From an article in The Hospitalist: "The Top 10 Things ID Specialists Wish Every Hospitalist Knew" & from a blogpost "6 high-yield ID clinical pearls" (blogpost has lots of references to peer-reviewed journals): 
1. Beta-lactam/b-lactamase (ie unasyn, zosyn) have excellent anaerobic coverage, no need to add flagyl or clinda. Unasyn's gram neg coverage is not as good as zosyn.
2. Staph Aureus bacteremia = 2 weeks of IV antibiotics, even if its assoc with removable line. Less may lead to relapse with infections of bone/valves. 20-25% cases of S.aureus bacteremia are complicated by metastatic dx or endocarditis. Consider TE echo to r/o valve involvement. If there is no source, or there is cardiac/bone/joint involvement = 4-6 weeks of IV antibiotics.
-Staph Aureus in urine, look for another source of infection, like heart valves/bone. Exception: history of foley or GU procedure
3. Sensitivity of C.Diff stool toxin = 80-90%, which means 10-20% false negative rate-- negative test does not r/o c.diff. Stool toxin test that is positive remains positive during and after cure, do not use it to confirm treatment, follow the clinical course instead.
-Diarrhea that develops more than 1-2 days after admission = c.diff, almost never is other bacteria (salmonella, shigella, yersenia, campy) or parasite unless someone is immunocomp or recently traveled abroad.
-Absence of diarrhea does NOT rule out C.Diff.
-C.diff causes leukocytosis (WBC 30-50). A hospitalized pt with a history of abx and a high white count = c.diff
4. Uncomplicated cellulitis is most commonly strep (often group A), including in diabetics.
-Group A strep can take 3-4 days to respond to antibiotics, and worsen for the first 1-2 days because of the secretion of tissue-damaging toxins. If systemic signs (fever, WBC) are improving but the wound looks worse, it doesn't need different/more potent antibiotics, it needs time and elevation.
-Cellulitis in the context of venous stasis/edema: elevate and diurese aggressively, as the infection won't improve until the edema is gone.
5. Quinolone monotherapy should not be used for serious GN infections because of expanding GNR quinolone resistance (incl >50% of pseudomonas in some hospitals).
6. VRE in the stool does not need to be treated, as most people will clear it on their own and not become asymptomatic. Unless you are a liver transplant recipient, in which case VRE in the stool needs to be aggressively treated.
7. Candida in the blood is always real (urine or sputum it might be a contaminant). Take it seriously, treat with mica (more effective than azoles), removing the line is not enough, get an optho evaluation. If there is candida in the urine, treat if there are symptoms.
8.  Coagulase-neg staph is a contaminant in blood the vast majority of the time; odds of getting a + culture before abx: ~40%, after abx: <20%
9. New guidelines for UTI tx: 
-Nitrofurantonin, 500mg BID for 5 days
-Bactrim 160/800mg BID for 3 days if local resistance rates are low (<20%)
-Fosfomycin trometamol 3g single injection: resistance rates are low worldwide, possibly less effective than the other treatments
-Pivmecillinam 400mg BID for 3-7 days
-Fluroquinolones are bigger antibiotics, consider if the others fail
-Do not use amp or amox, resistance is too high.
10. With normal vital signs, pneumonia is extremely unlikely. With one abnormal VS (temp, RR, pulse, O2), risk is ~12%, with 4 abnormal, it is 70%. (chart review, 2007 Am J Emer Med n>4000)

1. Causes of end-stage liver failure:
-Most common: Viral Hepatitis (B/C), alcohol (15-20% of heavy drinkers will develop cirrhosis)
-Increased back-pressure (ischemic and pressure damage)
---CHF: R heart failure, constrictive pericarditis
---Budd-chiari (hepatic vein thrombosis): lupus, polycythemia vera
---Veno-occlusive disease: injury to hepatic venous sinus endothelium (usu zone 3) leads to accumulation of clotting factors/fibrinogen -> veno-occlusion -> ischemia. Causes: high-dose cytotoxic therapy (bone marrow transplant), high-dose radiation to the liver (>30 gy), toxins like pyrrolizidine from herbal remedies (coltsfoot: flowers look like dandelions, leaves shaped like colts foot, used for respiratory symptoms, comfrey: fast-growing leafy green, called knit-bone in times past, used as topical and oral treatment for bone/skin concerns
-Direct damage to hepatocytes
---Ischemia (zone 3): shock (although if your shock is bad enough to lead to hepatic ischemia, you probably have bigger problems), hepatic artery thrombosis (i.e. sickle cell)
---Toxins (usu zone 1): amanita (zone 2), tylenol, methotrexate
---Viral: yellow fever (zone 2)
---Autoimmune hepatitis (+ANA, +a-smooth muscle antibody)
---Accumulation of toxic metabolites: hemochromatosis, wilson's, A1AT deficiency
---Accumulation of bile: PBC (a-mitochondrial ab), PSC, biliary atresia, choledochal duct cyst. In latter 2, need to diagnose and get Kasai by 2 mos.
---NASH
2. Complications of end-stage liver failure: Varices
-Pathophys: portal hypertension leads to back pressure into portosystemic anastamoses.
-Why you should screen for Esophageal varices: they're present in an estimated 30% of people with compensated cirrhosis and 60% of those with decompensated cirrhosis; annual first hemorrhage rate among those with varices is 12%, mortality from a variceal hemorrhage is 15-20%. Screen with endoscopy.
-if someone doesn't yet have a varix, timolol does not prevent them from getting varices or affect mortality/dev ascites/transplant need, and is associated with more b-blocker related serious complications {NEJM 2005, placebo-controlled RCT, n=213}
-If someone is found to have an esophageal varix, you can control it endoscopically (banding), or medically (prophylactic beta-blockers: they block b2 mediated vasodilation and allow unopposed alpha-1 constriction of splanchnic vessels). Nonselective b-blockers are effective in decreasing bleeding events (12 vs 23%), deaths due to bleeding (5 vs 10%), and are nearly significant in reducing overall mortality (21 vs 27%) {Lancet 1990, meta-analysis of RCTs, overall n=797). Recognize however that b-blockers are not benign, and suppress cardiac function, cause bronchoconstriction, impotence, fatigue.
-If someone is actively bleeding from an esophageal varix, you can band it endoscopically, or give octreotide (causes splanchnic vessel vasoconstriction somehow, possibly via suppression of vasodilatory hormones like glucagon) or vasopressin although that has more side effects.
3. Complications of ESLD: Ascites
-Pathophys: backpressure of fluid into vessels leading to liver combined with low albumin.
-Evaluate: abd u/s which can detect as little as 30mL of fluid. Make sure its not due to some other cause, like SBP, by taking a diagnostic tap: look at the cell counts, culture it/gram stain, albumin gradient<1.1 g/dL implies that it's not caused by portal HTN, look for another cause.
-Treatment: Diurese (lasix spironolactone) low-sodium diet to keep fluids off, paracentesis if the belly looks tense or it's causing symptoms (SOB, early satiety).
4. Complications of ESLD: Hepatic encephalopathy
-Accumulation of toxic metabolites, notably ammonia. Occurs in 50% of cirrhotics.
-Precipitants: alkalosis, hypokalemia (too much lasix), sedating drugs
-Treatment: lactulose, prevents absorption of ammonia,
5. Complications of ESLD: Hepatorenal syndrome
-Accumulation of blood in splanchnic vessels leads to steal phenomenon as blood is shunted away from kidneys, leading to prerenal syndrome.
-Additionally, it is thought that some toxin that accumulates in the face of decreased hepatic function acts as a renal vasoconstrictor. Direct NO injections into the renal arteries are not effective at reversing this condition, so it is either operating at a level deeper than NO, through an alternate and more potent pathway, or the NO injections were unsuccessful at reaching the full vasculature of the kidneys.
-Treat with ornipressin, vasopressin analogue which preferentially constricts splanchnic vessels. 2012 Cochrane review of multiple RCTs found terlipressin, another vasopressin analogue, decreased mortality (RR 0.76) and increased reversal of hepatorenal syndrome, but at the cost of increased cardiac complications (11% vs 0%)
6. Complications of ESLD: Spontaenous Bacterial Peritonitis (SBP)
-Pathophys: The ascitic fluid can become secondarily infected.
-Look for: fever, mental status changes, abd pain, vomiting, rebound tenderness.
-Diagnosis: paracentesis WBC>500, PMN>250, +gram stain or culture (although culture negative does not rule out
-Bugs: e.coli, klebsiella, s.pneumo
-Treat with antibiotics, repeat paracentesis in 2-3 days. symptoms should improve in 24-48 hours.
-Prognosis: 20-30% mortality rate, worse outcome if diagnosed late, can lead to sepsis.
7. Complications of ESLD: Coagulopathy: 
-Liver stops making coagulation factors; unresponsive to vitamin K.
-Treat with FFP (if its really bad, may need to run continuous infusion)
8. When doing a liver transplant, you want your patient to be volume-down, and you want to make sure their mean pulmonary artery pressure <35. The reason is that livers are very sensitive to back pressure, and the less volume there is the less there will be to back up from the heart into the liver. Once you put in the new liver and unclamp, reperfusion injury will wash inflammatory/pro-oxidant mediators from new liver (which just spent a long time in cold ischemia) into the lungs, causing some pulmonary vessel spasm. This will lead to a temporary increase in pulm aa pressure; if the baseline pulm aa pressure was already high, then it might go so high that the R heart can't push through it, blood will back up into the liver and damage it. And then you'll be left with choosing between pushing volume and significantly damaging the new liver, or not pushing volume and risking losing cardiac output.
9. MELD score was developed to predict survival of patients getting TIPS (Original study in Hepatology, n=231) now used to determine transplant list order for patients with chronic liver disease. MELD score: 3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.57[Ln serum creatinine (mg/dL)] + 6.43. If the pt has had dialysis at least 2x in the last week, Cr score is automatically increased to 4. Any value <1 is automatically assigned a 1, to prevent negative numbers coming out of the ln. Acute liver failure patients get priority over even the sickest chronic liver failure patients.
10.Blood type in solid-organ transplants: Rh factor is unimportant, only need to match blood type. In USA, blood types from most to least common: O, A, B, AB. As in blood, O's are universal donors and AB's are universal receivers.

