OBGYN & Surgery PDF

OBGYN & Surgery Obstetrics Antepartum Care Principles of Surgery Fluids and Electrolytes Multiple Gestation 1st Trimester Bleeding & Fetal Demise General Surgery...

OBGYN & Surgery Obstetrics Antepartum Care Principles of Surgery Fluids and Electrolytes Multiple Gestation 1st Trimester Bleeding & Fetal Demise General Surgery Acute Abdominal Pain 3rd Trimester Bleeding Chronic Abdominal Pain Preterm Labour Gallstone Disease PROM Anorectal Disease HTN in Pregnancy Colorectal Cancer Gestational Diabetes Breast Disease TORCH Infections Trauma Fetal Malpresentation Post Op Complications Normal L&D Infantile Vomiting Labour Induction & Augmentation Acute Abdo Pain in Children Fetal Heart Rate Monitoring Pediatric Fluid Resuscitation Post Partum Hemorrhage Shoulder Dystocia Orthopedics Fractures Post Partum Complications Bone Neoplasms Dislocations Gynecology Normal Menstrual Cycle Upper Limb Pain Hirsutism and Virilization Low Back Pain Infertility Joint Pain and Swelling Abnormal Uterine Bleeding Pediatric Orthopedics Endometriosis Amenorrhea Urology Scrotal Pathology PCOS, Ovarian Cysts Groin Lumps STIs Prostate Disease Pelvic Inflammatory Disease LUTS (Incontinence, Retention, Obstruction) Vulvovaginitis Hematuria & Bladder Cancer Cervical Cancer & Pap Test UTI Endometrial Cancer, Endometrial Hyperplasia Nephrolithiasis Ovarian Cancer Other Plastic Surgery Vulvar Cancer Burns Normal Pelvic Radiology Thoracic Surgery Pelvic Mass & Pain Vascular Surgery Urogynecology Cardiac Surgery Neurosurgery Stroke ENT  ANTEPARTUM CARE (1) Dx of Pregnancy Amenorrhea β-hCG: hormone produced by placental trophoblastic cells – maintains the corpus luteum during pregnancy +’ve in serum 9 d post-conception, +’ve in urine 28 d after 1st day of LMP plasma levels usually x2 every 2 days, peaks at 8-12 wks Lvls less than expected suggest ectopic pregnancy, abortion, inaccurate dates, or some normal pregnancies Lvls greater than expected suggest: multiple gestation, molar pregnancy, T21, or inaccurate dates U/S: Transvaginal: 5 wk GA – gestational sac visible 6 wk GA – fetal pole visible 7-8 wk GA – fetal heart activity visible Transabdominal: 6-8 wk GA – intrauterine pregnancy visible Ontario Perinatal Record Visit freq: q4wk before 26 wks, q2wk b/w 26-36wk, qwkly ≥36wks Initial Visit Hx: HPI: LMP, cycle q?, regular?, planned pregnancy?, assisted conception?, bleeding, N&V, rash/fever/illness OBGYN: GTPAL, last pap date & result, complications during past pregnancies (GDM, HTN, IUGR, shoulder dystocia, PPH, neonatal jaundice, birth defects), breastfeeding/duration, child’s current health PMH: DM, HTN, thyroid, VTE, mental health, breast, GU, MSK, STIs, Hep C, vaccinations FHx: DM, HTN, VTE, mental health, anesthetic Past surgical and anesthetic Hx Nutrition: Ca intake, Vit D intake, folic acid preconception, prenatal vitamin, food access/quality adequate, dietary restriction Social: supports, job, partner & partner’s job, smoking, drugs, EtOH, intimate partner violence PE: ht, wt, BP, abdo Investigations: CBC (Hb & PLT, MCV), ABO & Rh(D), Ab screen, rubella immune, HBsAg, syphilis, HIV, GC, chlamydia, urine C&S Additional tests as needed: TSH, HbA1C, Hb electrophoresis/HPLC, ferritin, B12, ID (HCV, parvovirus B19, varicella, toxo, CMV, syphilis/VDRL) F/U Trimester Visits: Hx: concern 1st T: N&V 2nd T: prenatal classes, preterm labour, PROM, bleeding, fetal mvt, mental health, VBAC consent 3rd T: fetal mvt, birth plan (pain management, labour support), type of birth/potential interventions/VBAC plan, admission timing, breastfeeding, mental health, contraception, newborn care/screening/follow up appnt, d/c planning, car seat, postpartum care Q visit: wt, BP, urine pt, SFH, presentation, FHR, fetal movement Table of Contents  ANTEPARTUM CARE (2) Prenatal Screening: Infection: Gestational age 8-12 wks: Maternal blood type, Rh and antibody screen Rubella IgG, HBsAg, HCV Ab (in women with a history of IV drug use), HIV Ab, VDRL (syphilis) Urinalysis and C&S, chlamydia and gonorrhea test Gestational age 35-37: GBS screen GA>10wk: NIPT: measures cell-free fetal DNA in maternal circulation Advt: v. sensitive for