the membranes between perilymph and endolymph and causing nerve firing, leading to fluctuating vertigo, tinnitus, ear fullness. 
-"Attacks of hydrops probably are caused by an increase in endolymphatic pressure, which, in turn, causes a break in the membrane that separates the perilymph (potassium-poor extracellular fluid) from the endolymph (potassium-rich intracellular fluid). The resultant chemical mixture bathes the vestibular nerve receptors, leading to a depolarization blockade and transient loss of function. The sudden change in the rate of vestibular nerve firing creates an acute vestibular imbalance (ie, vertigo).
The physical distention caused by increased endolymphatic pressure also leads to a mechanical disturbance of the auditory and otolithic organs. Because the utricle and saccule are responsible for linear and translational motion detection (as opposed to angular and rotational acceleration), irritation of these organs may produce nonrotational vestibular symptoms.
This physical distention causes mechanical disturbance of the organ of Corti as well. Distortion of the basilar membrane and the inner and outer hair cells may cause hearing loss and/or tinnitus. Since the apex of the cochlea is wound much tighter than the base, the apex is more sensitive to pressure changes than the base. This explains why hydrops preferentially affects low frequencies (at the apex) as opposed to high frequencies (at the relatively wider base). Symptoms improve after the membrane is repaired as sodium and potassium concentrations revert to normal." (medscape)
3. Criteria for menieres:
-Vary from possible to likely to probable to definite to certain-- certain requires temporal bone autopsy. 
-"definitely" menieres:
-2 or more spontaneous episodes of vertigo lasting > 20 minutes (but less than say, 8 hours-- the idea is that the vertigo is not continuous) 
-Low frequency hearing loss (<1 kHz)
-Tinnitus or fullness in affected ear
-Other pathology ruled out 
4. Caloric reflex test: you put warm or cold water (at least 7 degrees different from body temp) into the ear, and you will see nystagmus (warm => endolymph in the ipsilateral horizontal canal rises => increased firing vestibular afferent nerve => mimics a head turn to the ipsilateral side => eyes drift towards contralateral side => bat-back horizontal nystagmus to the ipsilateral ear). This test will be hyporesponsive in menieres disease
5. Treatment (acute event): vestibular suppressants 
-Antihistamines: meclizine is nice as it is safe and has few drug-drug interactions. Causes sedation and dry mouth
-Phenothiazines: phenergan, compazine -- dystonia side effects
-Benzodiazepines are stronger vestibular suppressants than antihistamines are. Valium has been shown to be effective. In acute usage, it can speed up resolution of symptoms/compensation, however in a small % of people the symptoms will get worse. Start at low dose (2mg/day) and titrate up. Cons: 10% addiction rate. Vontrol is a powerful vestibular suppressant that will suppress all vertigo, but it causes hallucinations so it can only be given in a hospital setting. 
-Anticholinergics
-Non vestibular suppressants: antiemetics for symptomatic management. 
6. Maintenance/preventative treatment (conservative)
-Diuretics, to decrease theoretically fluid in inner ear, esp K sparing. 
-Low sodium diet (<1 g/day)
-No caffeine, tobacco, alcohol
7. Treatment (non-surgical)
-Injection of vestibulotoxins in ear, i.e. gentamycin. Gent hits vestibular system harder than auditory, but hits both; the incidence of hearing loss in affected ear is 3-10%. This is for those who have failed medical treatment (i.e. 15g/day of valium). 1-3 injections, for unilateral disease only. For those who get hearing loss, you can try steroids but theres no evidence they work
-Meniette device: applies pulses of low pressure to middle ear via PE tube. Treatment is 5 minutes TID. $$$$$. Discovered when people realized that airline travel resolved their symptoms. 
-Systemic vestibulotoxins for bilateral disease-- i.e. IM streptomycin. Streptomycin is much more vestibulotoxic than ototoxic, but it's both. Do not use dihydro-streptomycin, its really ototoxic. This paper from 1964 details the side effects of the drugs of the streptomycin family... it's strange to see kanamycin discussed as a drug to be used in people rather than a lab tool. Apparently its toxic to the cochlea. All of the streptomycin family of drugs (dihydro, kan, vanc, vio, neomycin, etc) are more ototoxic than vestibulotoxic except the original. 
-When you are using vestibulotoxins, titrate carefully-- if you completely destroy the vestibular system you will get oscillopsia. 
8. Treatment (surgical)
-Endolymphatic sac decompression shunt-- 66% effective 
-Cut vestibular nerve behind the labyrinth- 96% effective because in 4% of people, the 8th nerve goes to the cochlea before it goes to the labyrinth. To do this, you need a normal sigmoid sinus and well aerated mastoid. You can also cut the vestibular nerve in the brain, but you need to do a craniotomy via a retrosigmoid/posterior fossa approach. 
-Transcanal labyrinthectomy: drill out the canals, stuff cavity with gelfoam infused with gentamycin. 95% effective
-Total labyrinthectomy: you drill out the entire inner ear. If this is not effective, you have the wrong diagnosis. 
9. Facial nerve anatomic landmarks:
-First genu around geniculate
-Passes by stapedius bone 
-Exist stylomastoid foramen
-External bony landmark for finding trunk of facial nerve - tympanomastoid suture 
10. Superior canal dehiscence:
-Overlying temporal bone thins out. The membrane is intact, and leads intermittent vertigo (esp with pressure changes) and conductive hearing loss. 
-"Third window hypothesis": additional window in addition to round and oval window, so the conduction of signal through perilymph is less effective. 
-On the same hypothesis, you can treat otosclerosis with a foraminectomy (remove bone but leave membrane) to create a second window if you lose one.