1. Kidney trauma grading: 
-Grade I: contusion
-Grade II: <1 cm cortex laceration
-Grade III: >1 cm cortex laceration
-Grade IV: laceration through cortex, medulla; renal aa/vv damage
-Grade V: shattered kidney, significant hilum injury leading to ischemia
2. Kidney trauma surgical management: 
-Attempt salvage surgery whenever possible: cut out damaged parts, approximate remaining viable tissue, omental overlay.
-Indications for nephrectomy: bleeding leading to hemodynamic instability (be careful in kids-- they can lose a lot of blood without hemodynamic compromise, and decompensate very quickly), shattered/completely devascularized kidney. Watch out for single kidney!
3. Bariatric surgery: two mechanisms of weight loss.
-Restriction, i.e. gastric sleeve: decreases the size of stomach, reduces amount of food it can hold. Good for people who are not as heavy, or for people who are very heavy but are not healthy enough for a more extensive surgery. Gastric sleeve procedures are also an excellent treatment for reflux, since it both reduces acid-secreting cell content and
-Malabsorption, i.e. roux en y, duodenal switch: bypass absorptive segments of bowel.
Gastric bands do not work.
4. AV fistulas in hemodialysis: because both the intake and output lines of dialysis are into veins (too risky to stick an artery), AV fistulas are made to increase volume flow across the source vein. Up to 10-20% of patients will have vascular steal phenomena (i.e. distal ischemia due to decreased blood flow to capillary bed), but the rate of serious ischemia requiring intervention (i.e. bypass graft) is much lower, <5%. Patients with peripheral artery disease (arteriolosclerosis, advanced DM) are more predisposed because of more stenotic vessels as well as decreased collateral formation.
5. Criteria for kidney transplant in an HIV-positive person:
-Undetectable viral load
-CD4>200-250
6. HIV+ patients have a higher kidney rejection rate than non-HIV infected patients, according to this 2010 non-randomized prospective trial in the NEJM, which at n=150 is the largest study to date of kidney transplant in HIV+ people. They chose people that met the above criteria, and found 1- and 3- year survival rates (97 and 88% respectively) and graft survival rates (90% and 74%) that were comparable with the general population of kidney recipients, however they found a significantly increased graft rejection rate-- 31% and 41% at 1 and 3 years, respectively. From the discussion:
"The main finding of concern in this study...was the unexpectedly higher rejection rates (by a factor of 2 to 3) in the HIV-infected kidney recipients, as compared with recipients who did not have HIV infection. About half these episodes were glucocorticoid-resistant, which is characteristic of aggressive rejection. Aggressive acute rejection within 6 months after transplantation suggests an inherently enhanced response to donor antigens. The subsequent gradual and steady increase in rejection despite low CD4+ T-cell counts may represent a memory response. Multiple explanations for this type of response can be hypothesized. First, HIV contains human leukocyte antigen molecules of the host, and their transmission to another host may induce allosensitization. Second, the homeostatic expansion of T cells in HIV infection is often coupled with the acquisition of memory phenotype, which in turn is associated with increased responsiveness of the T cell and nonspecific enhancement of alloimmunity. Third, prior infections can lead to the generation of memory alloreactive T cells as a result of cross-reactivity" Additionally, since many HAART drugs inhibit the cyp-450 system, dosing of immunosuppressive drugs had to be less frequent. Although monthly trough levels of these drugs were therapeutic, there is still a possibility there was inadequate immunosuppression.
7. Most common infectious agents after liver transplant: enterococcus, citrobacter, klebsiella, fungus. Cefepime generally covers citro/kleb, try amp or vanc for the enterococcus if its not VRE. If it's VRE, go to linezolid or daptomycin; linezolid has better lung penetration but carries the risk of anemia (via erythrosuppression) and thrombocytopenia (via consumption/autoimmune) and serotonin syndrome. So if someone's platelets are low, don't use it.
8. Sequelae of immobilization:
-Muscle: atrophies: 1-3% in a day, 10-15% in a week, 50% in a month in young healthy males; in older, frailer people it's probably even faster.
-Bones: Contractures and disuse osteoporosis
-Pulm: lying down decreases breath movement into lower lobes and increases atelectasis. Increased risk of aspiration. Prone positioning in patients with ARDS increases oxygenation (PaO2) and decreases needed FiO2, may decrease mortality in very ill patients. {Crit Care Med, 2008, meta-analysis total N>1000}
-CV: initially, increased venous return, leading to diuresis and volume depletion, orthostatic hypotension
-Heme: hypercoagulable state
-GI: increased GI motility dysfunction, diarrhea/constipation. Increased acid production, decreased appetite.
-GU: increased risk of UTI, stones, urosepsis
-Extremities: bedsores
9. Early exercise/PT intervention in clinically ill ventilated patients results in faster recovery and decreased morbidity and mortality, according to a 2009 RCT in the Lancet. This study randomized people who were in the ICU, on ventilators, to be woken up out of sedation daily and given whole-body PT. Return to functional status at discharge: 59% (intervention) vs 35% (control); duration of delirium: 2 days (intervention), 4 days (control); ventilator-free days: 23.5 days (intervention), 21.1 days (control).
10. Digoxin levels are usually targeted for between 0.8 and 2.0 depending on the intervention. Levels should be checked, often to monitor for toxicity rather than efficacy, especially if the patient is in renal failure. If the kidneys are fine, levels checked once per week is OK. If they have renal impairment, empirical spacing of dosing may be appropriate, to once every 48-72 hours, since constant checking also carries risk.

1. Fluid resuscitation per surgery:
-4 cc of infused isotonic crystalloid equates to 1 cc of increased intravascular volume
-1 cc of 25% albumin infused raises the intravascular volume by 4 cc
-use crystalloids, albumin costs 50x more than NS, and in large trials has not been shown to be superior (SAFE trial)
-Don't use dextrose-fluids intraop, since the stress of surgery leads to increased endogenous glucose release and insulin resistance
-Maintain with D4,0.25NS, with daily BMPs to monitor for hyponatremia or hyperkalemia, which may worsen postop ileus
-Replacement fluids intraop- 3:1 crystalloid:EBL. 1:1 colloids.
2. Too much fluid leads to...
-Hemodilution
-Dilution of clotting factors
-Hypothermia from infusion of unwarmed fluids, which can worsen coagulopathy
-Pulmonary edema (~10L excess)
-Cardiovascular instability (HTN, CHF)
-Poor perfusion at cellular level, poor wound healing
-Bowel edema
3. Selected effects of anaesthesia: 
-Isoflurane leads to increased fluid extravasation, increased third spacing.
-Many anesthetic agents cause myocardial depression, and can push patients in borderline heart failure into frank heart failure
-Spinal anesthesia can cause a chemical sympathectomy, leading to loss of sympathetic tone in venous system, pooling of blood, decreased preload. Treat with fluid before you treat with pressors
4. Transfusion. 
-IN a large meta-analysis of extant trials examining liberal (transfuse when HgB<10) or restrictive (transfuse <7-8) transfusion practices, Carlson et al in a 2012 paper in the [Ann Intern Med] recommend the following guidelines:
-1: The AABB recommends adhering to a restrictive transfusion strategy (7 to 8 g/dL) in hospitalized, stable patients (Grade: strong recommendation; high-quality evidence).
-2: The AABB suggests adhering to a restrictive strategy in hospitalized patients with preexisting cardiovascular disease and considering transfusion for patients with symptoms or a hemoglobin level of 8 g/dL or less (Grade: weak recommendation; moderate-quality evidence).
-3: The AABB cannot recommend for or against a liberal or restrictive transfusion threshold for hospitalized, hemodynamically stable patients with the acute coronary syndrome (Grade: uncertain recommendation; very low-quality evidence).
-4: The AABB suggests that transfusion decisions be influenced by symptoms as well as hemoglobin concentration (Grade: weak recommendation; low-quality evidence).
Generally, the following groups are transfused when Hb<10: Neonates in the NICU, patients with active hemorrhage, and patients with active coronary ischemia symptoms.
5. Pulmonary artery catheters...
...are not associated with survival benefits, or benefits in ICU/hospital length of stay, but are associated with catheter-related complications {Lancet 2005, RCT n=1041} {NEJM 2003, RCT n=1994}
...are associated with increased mortality (OR 1.24), increased cost, and increased ICU LOS SUPPORT study {JAMA 1996, prospective cohort n=5735}
-less invasive way to get information about LVEDV- echo, although inter-rater reliability isn't great
-can be associated with falsely negative reads if the heart is very stiff, or if there is positive pressure ventilation
6. Venous O2 saturation is an earlier sign of shock compared to lactate, other labs. If there is decreased delivery of oxygen to tissues, the tissues will begin to extract more, leading to decreased SvO2. Normal arterial saturation is around 100, normal venous around 80, for an extraction ratio of 20%
7. Sepsis::
-associated with +blood cultures in only 40% of patients
-associated with systemic inflammatory mediators (IL-1, TNF, etc) that lead to vasodilation, increased vascular permeability, and decreased cardiac contractility
-preload, afterload, and contractility are all decreased.
-heart will compensate by increasing HR, combination of that and decreased intrinsic contractility leads to decreased stroke volume. Also, increasing HR will lead to a significant increase in myocardial O2 demand
-overall effect is warm, bounding pulses,
8. Treatments targets for sepsis: (from Surviving Sepsis 2012)
-MAP (best measure of afterload) >65. Below, end organs stop autoregulating pressures.
-CVP 8-12
-Urine output >0.5 cc/kg/hr
-SvO2 >70 (central venous), >65 (S vena cava)
9. Treatments for sepsis: (from Surviving Sepsis 2012)
-Fluids: crystalloids, albumin only if already volume-overloaded with crystalloids.
-Pressors: norepi first choice, epi when you need more, can add vasopressin to norepi for more pression or to decrease norepi dose (not first line), dopamine only if they're low risk for bradycardia/tachyarrythmia, dopamine doesn't protect the kidneys at all according to the data, and does lead to increased risk of arrhythmias.
-Inotropes if the above methods aren't enough and you have evidence of decreased cardiac contractility. Dobutamine 20 mcg/kg/minute
-If everything fails, try steroids (200mg/day, continuous infusion)
-Antibiotics in sepsis: get cultures first, then do broad-spectrum. Particular therapy (i.e. vanc + 4th gen ceph + flagyl vs vanc + b-lactam/b-lactamase) will be dependent on sensitivities and hospital fauna susceptibilities in general.
10. Clindamycin is an effective anti-toxin for tissue-destructive toxins in necrotizing fasciitis. Add it to broad spec antibiotics (not just for nec fasc but also likely staph superinfection), or community acquired MRSA is often suscept to clinda.