T21, can also test for T12, Turner’s, DiGeorge, Cri Du Chat, Prader-Willi, Angelman, XY d/o Covered in ON and BC but not in other provinces Disavtg: no screening for ONTD, need invasive tests to confirm Dx, not applicable to donor eggs GA 11w to 13w+6d: Enhanced First Trimester Screening: DS, trisomy 18, placental growth factor, MSAFP, βhCG eFTS doesn’t measure risk of ONTD and should be combined with MSAFP at 15-20 wk Useful if Pt wants results in T1 More accurate test for T21 than MSS 5% false +’ve rate → if +’ve test, offer Pt CVS, amniocentesis, or NIPT IPS Part 1: DS, T18, βhCG, open neural tube defects 2% false +’ve rate → if +’ve test, offer Pt CVS, amniocentesis, or NIPT Nuchal translucency US GA 15w to 20w +6d: IPS Part 2: MSAFP, βhCG, unconjugated estrogen, Inhibin A Maternal Serum Screen: MSAFP, βhCG, unconjugated estrogen, Inhibin A, detects DS, T18, open neural tube defects Only offered alone if Pt missed time window for IPS or eFTS 8% false +’ve rate for T21, lower for NTD and T18 → if +’ve test, offer Pt CVS, amniocentesis, or NIPT GA 24-28wk: Gestational DM 50g OGTT Labs: CBC (Hb, PLT), ABO & Rh(D), repeat Ab, 1hr OGTT ± 2hr OGTT if +'ve 1 hr OGTT Invasive Diagnostic Tests: Amniocentesis: US guided transabdominal extraction of amniotic fluid done ≥15wk GA Indications: confirm +’ve eFTs/IPS/MSS/NIPT, assess fetal lung maturity in T3 Also screens for ONTD In F>35, the risk of chromosomal anomaly is greater than the risk of miscarriage from procedure Disadvtg: 1/200-900 chance of pregnancy loss (depends on experience of MD), results for QF-PCR or FISH can take 14-28 day (chromosomal tests give preliminary results in 48hr) Chorionic Villus Sampling: biopsy of fetal-derived chorion using transabdominal needle or cervical catheter at 10-12 weeks Enables pregnancy to be terminated earlier than with amniocentesis Rapid karyotyping and biochemical assay within 48hr, including FISH analysis Disadvtg: 1% risk of procedure-related pregnancy loss, doesn’t screen for ONTD, 1-2% false negative results Table of Contents  MULTIPLE GESTATION Epidemiology Incidence of twins is 1/80 and triplets 1/6400 in North America 2/3 of twins are dizygotic (fraternal) RF: IVF, ↑maternal age, newly discontinued OCP, certain African regions Role of US Ideally b/w 8-12 wks GA, done to determine if each fetus has its own chorion and amniotic sac Dichorionic–diamniotic: Twins who have their own chorions and amniotic sacs. They typically do not share a placenta and can be fraternal or identical. Monochorionic–diamniotic: Twins who share a chorion but have separate amniotic sacs. They share a placenta and are identical. Monochorionic–monoamniotic: Twins who share one chorion and one amniotic sac. They share a placenta and are identical. During pregnancy need serial US q3-4wk from 22 wk GA to assess growth (uncomplicated diamniotic dichorionic) If monochorionic, need ↑ US freq Other investigations: Doppler flow studies weekly if discordant fetal growth (>30%), BPP as needed Complications: usually due to doubling of placental mass Maternal: hyperemesis gravidarum, GDM, gestational HTN, anemia, ↑physiologic stress, ↑ compressive Sx, C/S (~50% of all twin deliveries) Uroplacental: ↑PROM/PTL, polyhydramnios, placenta previa, placental abruption, PPH (uterine atony), umbilical cord prolapse, cord anomalies (velamentous insertion, 2 vessel cord) Fetal: prematurity, IUGR, malpresentation, congenital anomalies, twin-twin transfusion, increased perinatal morbidity and mortality, twin interlocking (twin A breech, twin B vertex → vertex vertex is normal and most common presentation), single fetal demise Twin-twin transfusion syndrome: In monochorionic-diamniotic babies, one twin can donate blood to the other causing the donor to get too little blood and the recipient twin getting too much blood Due to formation of vascular anastomoses Donor twin: IUGR, hypovolemia, hypotension, anemia, oligohydramnios Recipient twin: hypervolemia, HTN, CHF, polycythemia, edema, polyhydramnios, kernicterus in neonatal period Epidemiology: 10% of monochorionic twins; concern if >30% discordance in estimated fetal wt Tx: therapeutic serial amniocentesis