1. Succinylcholine is a fast-on (60 seconds), fast-off (10 minutes) paralytic. It is metabolized by plasma acetycholinesterases, not by synaptic AChE, which is why it lasts minutes rather than seconds. It causes membrane depolarization, and thus increases serum K. Normally, it will increase serum K by 0.5-1 mEq, which may not be tolerable in someone with ESRD running high baseline K. In certain patients, however, it increases serum K significantly more, up to 10 mEq-- notably, in patients who have suffered burns >15-20% of their body, or pts who have suffered crush injuries.
2. Active cardiac lesions that necessitate cardiac workup before surgery: 
-Heart failure
-Unstable angina/MI within 30 days of surgery
-Malignant arrhythmias (afib with RVR, v-tac, 3rd-degree block, as it may progress to bradycardia)
-LV outflow obstruction (Aortic stenosis), mitral stenosis
If someone doesn't have any of these lesions, and is capable of walking up a flight of stairs without cardiopulmonary symptoms, and is asymptomatic with a benign history, a cardiac workup is not necessary. In cases where exercise tolerance is not able to be determined (i.e. joint pain that precludes exercise), a workup may be indicated.
3. Predictors for difficult intubation: 
-Mallampati score of 3-4 (1: whole uvula visualized, 2:  most uvula, 3: some uvula, 4: no uvula visualized)
-Obesity: since fat is not added to the back of the head, the head will be extended when the patient is supine, need to stack pillows under head to push head forward into position
-Receding jaw: tongue/tissues compacted into smaller area, harder to maneuver
-Unable to open jaw: can attempt nasal intubation. Nasal intubation-- push scope horizontally, don't push up towards turbinates. Never attempt nasal intubation on someone with confirmed/suspected basilar skull fracture.
-Bloody field: fiberoptic scopes do not work if you can't see. If it's significantly bloody, go to trach.
-Smoker or asthmatic or any history of reactive airway disease. Laryngoscope/ET can trigger bronchospasm.
4. Indications for intubation
-need for positive-pressure ventilation (vs continuous 24/7 bag-mask)
-need for ventilator-assist/PEEP
-need to protect airway
-need to keep airway patent
-pulmonary hygiene (keep mucus and secretions out of airways)
When intubating, pull mandible forward (relative to maxilla), as the tongue is attached to the mandible and it will pull the tongue off of the posterior pharynx. Put the end of the laryngoscope into the vallecula, and pull the tongue upwards.
5. Most MIs happen 2-3 days postop, since the patient is moving around more, cardiac output is increasing, fluids are being mobilized.
6. NPO rules before surgery for people who have normal gastric emptying:
-2 hours: clear fluids
-4 hours: breast milk for infants
-6 hours: cow's milk, light carbohydrate meal
-8 hours: solid meal with fats and proteins.
The half life of clear fluids in the adult stomach is 11 minutes.
7. The maximum non-humidified airflow that can be comfortably tolerated by nasal cannula is 2-3 L/min. This rate is far below the rate of normal breathing, such that a significant portion of inhaled air will come from room air. This will dilute out the administered oxygen, thus the maximum %total inhaled oxygen caps out at about 30%. In someone who has obstructive lung disease, even small increases in % inhaled oxygen may have a significant impact on their saturation, bringing them from 80s to 90s, if they are at the straight part of their curve. Clinically appreciable/visible cyanosis happens at a saturation of about mid-80s.
8. Generic guidelines about medications to stop vs continue through day of surgery:
-anti-HTN: continue taking, except for ACE/ARB since they can inhibit compensatory mechanisms for hypotension in surgery
-cardiac drugs (digoxin, sotalol, amiodarone): continue taking
-oral hypoglycemics: stop the day of surgery. Fasting before surgery can lead to hypoglycemia, which is hard to assess in someone who is unconscious from surgery, and can cause significant morbidity.
-insulin: take 1/2 a dose the day of surgery. The stress of surgery causes hyperglycemia (via endogenous steroids/cortisol, epinephrine, GH), and people who need insulin are at baseline less well controlled on their sugars vs people on oral hypoglycemics. Monitor fingerstick glucoses during surgery and post-op.
-Asthma/COPD maintenance medications: continue taking
-Anticoagulants: difficult to ascertain. Must evaluate specific patient history, conditions, type of surgery, balance clotting (surgery =>hypercoagulable state) vs bleeding. Generally aspirin is continued, coumadin is not, but it really depends.
-Herbals/vitamins: stop 7-10 days before surgery.
9. Revised cardiac risk index to determine risk of perioperative major cardiac event: 
Equally weighted factors, derived from a cohort of 4300 people aged >50. [Circulation]
-History of ischemic heart disease
-Heart failure
-Renal failure (cr>2.0)
-DM I/II (requiring insulin)
-CVA
+high-risk non-cardiac surgery (suprainguinal vascular, thoracic, abdominal)
3+ risk factors- 11% chance of major cardiac complication
2 risk factors- 7%
1 risk factor: 0.9%
0 risk factors: 0.4%
10. Meta-analysis examining ability of revised cardiac risk index (RCRI) to predict cardiac complications: From the abstract of a meta-analysis in the [Ann Intern Med, 2010] examining over 20 studies involving over 700,000 subjects: "The RCRI discriminated moderately well between patients at low versus high risk for cardiac events after mixed noncardiac surgery (area under the receiver-operating characteristic curve [AUC], 0.75 [95% CI, 0.72 to 0.79]); sensitivity, 0.65 [CI, 0.46 to 0.81]; specificity, 0.76 [CI, 0.58 to 0.88]; positive likelihood ratio, 2.78 [CI, 1.74 to 4.45]; negative likelihood ratio, 0.45 [CI, 0.31 to 0.67]). Prediction of cardiac events after vascular noncardiac surgery was less accurate"

1.Bees can see the direction of plane polarized light and use it to navigate. [Nature, Rossel et al 1986] From the abstract: "The mechanism involves the transformation of polarization information into modulations of perceived brightness while the bee scans the sky by rotating its field of view." Some invertebrates are able to detect the plane of polarized light because they have polarization-sensitive photoreceptors, where pigment molecules (i.e rhodopsin) are oriented parallel to the vector of incident light. In vertebrates, like lowly humans, our rhodopsin molecules are oriented randomly in all our photoreceptors (womp womp). In bees, there is a patch of retina containing polarization-sensitive photoreceptors that are aligned in a graded manner. The angle of polarization of light from the sun is (generally) perpendicular to the plane containing the sun. So bees can sweep their eyes across the sky and turn around its vertical axis, and when the vectors of incident sunlight match up with the orientation of their eyes, the light will be brightest, allowing them to discern cardinal directions.
2. Mantis shrimp can see circularly-polarized light, and even differentiate R vs L handed circularly-polarized light: excerpt from a summary in [Cell: Current Biology by Michael Land] on a paper authored by Chiou et al in the same journal. "Circularly polarised light is not directly identifiable by oriented rhodopsin molecules, because the electric vector is not confined to one plane, but rotates continuously… circularly polarised light can be converted back to plane polarised light by passing it through a quarter-wave plate so that the delay between the two orthogonal components is eliminated… This, according to Chiou et al is exactly what happens in the eyes of stomatopods... Running through the centre of each eye is a band of six rows of special ommatidia. Four of these constitute a remarkable colour vision system, containing a total of 12 different visual pigments; the two further rows appear, from the arrangement of the microvilli, to be concerned with the analysis of polarised light. The receptors in these ommatidia are in two tiers. Seven of the eight receptors have their microvilli arranged at right angles in alternating blocks, so that they have the capability to respond differentially to incident light polarised in different planes. Above these, in the light path, is an eighth cell containing a single block of parallel microvilli, all aligned the same way. As Chiou et al.[3] show ...en bloc they introduce a quarter wavelength phase difference into the light passing through. Consequently, they convert circularly polarised light into plane polarised light, which the underlying seven receptors are then able to detect. Interestingly, the eighth cell microvilli are orthogonal to each other in the two ommatidial rows, meaning that they introduce orthogonal retardations into circularly polarised beams. Referring back to Figure 1C, this means that one will produce plane polarised light from a right-hand helix, and the other from a left-hand helix. This accounts for the animals' ability to distinguish right-hand and left-hand polarised light."
3. Some speculation as to why it may be useful to be able to see circularly polarized light, again from Chiou et al: light may become circularly polarized in turbid water, so being able to differentiate R from L handed circularly polarized light may enhance contrast and allow the shrimp to see better. Additionally, certain materials (such as arthropod exoskeletons, most notably scarab beetles) have the ability to circularly polarize light. Apparently, male mantis shrimp (but not females) have patches of exoskeleton that are able to do this, so perhaps they use them in communication or for behavior displays.
4. Scarab beetle shells reflect L-handed circularly polarized light. According to a paper in [Biol Rev], this occurs because the exoskeleton proteins (chitins) are organized in a helical manner. What this means is that there are many layers of microfibril protein. Each layer is composed of proteins that are oriented parallel to each other; below that, there is an identical layer of proteins that are all parallel to each other but oriented at an angle relative to the layer above them. And so on, so forth, many layers.
5. Cuttlefish can see polarized light, and use it to see through the camouflage of silvery fish (pun intended). Many fish employ radiance-matching camouflage, whereby silvery darker scales on their back and lighter scales on their bellies make it such that if they're seen from above or below, they blend in with their background. As reported by a paper in [Vision Research by Shashar et al], this reflected light is partially polarized, and cuttlefish (and some other cephalopods) can see polarized light (by the aforementioned mechanism-- pigment proteins oriented parallel to vector of incident light) and thus take advantage of this fact to hunt their prey. This paper reported findings that cuttlefish preferentially chose polarized-light reflecting fish to prey on. Also mentioned in this paper is the intriguing fact that some species of fish have evolved scales that only reflect light polarized to a small-degree, adding a second layer of camouflage.
6. Squid are able to detect transparent prey via polarization-sensitive vision. In another paper by Shashar et al in [Nature], it was found that while the bodies of many zooplankton are transparent, some tissues within them do polarize light, notably muscle fibers and ironically, rhabdomeric photoreceptors, and squid predators are able to see this light and use it to catch prey.
7. There is some evidence that humans have a preferred chewing side. One paper out of Japan found that the preferred chewing side was influenced by subclinical displacement of the articular disk in the TMJ, but only for hard food; (chewing on one side places an increased load on the contralateral TMJ). Another paper out of China found that chew-side preference may be related to the dominant brain hemisphere.
8. An extract of an african tree root used in traditional medicine for pain relief has been found to contain a compound that is identical in structure to Tramadol (Nature) The tree in question is the pincushion tree (Nauclea latifolia)
9. Eating whole fruit is associated with a slightly lower risk of diabetes, but drinking fruit juice is associated with a slightly higher risk, according to a paper in BMJ. In the form of HR(95% CI) for developing type 2 diabetes-- "0.74 (0.66 to 0.83) for blueberries, 0.88 (0.83 to 0.93) for grapes and raisins, 0.89 (0.79 to 1.01) for prunes, 0.93 (0.90 to 0.96) for apples and pears, 0.95 (0.91 to 0.98) for bananas, 0.95 (0.91 to 0.99) for grapefruit." The 95% CI for stone fruits (peaches, plums, apricots), oranges, strawberries and cantaloupe crossed 1.0; drinking fruit juice had a HR of 1.08 (1.05-1.11).
10. Naegleria fowleri found in municipal drinking water in Louisiana. (NPR)

1. During the most recent ice age, monsoons in northern africa may have brought enough rain to create three major river systems that ran north across the sahara to the mediterranean, creating a path for human migration out of africa. "This paper uses a novel palaeohydrological and hydraulic modelling approach to test the hypothesis that under wetter climates c.100,000 years ago major river systems ran north across the Sahara to the Mediterranean, creating viable migration routes. We confirm that three of these now buried palaeo river systems could have been active at the key time of human migration across the Sahara. Unexpectedly, it is the most western of these three rivers, the Irharhar river, that represents the most likely route for human migration. The Irharhar river flows directly south to north, uniquely linking the mountain areas experiencing monsoon climates at these times to temperate Mediterranean environments where food and resources would have been abundant." (PLoS One c/o Nature news)
2. In a big RCT (n=657) electronic cigarettes were associated with a 7.3% quitting rate at 6 mos compared to nicotine patches (5.8%) and placebo in the form of e-cigarettes with no nicotine (4.1%). (Lancet, c/o Hopkins podmed podcast) It'd be interesting to know what the baseline quitting rate is without any intervention.
3.Whale earwax-- like an ice core, but made of earwax, and for a whale. Whale earwax apparently accumulates over time, and can be extracted in one piece after its death and analyzed much like an ice core or a tree core. Concentrations of various substances can be measured and correlated with time-- from pollutants like mercury and pesticides to endogenous hormones like cortisol. A group from Baylor reported the findings on an earwax sample from a 12 year old blue whale, finding increased concentration of toxins in its first year of life (possibly from maternal transfer in milk), and increased cortisol levels corresponding with sexual maturity. (Nature news)
4. Surgical tool analyses smoke from electrocautery to provide real-time data on the content of tissues-- including the presence of cancer cells. The tool is an electrocautery knife (iKnife) connected to a mass spec that analyses lipid ratios in the vaporized tissue; it's able to identify the nature (neoplastic vs benign) and even the origin of the tissue if it was metastatic. Trials of the tool in live resections yielded promising findings-- "Tissue identification via intraoperative REIMS matched the postoperative histological diagnosis in 100% (all 81) of the cases studied. The mass spectra reflected lipidomic profiles that varied between distinct histological tumor types and also between primary and metastatic tumors." (Science trans med) This is pretty impressive, given that the tool does in 1-3 seconds what a surgical pathologist takes 30+ minutes to do. (c/o Science news blog)
5. Low risk ankle rule: currently about 95% of kids who present to an ER with an ankle injury will receive an x-ray, while only 12% of them actually have a fracture that requires treatment. This paper in the Lancet (prospective trial, n=607) found a 100% sensitivity, 100% NPV of the low-risk ankle rule in ruling out high-risk ankle injuries, and argue that in implementing this rule could lead to over 60% reduction in x-rays, vs only 12% reduction in the ottowa rules. However, another study in the Annals of Emergency Med (prospective, n=272) found only an 87% sensitivity of the low-risk ankle rule. Perhaps variation in examiner technique or patient population explains the discrepancy.
The low-risk ankle rule: if tenderness/swelling is limited to distal fibula or the 3 ligaments around it (distal to tibial anterior joint line)
High-risk injuries: fracture of the foot, distal tibia, and fibula proximal to the distal physis; tibiofibular syndesmosis injury; and ankle dislocations.
Low-risk ankle injuries: lateral ankle sprains; nondisplaced Salter-Harris types I and II fractures of the distal fibula; and avulsion fractures of the distal fibula or lateral talus. (c/o contemporary pediatrics)
6. Methylprednisone injections were able to reduce symptom severity in patients with carpel tunnel syndrome at 10 weeks but not at 1-year, according to a new double-blind randomized placebo-controlled trial published in the Annals of Internal Med. At 1-year, surgery rates were 73%, 81%, and 92% for patients who had received 80mg steroid, 40mg steroid, and placebo injections respectively. (c/o Hopkins PodMed)
7. Useful meta-analysis published in JAMA found a few simple clinical exam findings to be predictive of rotator cuff injury-- a great video narrates the findings of the paper and illustrates (literally) the relevant exams and findings. (c/o Hopkins PodMed)
Findings:
--1. Presence/absence of pain is NOT useful in identifying those with rotator cuff tears
--2. Infraspinatus atrophy made rotator cuff disease more likely
--3. Painful arc test was the only finding with a likelihood ratio>2 for positive rotator cuff injury; negative painful arc test had the lowest negative LR (0.36). To do this test, you have the patient start fully adducted, and abduct their arm 180 degrees. Pain between 60 and 120 degrees is considered a positive finding. Pain at 45 degrees suggests significant impingement (of rotator cuff tendons and subacromial bursa), pain at 60-70 degrees suggests moderate impingement.
Other pain tests were not found to be useful in detecting RC disease, notably: Hawkins test (pt flexes elbow and shoulder 90 degrees, examiner internally rotates arm) and Neer test (examiner fully flexes arm that is slightly abducted, internally rotated, and pronated)
--4. Positive external lag test (pt cannot maintain flexed elbow externally rotated to the side) or internal lag test (pt cannot maintain arm internally rotated behind back) were diagnostic of a full-thickness RC tear. Negative internal lag test excluded RC tear.
--5. Positive dropped arm sign (pt cannot resist downward pressure on an arm abducted 90 degrees, arm drops) increases likelihood for any RC injury.
--6. Positive external rotation resistance test (pain or weakness when trying to externally rotate arm against resistance) was accurate in diagnosing disease.
In sum: do the painful arc test, the internal and external lag test, dropped arm test, and external rotation resistance tests.
8. Catfact: Tibetan monks are better at protecting snow leopards than government agents hired to protect snow leopards. (Economist)
9. A team in japan is using GC-Mass spec to authenticate poop coffee (Economist) (J Ag Food Chem)
10. An immense shield volcano, of a size comparable to the largest known volcano in the solar system (olympus mons), discovered off the coast of Japan. (Nature c/o NPR). From the abstract: We show that the Tamu Massif is a single, immense volcano, constructed from massive lava flows that emanated from the volcano centre to form a broad, shield-like shape. The volcano has anomalously low slopes, probably due to the high effusion rates of the erupting lavas."

1. Differential of syncope in a pediatric patient:
-General: dehydration, vasovagal, orthostatic, heat, hypoglycemia
-Cardiac: structural (HOCM) vs arrhythmogenic (WPW, long QT)
-CNS: seizures
-Psych
-Tox
-Pregnancy
2. Sarcoidosis: non-caseating granulomas that can cause restrictive heart/lung disease, LAD particularly in parotid/salivary glands, and sjogren's like symptoms. It can also be associated with vitamin-D toxicity (from macrophages).
3. Males that present with classic congenital adrenal hyperplasia will present at birth with (subtle) scrotal darkening, and will present 1 week later with symptoms of salt wasting-- they will appear toxic, will be vomiting, dehydrated. DDx for these symptoms: sepsis, congenital heart failure, metabolic syndromes.
4. Primary amenorrhea: defined as lack of onset of menses by age 14 (absence of other secondary sexual characteristics) or age 16 (in presence of secondary sexual characteristics). Differential:
-Anatomic: lack of uterus (mullerian agenesis, androgen insensitivity, etc), imperforate hymen
-Hormonal: turners (most common cause of primary amenorrhrea-- look at growth chart), hyper/hypothyroid, CNS tumors affecting pituitary/hypothalamus.
Workup: FSH, LH, TSH, bone age.
5. Differential of acute-onset scrotal pain:
-Torsion: very acute onset, afebrile, no cremasteric reflex, nausea is frequent
-Epididymitis: slightly less acute onset, febrile, +cremasteric reflex, +prehn's sign (questionable how good it is to differentiate epididymitis from torsion; upward lifting of scrotum alleviates pain)
-Trauma
-Incarcerated Hernia
-Orchitis
6. Most common causes of dysfunctional uterine bleeding-- menorrhagia, metrorrhagia, menometrorrhagia
-bleeding diathesis-- 25% of cases of von willebrand's disease are diagnosed at the onset of menses
-foreign object (tampon)
-trauma
-pregnancy-related: ectopic, previa, abruption
-PID
-birth control, esp progesterone-only
7. Management of DKA in kids: first NS bolus 10mg/kg in first hour, if necessary another 10mg/kg over the next hour. After the fluid repletion is complete, insulin drip 0.1 units/kg per hour. Do not bolus insulin.
8. Ecoli sepsis in a newborn-- think galactosemia
9. Latrotoxins (venom of the black widow family of spiders) contain tetrameric proteins that bind receptors at presynaptic nerve terminals and form pores that allow the influx of divalent cations, notably Ca, causing continuous nerve depolarization.
10. Fox fact: foxes belong to the canidae family. Male foxes are called reynards, and females vixens. They live in small family groups, and they are omnivores, hunting small game (rodents), but also eating insects and fruits.

1.Evaluating neonatal jaundice, categorized by time of first appearance:
-First 24 hrs: hemolysis until proven otherwise. ABO, G6PD, spherocytosis, etc. Workup: CBC with diff and smear and retics, coombs, G6PD, fractionated bilirubin.
-Approx day 1-2: likely physiologic. Workup: transcutaneous bili, followed by serum if levels are high
-Approx day 3-5: likely "breastfeeding jaundice" aka dehydration jaundice. Increase feedings, supplement with formula. Do not give IV fluids unless there are signs of dehydration... hooking a kid up to an IV will only encumber further breastfeeding efforts by mom and worsen then problem.
-Approx weeks 1-3: likely breastmilk jaundice. Can switch to formula for a day or two and go back to breast milk, jaundice shouldn't return; alternatively, can breastfeed through it.
-If the kid has been jaundiced at a low-grade level for 4-5 weeks after birth continually/without resolution, consider a chronic process like biliary atresia (conjugated) or hypothyroid (unconjugated). Work this up, because if it is a biliary atresia, the Kasai needs to be done by 2 mos for good outcomes.
2. Hypothyroidism facts:
-Newborn screen checks for T4 levels, to be followed by TSH if T4 was low.
-Only 60% of kids with positive newborn screen for hypothyroid are actually hypothyroid; maternal antibody transfer can result in a false positive.
-In kids who are unscreened, symptoms will first appear around 8-12 weeks: hypotonia/decreased suck leading to FTT, constipation, jaundice, macroglossia, hoarse cry/lethargy, big fontanelles. The facial features usually do not appear until very late.
-Most common type of hypothyroid in this country is acquired: hashimoto's. Symptoms that kids usually present with: constipation, lethargy/decreased school performance, weight gain, decreased growth velocity, delayed puberty.
3. Hyperthyroidism facts: 
-Most common is Graves, which archetypally presents in a teen girl (F:M = 5:1), with a family history of autoimmune disease.
-Symptoms of presentation are not the same as in adults. Kids do not usually get the proptosis. Instead, they may present with an ADHD type story, of decreased school performance, inattention, insomnia, emotional lability, plus diarrhea, sweating, palpitations, amenorrhea. There will be weight loss, but that is not a symptom patients (esp teen girls) will usually complain of to their physicians.
-Be suspicious of any teenager who presents with "ADHD", for that is nearly always diagnosed at a younger age. In such a case, always run: thyroid, lead, and hearing/vision tests.
-In kids, we manage hyperthyroid medically rather than with surgery/radiation. PTU causes agranulocytosis and lupus-like picture, methimazole can also cause agranulocytosis but is preferred because it has qd dosing and is easier to titrate.
4. The Erythemas...
-Marginatum: serpiginous, expanding borders, largeish (rheumatic fever)
-Migrans: smaller, rounder/nonserpiginous borders, annular (lyme)
-Nodosum: painful, red, nodular, pretibial (IBD, sarcoid, infections- strep)
-Multiforme: targetoid, urticaria-like, multiple. Large differential: viral (herpes, HIV), bacterial (strep, staph), fungal/parasitic (toxo), drug reactions (penicillins, sulfa drugs, AEDs, aspirin, allopurinol, anti-TB), autoimmune or neoplastic.
-Toxicum: vesicles on erythematous base, common in neonates.
5. Facts about rheumatic fever: 
-Chorea can occur up to a year after a strep infection, and is the only symptom that can diagnose RF in the absence of any other signs. Penicillin, for an unknown reason, treats chorea.
-Minor criteria: arthralgia (without swelling), increased PR interval, fever.
-The migratory polyarthritis-- joints are swollen and painful, and the pain migrates by the day, which is a relatively unique identifier. Other causes of migratory polyarthralgia: rat bite fever, disseminated gonoccocus
-the N&E criteria of JONES criteria (subcutaneous nodules and erythema marginatum) are always accompanied by carditis. If these symptoms are present, search for the carditis.
6. Pauciarticular/Oligoarticular juvenille RA
-most common subset of JRA (~50%), affects 1-4 joints.
-F>M, peak age 2-3 years, rare >10 years
-Usually affects large joints, rarely hip
-Uveitis is really common in this group-- 20% overall, up to 50% in kids who are ANA+. Get a slit lamp if you suspect.
-Lab findings: not too many; may have a low ESR or low ANA titer.
-Rarely progresses to destructive arthritis.
7. Polyarticular JRA: 
-Second most common subset of JRA (30-40%), affects 5+ joints
-F>M, bimodal peak age: 2-5 years, and then again in preteen years (10-14)
-Can affect any joints, but usually doesn't start in the hips
-Uveitis less common
-Labs: 10-20% will have +RF, many will show a mild elevated ESR, the younger kids will often have +ANA titer (low)
-Destructive arthritis is common (>50%), DMARD use common
8. Systemic JRA:
-Least common subset of JRA (10-15%), affects any age, all joints
-Diurnal fevers, evanescent salmon-pink rash, HSM, LAD
-Uveitis is rare.
-Labs: elevated WBC with left shift, anemia, elevated ESR. ANA/RF are usually negative!
-Destructive arthritis/DMARD use are common.
9. SCFE vs LCP: 
-SCFE: overweight preteens
-LCP: underweight 5-7 year olds
Frog-leg AP pelvic x-ray to differentiate
10. Osteomyelitis vs Septic joint: MRI for definitive determination.

1. Interesting facts/excerpts from a medscape article on neonatal hematology:
-At birth, normal hemoglobin is 19, hct is 60, and retics are 4-7% (dropping to 0 by 4 days of age perhaps due to the drop in epo 2/2 increased oxygen tension in blood)
-MCHC > 35 implies spherical RBC, since more hgb/cell=fatter cell.
-"Immediately following birth, the neonate's H/H levels increase about 10% over the first 6 to 8 hours of life. This increase represents equilibration from a placental transfusion (from mother to neonate) occurring at the time of birth. When infants are born prematurely, the umbilical cord is cut more quickly... so this phenomenon does not occur."
-"Neonates... erythrocyte levels differ depending on the site of sampling. Capillary (heelstick) samples range from 5% to 25% higher than simultaneous samples taken from veins, arteries, or umbilical vessels. The neonate's generally larger RBCs tend to sludge in the smallest blood vessels, so capillary blood samples contain higher erythrocyte counts. If the infant's heel is warmed prior to lancing, blood vessels dilate, and the resulting capillary hematocrit is closer to venous or arterial values. The site of blood sampling must always be taken into consideration when interpreting the neonate's RBC parameters"
2. Pearls about sodium: 
-increased glucose, protein, lipid, or urea can falsely deflate your Na levels-- "pseduohyponatremia". In the case of glucose, high glucose levels pull water out of cells (since glucose equilibrates across cell membranes slowly in the absence of insulin), diluting out the serum Na. For every 100 mg/dL over normal glucose, add 1.6 mEq to your sodium. in the case of protein or lipid, sodium concentration is only measured in the fraction of free water (normal: 93% of serum), and lipids/proteins take up space and reduce the % of free water per unit of serum. In patients with severe hyperlipidemia or hyperproteinemia (i.e. multiple myeloma), the % of free water in serum may go below 80, artificially reducing the measured sodium.
-If someone is seizing from hyponatremia, they won't stop until you correct the Na-- AEDs will not help you. If they're <120, correct to 120 with 3%NaCl. If you don't have 3%NaCl, you can use sodium bicarb, which is by volume 8%NaCl. Give 1cc/kg boluses until they stop seizing.
-Acute hyponatremia: correct 0.5-1 mEq/hour. Chronic: 0.5mEq/hr
3. Pearls about fluids: 
-Best way to detect changes in fluids in infants and small children is by weight, since it can be hard to find edema on exam.
-NS: 154 Na/Cl, LR: 130 Na, 110 Cl, 4 K, 28 bicarb.
-No difference in outcomes [death, hosp LOS, ICU LOS, vent time, dialysis time] between colloidal and crystalloid solutions in the ICU. SAFE trial: RCT, 28 days, n=7000 NEJM)
-GI>>>IV for fluid resuscitation. If they can drink, make them drink.
4. Resuscitate with isotonic solutions (rather than hypotonic):
-stress => increased ADH/increased sensitivity to ADH, diluting their blood. You don't want to dilute more by giving hypotonic solutions.
-it takes less hyponatremia to cause cerebral edema in a kid vs adult-- their skull/brain ratio is smaller, they have less room to expand. While adults may be able to tolerate sodium into the low 110, with kids its more like 120s.
5. Neonatal fever: how to figure out if a neonate with a fever is harboring a serious bacterial infection. The boston (n>500), philadelphia (n>700), and rochester criteria (n>900) were all based on large retrospective data analyses trying to determine who was at high vs low-risk. '
6. Rochester Criteria for detecting neonatal sepsis: negative predictive value: 98.9, sensitivity 92%, PPV=12%, n=931.
-infants age<60 days, T>38.0
-History: term infant, no illnesses, went home with mom at birth, no perinatal antibiotics
-Exam: well appearing, no ear/bone/tissue infections.
-Labs: WBC 5000-15000, absolute bands <1500, UA wbc <10/hpf, stool smear wbc<5/hpf  [NO LP needed]
-Management: if all above criteria are met, they are "low risk" and can go home with no antibiotics, f/u in a few days.
-Outcomes: no adverse outcomes.
7. Philadelphia Criteria for detecting neonatal sepsis: NPV 99.7, sensitivity 98%, PPV 14%, n=747
-age 29-60 days, T>38.2
-Exam: well appearing, unremarkable exam
-Labs: WBC<15, band-neutrophil ratio <0.2, UA<10 wbc/hpf, urine gram stain neg, CSF wbc<8, CXR no infiltrate, stool smear (if they had diarrhea): no blood, few wbc.
-Management: if all criteria are met, home with no antibiotics
8. Boston Criteria for detecting neonatal sepsis: n=504
-age 28-89, T>38.0
-History: no immunizations/antibiotics within last 48 hours, no dehydration
-Exam: well appearing, no ear/tissue/bone infections
-Labs: WBC<20, CSF wbc<10, UA<10, CXR: clear
-Management: home, WITH empiric antibiotics (in the study: 50mg/kg IM ceftriaxone)
-Outcomes: this group was the most liberal, and as would be expected, a relatively larger false-negative rate. Overall, 5% of the cohort deemed "low risk" eventually were found to be harboring serious bacterial infections, however there were no adverse outcomes.
9. Management of SVT in children:
-If they are well perfused (good cap refill, good mental status): for the older kids, you can do carotid rub; younger kids, cold packs on their neck. If that fails, adenosine (start with 0.1mg/kg, then do 0.2, 0.3, etc. Once you get to 0.4-0.5, consider cardioversion)
-If they do not look well perfused (poor mental status, etc): synchronized cardioversion if getting the defib is faster than getting a line. Otherwise, try adenosine
10. Pearls about steroids: 
-They impair bone healing: i.e. if someone has asthma and just had orthopedic surgery, consider holding the steroids unless they really need it
-Max dose in kids is 60mg/day, so if they're 60kg, they will get 0.5mg/kg BID instead of 1 or 2.

1.Hilarious Paper #1 "Survival of acute hypernatremia due to massive soy sauce ingestion"...A 19-year-old man presented to the Emergency Department in a comatose state with seizure-like activity 2 hours after ingesting a quart of soy sauce. He was administered 6 L of free water over 30 min and survived neurologically intact without clinical sequelae. Corrected for hyperglycemia, the patient's peak serum sodium was 196 mmol/L, which, to our knowledge, is the highest documented level in an adult patient to survive an acute sodium ingestion without neurologic deficits..."
2. Hilarious Paper #2:"Misidentification of vagus nerve stimulator for intravenous access and other major adverse events." We reviewed our experience with major adverse events, after accidental puncture of a stimulator wire by an emergency room physician seeking intravenous access to treat status epilepticus..."
3. Ebstein's anomaly is the most fascinating congenital heart defect: 
-the tricuspid valve is displaced downwards (valves in a sense "fused" to ventricular wall, fail to separate adequately to "rise" up to normal position)
-tricuspid ends up being severely regurgitant, from a combination of being displaced and atrial enlargement.
-why Ebstein's is associated with cyanosis: increased pulmonary resistance at birth (and for first few months of life) means that blood from the RV preferentially regurgitates back to RA rather than going into pulmonary vasculature. Blood from RA shunts R to L through PFO, into LA, LV, through aorta, and then back through PDA (since resistance in pulm vasculature is lower than systemic), and then because resistance in the RV is lower than pulm, it regurgitates back into RV, and then back into RA, in this unique circular shunt.
-this circular shunt is only in place while the PA resistance is high, i.e. in the first months of life. Thus, it has a high perinatal mortality, but once a child ages out of this phase, s/he can live a healthy and asymptomatic life.
-Ebstein's is frequently associated with wolff-parkinson-white
4. Transposition and TAPVR are not ductal-dependent congenital heart defects, they're PFO dependent. In these two defects, there are 2 separate circulations that are not communicating, and the way to fix it is via mixing of blood in the chambers, which a PDA will not do. PDA will only shunt blood from the higher to lower pressure sides, which is useless in this case. A PFO will ensure good admixing, since the atria are both low pressure systems. If the PFO is closing, an emergent balloon atrial septostomy is necessary.
5. Duct-dependent lesions are those where there is severe outflow obstruction from either the R or the L, due to severe stenosis (TOF, bad pulm or aortic stenosis, bad preduct coarctation) or lack of propulsion-- i.e. hypoplastic L or R heart (tricuspid atresia). In other words, lesions where it would be useful to shunt large amounts of blood mostly unidirectionally from systemic to pulmonary systems (or vice-versa).
6. Cyanotic heart lesions are those that have a R => L shunt, which requires (1) pulmonary outflow obstruction and (2) a shunt so blood goes to L side instead. Non-cyanotic heart lesions are those that have a L => R shunt, or those that have outflow obstruction but no shunt/admixing (i.e. pulm stenosis without VSD/ASD/PFO)
7. Refeeding syndrome: when someone has been in starvation for a long time, body stops making insulin; when it gets fed again, insulin goes up, which can cause electrolyte abnormalities:
-decreased phosphate, since the increased generation of ATP will lead to cellular uptake of blood phosphate. People can drop their phosphates very low, leading to bradycardia, lethargy.
-decreased calcium, which can lead to convusions, arrhythmias, tetany, numbness.
-decreased potassium, which can lead to arrhythmias. Insulin leads to K uptake
-decreased mag
8. The murmur of a VSD is not heard until a few months of life, because the increased pulmonary resistance means that there is little shunting of blood (L->R) across it, even though there is a pressure differential.
9. Acrocyanosis is normal in newborns and infants, can be thought of as a "physiologic reynaud's" as the body is still learning how to autonomically regulate heat and perfusion.
10. If you are attacked by a polar bear and are out of options, try shining your iphone light into its eyes to scare it off. [NPR] Disclaimer: this is definitely the worst idea ever, and will not work

1. Edema: 
-Decreased oncotic pressure (nephrotic, malnutrition, liver failure, protein losing enteropathy)
-Increased hydrostatic pressure (volume overload, CHF, cirrhosis, obstruction, hypothyroid)
-Increased permeability (sepsis, anaphylaxis, burns, SJS, angioedema)
2. In cases of bacteremia, odds of your blood cultures being positive are:
~67% x24 hours:
~94% x36 hours
~95% x48 hours
3. Probability of having meningitis:
-Definite: +LP culture/gram stain
-Probable: +blood culture AND CSF parameters: (WBC >5, glucose <40, or protein >100)
-Possible: -blood cultures AND CSF (WBC >100, gluc <40 or prot >100)
4. Lemieres's disease:
-Fusobacteria
-oropharynx-> burrows through neck tissues to IJ-> septic thrombophlebitis
-can cause cerebral infarcts somehow.
-Tx with 28 days of IV metronidazole
5. In someone with a L->R shunt, try to avoid giving oxygen. Oxygen will cause pulm vasodilation and systemic vasoconstriction and thus worsen the L to R shunt and hasten the onset of eisenmenger's. Goal sats will be high 80s/low 90s. Diurese a lot (lasix lasix lasix lasix). You will likely see pulmonary vascular markings on CXR.
6. Workup of UTI in a kid: when to get a renal/bladder u/s: 
 -Febrile UTI in a kid <24 mos
-Multiple febrile UTI
-Febrile UTI + fam hx of renal/bladder conditions (including HTN, FTT)
-Non-responsive to antibiotic treatment
7. Workup of UTI in a kid: when to get a VCUG: 
-Abnormalites found on renal/bladder u/s (hydronephrosis, scarring, high grade reflux, obstruction)
-Complex or atypical clinical sx
-Non-e.coli UTI
-Family history/recurrent/unresponsive to treatment.
8. Management of UTI in a kid:
-prophylactic abx only indicated in patients with grade 3-4 reflux.
-repeat cultures (i.e. post treatment) are not indicated unless they failed antibiotics
-UTI with fever in a <24 month old: treat with 7-14 days of antibiotics.
9. Charcot joints: damage to bone from loss of nerves: DM, syrinx/SC injury, B12 def, tabes dorsalis, peripheral nerve dx)
10. Uses of magnesium:
-torsades
-CP prophylaxis
-eclampsia (prev seizures, diuretic; not effective as tocolytic [cochrane])
-asthma (can also use terb, relaxes bronchial smooth mm)

1. Criteria for diagnosing DKA
-have to have diabetes (blood gluc>200)
-have to have acidosis... from ketones... (pH<7.3 or bicarb<15)
...hence "diabetic... keto...acidosis..."
2. DKA severity is based on degree of acidosis: 
-Mild: pH 7.2-7.3 / bicarb 10-15
-Moderate: pH 7.1-7.2 / bicarb 5-10
-Severe: pH <7.1, bicarb <5
You can get a sense of how insulin deprived the person is by the severity of DKA. Usually their A1Cs will be pretty high (>10-11). If they have a relatively good A1C and they're presenting in DKA, it means they didn't take their insulin recently (intentionally/accidental), or they're really acutely sick from something else. Monitor urine for ketones-- need to have 2 voids that are negative for ketones before they're OK to get off IV fluids and go home.
3. For pain management in sickle cell pain crises: a good regimen is alternating max dose toradol (30mg IV) with tylenol. If that doesn't work, go to opiates.
-"aplastic crisis" in sickle cell does not mean pancytopenia, it means severe anemia with low retics, with nl white cells/platelets, can be caused by parvo.
-"hyperhemolytic crisis" = severe anemia with high retics
-"splenic sequestration crises" are exactly what they sound like. They are terrifying, with a 10-15% mortality rate: kids can hemorrhage into their spleens (and/or livers), and in the span of an hour, lose half of their hematocrit and crash. Monitor vitals (esp BP) and hct hourly, if they are in shock, push crystalloids with one hand, get O- blood stat with the other, and if you can't stabilize, with third hand call surgeons while wheeling towards OR for splenectomy. If you can stabilize, do prophylactic splenectomy when pt is fully chipper and HDS-- splenic sequestration have a 50% recurrence rate, so splenectomy is indicated after first event.
4. Retrocecal appendicitis can mimic pyelonephritis. The WBCs can migrate into the ureters and cause pyuria, can present with back pain.
5. Antibiotics Pearls:
-Omnicef covers HiB better than amox in someone who isn't vaccinated.
-The treatment for uncomplicated cellulitis is 7-10 days of PO antibiotics. 
6. Systolic heart murmurs:
-Holosystolic: "blood is going somewhere it shouldn't", since there should be no movement of blood during isovolumetric contraction/relaxation at the beginning and end of diastole. DDx: VSD, AV valve regurg
-Mid Systolic ejection: must r/o HOCM.
---Benign: "increased flow across normal valves"-- fever, anemia, states that produce increased cardiac output (hyperthyroid, anemia) or super healthy young people who just have very high CO baseline. Also can be still's (LLSB, louder supine, age 2-6), PPS (pulmonic window, radiates everywhere, kids <6 mos of age, more common after respiratory illness. )
---Pathologic: outflow tract obstruction: aortic/pulmonic stenosis, HOCM
-Early Systolic ejection: small, muscular VSD, closes upon heart contraction
7. Diastolic Heart Murmurs: always pathologic
-Early diastole: A/P valve regurg
-Mid diastole: increased flow across M/T valves,
-Late diastole: stenotic AV valves.
8. Continuous Heart Murmur:
-PDA, AVM/fistula
-Venous hum: from blood crashing through jugular vein. Diagnosis: Press finger over jugular, sound stops.
9. If you have a sick newborn (<2 weeks old) who presents with a sepsis-like picture, always keep duct-dependent heart defect high on your differential; the two can present with very similar clinical features. Your threshold for giving prostaglandins should be low, because they have very few side effects.
10. Asthma controllers:
-When someone is not well controlled on med-dose inhaled steroids, add LABA before going to high-dose steroids.
-Singular: 20-30% nonresponders. Esp good for asthma/allergic rhinitis or cough-predominant asthma types.

1. Kocher criteria for septic joint: 
-Non weight bearing
-ESR>40 (alt: CRP>20)
-T>101.5/38.5
-WBC>12
1/2/3/4 criteria correspond with 3/40/93/99 percent chance of septic joint
2. Acute onset of limping in a child: ddx
-transient synovitis (postviral)
-septic joint (see kocher criteria)
-leukemia
-osteosarcoma/mets (older kid)
-avascular necrosis of femoral head 2/2 legg-calve-perthes, steroids, sickle cell, gaucher, alcohol, lupus. Note: younger kids have dual blood supply to femur (foveal aa) that eventually closes, and so are less likely to get avasc necrosis.
3. Ativan toxicity: 
-BP/RR/mental status: often go down
-HR can go up or down, same with bowel sounds/pupils
adults will show hyporeflexia, kids can be obtunded.
4. In ingestions with significant pill burdens, the pills can coalesce and form a pill bezoar in the stomach, leading to release of drug over long time.
5. Aminglycosides can have a post-antibiotic effect, whereby they continue to kill bugs even after their blood levels drop to undetectable (adults estim ~4 hours, younger kids ~8). For maximal effectiveness in CF patients, you want a really high peak to increase absorption into tissues (fibrotic lungs) and to be significantly higher than MIC. Watch peaks on patients that are pregnant/burn patients who have different volumes of distribution.
6. Berlin heart: extracardiac pump, b/l assist, bridge to transplant in kids. Outcomes after 2 years in one study: 26% death, 60% transplant, 5% weaned, 8% still on device. Preferable to ECMO because lower surface area requires less heparin, lower risk of intracranial bleed. Preferable to LVAD because bilateral assist, kids' rib cages have limited space.
7. In someone who is tachypneic (like asthma) you expect blood gases to show respiratory alkalosis, with low CO2s (20s) and pH somewhere around 7.45-7.5. If you see an asthmatic kid, breathing fast and with a "normal" blood gas, i.e. pH 7.4 and CO2 of 40, that means they are retaining CO2, not doing good gas exchange.
8. Azithromycin has immunomodulating effects, as well as antibiotic. It can increase neutrophil apoptosis, decrease neutrophil migration; it has been shown to decrease eosinophils in the sputum of asthmatics and even decrease bronchial hyperreactivity.
9. Linezolid: thrombocytopenia, serotonin effects that can lead to serotonin syndrome in combo with other drugs.
10. Pedi meds that taste bad: flagyl, penicillin V, ferrous sulfate, linezolid, prendnisolone...

1. Hypertrophic cardiomyopathy
-usu genetic, freidrich's ataxia, IDM - transient (insulin is a growth factor)
2. Dilated cardiomyopathy
-ABCCCD: alcohol, beriberi (wet), cocaine, cobalt, coxsackie, doxorubicin (+anthracycline)
-muscular dystrophy, mitochondrial dx
3. Restrictive cardiomyopathy
-infiltrative processes: amyloid, sarcoid, hemochromatosis, wilson's, pompe's disease.
4. Arrythomogenic cardiomyopathy
5. LV Non-compaction: 
-in embryonic state, ventricular tissue is spongy and has deep clefts; over time, it compresses down into a tight, efficient muscle. Failure of this process (poss due to mitochondrial defects and decreased ATP) leads to a non-compacted, poorly contractile heart. Can present in infancy or adulthood.
6. Treatment for LV non compaction: reduce need for cardiac output, increase CO
-afterload reducers: ACE/ARB, milrinone, nitrates, synthetic BNP (diuretic)
-sympatholytics: B-blockers
-digoxin (inotropic, not chronotropic-- to increase relative cardiac perfusion)
-ultimately, only treatment is transplant
7. Excessive time under bili lights can degrade water-soluble vitamins and can lead to B vitamin deficiency, so alternate time under lights with time out.
8. Zinc deficiency: intense read rash perineally and periorally, +diarrhea.
9. Suspect mec ileus: enema with water-soluble contrast.
10. Pyloric stenosis presents in a few weeks of life; continued pressure against pylorus further encourages hypertrophy.

1. To prevent mollusks and other sea things from sticking to submerged structures, like ships and docks, there are many kinds of coatings you can apply: one is a "peeling layers" coating, where you have polymers that are cross-linked via oxygen-metal ion bridges (Sn, Zn, Cu, etc-- Sn is banned in EU waters); these bonds hydrolyze relatively easily and when sea creatures go to attach, the polymer layers peel off. You can also teflon coat (or other super low surface tension substances, like certain silicon-based compounds) surfaces to prevent attachment; but these things depend on strong currents to sweep away animals. It works for shipping vessels, which are always on the go, but not for more stationary vessels (military). You can also create a dynamic/soft surface (like sea sponges don't get mollusk attachment) or certain patterned surfaces (like shark skin).
2. MRSA dosing of clinda: 40mg/kg.
3. Failure to thrive: first you fall off the growth curve for weight, then height, finally head circumference.
4. If someone presents with a neck mass + local lymphadenopathy: 
-Viral: (EBV, esp if they have strep throat since strep often happens in people with EBV), HIV (causes parotitis and generalized LAD), VZV, CMV, Adeno
-Fungal: histo, blasto, TB, atypical mycobacteria like MAI
-Parasitic: toxo
-Bacterial superinfection- staph, strep
-Rheum: sarcoid (parotid mass- can be sarcoid even if ACE is normal), kawasaki
-Superinfected congential lesion: brachial cleft cyst/cervical sinus, hypoglossal duct cyst or other thyroid anomaly
-Neoplastic: hodgkin's/non-hodgkin's.
-Abscess: retropharyngeal (look for pain on extension of neck, difficulty/painful swallowing, drooling), paratonsillar.
5. Elevated alk-phos in a pediatric population, think about where alk-phos comes from: 
-Liver: check LFTs, GGT, bili, to see if there's any sort of hepatic or biliary process. Check for clinical stigmata of cholecystitis or stones (murphy's sign, colicky URQ pain)
-Bone: check PTH, Ca (tchovek's sign), phosphate levels to look for primary bone dx; check renal function.
--Ask about pain, fully examine (press on) all bones to elicit point tenderness-- to r/o fracture or cancer (primary/met)
--Check vitamin D levels (check 25-OH vit D which is the storage form; 1,25 is active form with v short half life) for rickets. Clinical stigmata of rickets: genu varum, thickening of wrists (one of the first signs), cuffing/fraying of distal ends of long bones on xray esp radius/ulna, rachitic rosary; also ask the kid about his diet, is he eating enough ca/vit D, does he get enough sunlight, is he chubby and active or failure to thrive?
-Placenta: pregnancy test.
-Leukocytes: tumor lysis syndrome, chemo, mono.
-Gut- ask about GI sx (pancreatic CA, celiac can present like this)
6. Isolated ulnar fractures are rare, unless the pt raises his arm to block a hit (i.e. from a blunt object). If you see an ulnar fracture, check for radial head dislocation -- "monteggia fracture"
7. Salter-Harris fractures: 
diaphysis -> metaphysis -> physis -> epiphysis. Physis is another term for epiphyseal/growth plate.
I: Straight through the physis
II: Above the physis (diaphysis) + physis
III: Lower than the physis (epiphysis) + physis
IV: Through all 3: metaphysis/physis/diaphysis
V: Ram- compression fracture of physis.
It can be hard to tell the difference between S-H 1 and 5, but the outcomes are different. 3,4, and 5 are worse.
8. To fix nursemaid's elbow: flex the affected arm 90 degrees, grasp radial head in one hand, and either hyperpronate or flex/supinate simultaneously; some people think the former is less painful. Do it fast, because it hurts and you want the pain to be as quickly over as possible. The kid should be no longer in pain and able to use the arm again in a few minutes. Counsel parents on not letting the injury recur (i.e don't swing your kid around by the arms, etc)
9. If someone is in the ICU and needs inotropes and sedatives, you should put them in different lines. If you only have one line, put the sedative in front of the inotropes. If the sedatives are behind, when you bolus them (i.e. for acute pain control for an exam or quick procedure), you will push everything in front of the sedatives on the line into the patient, i.e. bolusing the inotropes too, and that's dangerous. You can't just temporarily stop whatever is in front of the sedatives-- if they're sick enough to need inotropes, even a few seconds off of the IV drip will lead to hemodynamic instability.
10. TPN causes cholestasis and subsequent liver damage. The pathogenesis is incompletely understood, but here are some theories:
-Loss of enteral intake: reduced release of GI hormones/growth factors that are normally released by peristalsis/food in gut that maintain overall GI health, no CCK -> bile stasis in GB, bacterial overgrowth due to stasis/less developed GI immuno (also worsens cholestasis by deconjugating bile acids), bacteria also stimulate inflammation.
-TPN components may be toxic, too high, or too low: i.e. lipids may lead to hepatic steatosis and cholestasis (lipids >1g/kg/day corr with inc hepatic dmg), certain amino acids are not metabolised well by preemies and must be dropped (methionine) or are missing and need to be replaced (taurine), less vitamin antioxidants, certain minerals/metals may be toxic.
Finally, whatever underlying dx that necessitated TPN, such as short gut, will contribute to the poor outcomes. (clin liv disease)

1. In a young patient, athlete, with development of UE DVT and symptoms consistent with chronic PE, like SOB and even hemoptysis, and perhaps CT findings of what could be old consolidated blood in dependent parts of the lung, think paget-schroetter syndrome. Hypertrophy of the anterior scalene or subclavian muscle, and/or excessive movement of the clavicle and first rib against the axillary v, (i.e. in young athletes like baseball pitchers or mechanics who have their hands up a lot). Repetitive crushing of the vein leads to vessel inflammation, damage, and eventually intimal hypertrophy. The tissue surrounding the vessel, normally loose, can become fibrotic and further worsen damage.(J Vasc Surg)
2. Treatment for paget-schroetter is generally agreed to be anticoagulation followed by surgery to remove first rib and anterior scalene. Surgery is the definitive treatment; without it, the symptoms/clots inevitably recur. They used to wait 6 mos before surgery, but there's some data out now that it can be done immediately upon diagnosis with no difference in outcome. With regard to how to manage the clot/prevent more thrombosis before definitive surgical treatment, one retrospective study out of Hopkins (n=110) compared endovascular intervention (thrombolysis/venoplasty) and vs medical management (usu warfarin, sometimes lovenox) before surgery, and found no difference in eventual outcomes. (J vasc surg) Of course as a retrospective chart review study at a big referral center, there was neither randomization nor homogeneity in the type or duration of intervention. Stent/balloon angioplasty usually leads to worse outcomes, as it creates an even more thrombogenic surface that will inevitably clot off again;  (Ann thorac surg).
3. Acyclovir hits the kidneys really hard (crystallizing in the tubules) so if you're going to give it, blast the patient with IV fluids to get it out and increase solubility, and do not use any other drug that harms the kidneys like NSAIDs. I.e. even if they're spiking past 104 and you're maxed out on acetaminophen (15mg/kg in kids q4, 90mg/kg/day), do not give NSAIDs. Treating fever is a comfort thing anyways; even up to 104, there's little evidence that it leads to increased morbidity or mortality.
4. If a newborn is at high risk for kernicterus due to UCB, you can give them light therapy, which is a blue-light (560nm). You can give them one lamp at 65uW, or two lamps, and/or a reflective blanket to lie on. Absolute contraindication for phototherapy: porphyria cutanea tarda. If their UCB is really high (ballpark >25, although it depends on age), you can exchange transfuse.
5. Bhutani nomogram scale (for bili) doesn't reliably begin until around 24 hours of age, so measurements earlier than that will not find clinical correlates on this scale.
6. Major risk factors for kernicterus (i.e. factors that can cause your bili to go up high, or increase suddenly):
--Sepsis & associated factors: temperature instability (esp hypothermia since many newborns can't mount a fever), lethargy/hypotonia, acidosis
--G6PD
--Hypoalbuminemia (<3). You don't want to just infuse albumin-- too much colloidal infusion will dry out tissues by drawing all the fluid intravascularly, also the increased intravascular pressures will damage friable/sensitive vessels in lungs and brain and may lead to pulm or cerebral edema.
--ABO incompatibility (def exchange transfuse to get mom's antibodies out)
--Perinatal hypoxia-- i.e. nuchal cord.
7. Minor risk factors:
--Family hx
--Race
--Bleeds-- i.e. cephalohematoma
--IDM (polycythemia)
--many others
8. Wait 1-10 minutes between albuterol inhaler treatments: the first one gets the bronchioles open, so the second can go further. 4 puffs of MDI/spacer = 1 neb
9. Serologies for coxsackie are an inefficient allocation of limited hospital resources: there are dozens of variants of coxsackie that you have to send for, plus sensitivity and specificity are not great. If you really want an answer, you're better off with a PCR or a viral culture (takes forever).
10. Neck/Axillary LAD more likely viral, inguinal more likely bacterial.