to decompress polyhydramnios of recipient twin and ↓pressure in cavity and on placenta intrauterine blood transfusion to donor twin if necessary laparoscopic occlusion of placental vessels fetoscopic laser ablation of placental vascular anastomoses when indicated and if available Most mothers will need a C-section Table of Contents  FIRST TRIMESTER BLEEDING & FETAL DEMISE (1) Etiology of 1st trimester bleeding: Obstetrical: Spontaneous abortion: threatened, inevitable, incomplete, complete, missed, septic Ectopic pregnancy Implantation bleed: Dx of exclusion Non-obstetrical Anatomically: cervix/vagina/vulva, GI, GU Etiology: neoplasm, trauma, infection, warts, cervical polyps, extropion Hx & PE: Questions to ask when getting the consult: vitals, #pads soaked/hr, LMP to calc GA Hx: HPI: LMP, details of bleeding (amount, duration, improve/getting worse), pain (crampy, constant), passing tissue, US results of this pregnancy, fevers, chills Gyne Hx: GTPAL, menstrual Hx, STI, paps PMH: bleeding d/o Past surgical Hx, social, meds, allergies, FHx PE: General appearance, vitals and POSTURAL VITALS Abdo exam: palpable uterus? Tenderness, guarding Speculum exam: amount of bleeding, cervix open/closed, visible tissue, other causes of bleeding Bimanual: uterus size, adnexal mass, uterine/adnexal tenderness, cervical motion tenderness Investigations: depends on Hx and PE but usually includes CBC, T&S (mandatory), serum (quantitative) βhCG (≥66% ↑ (N = x2) q48 hrs in viable intrauterine pregnancy) Progesterone: 1500 IU/L Transabdo US: βhCG >6500 IU/L If Pt requires methotrexate (medical abortion), add: lytes, BUN, Cr, LFT Management: Expectant: must be stable and reliable Pt Pregnancy of unknown location (βhCG below discriminatory zone): repeat βhCG in 48 h, repeat TVUS when βhCG > 1500 IU/L βhCG low and ↓, negative TVUS: weekly βhCG until 0 Medical: Misoprostol Methotrexate 50mg/m2 IM; (25% require 2nd dose) Candidates: stable, reliable, lives close to hospital, βhCG 12-14wk GA), salpingectomy for ectopic Indications: hemodynamic instability, impending or ongoing rupture of an ectopic mass, contraindications to MTX, unable to comply with MTX f/u, lives far from hospital, desire for permanent contraception, failed medical therapy Table of Contents  FIRST TRIMESTER BLEEDING & FETAL DEMISE (2) Types of Abortion: In 1st pregnancy, the risk of miscarriage is 11-13%. After 1 miscarriage, risk if 14-21%, after 2 = 24-29%, after 3 = 31-33% Type Definition Findings Management Threatened Process of miscarriage that has started but Vaginal bleeding Expectant Tx, bed rest, wkly pelvic US potentially reversible, before 20wks GA Fetal activity r/o treatable causes of vaginal bleeding Closed cervical os WinRho for Rh –’ve mothers Inevitable Vaginal bleeding and cervical dilation without Vaginal bleeding & visible/palpable POC Depends on Pt preference expulsion of products of conception (POC) that Fetal activity may be present Expectant management (serial clinical monitoring; occurs before 20wk GA, which is typically Closed cervical os option for 12wks GA Complete Complete passage of all POC before 20wks GA Vaginal bleeding: POC outside uterus WinRho if Rh – Closed cervical os Should resume menses in 4-6 wks, if not see MD Usually occurs 500g if unknown GA (aka stillbirth) Cervical os variable intrauterine fetal death Pls see next slide for more details Vaginal delivery safer than C-section Induced Abortion Medical or surgical termination of pregnancy Indications: Failed pregnancy: fetal demise, incomplete abortion Maternal health: e.g. severe cardiac disease in mother Personal choice Table of Contents  FIRST TRIMESTER BLEEDING & FETAL DEMISE (3) Ectopic Pregnancy: pregnancy that occurs outside the uterus, baseline risk of 1% 98% tubal: 70% ampullary, 13% fimbrial, 13% isthmic, 2% interstitial 2% other locations: ovarian, abdo, Caesarean scar Heterotopic: intrauterine and ectopic (2 babies) Presentation: Typically b/w 6-8wk GA Pain: acute, severe, on side of ectopic *need to r/o ectopic pregnancy in any F presenting with pain in 1st trimester Bleeding: usually not heavy Many aSx May present with hemorrhagic shock if ruptured RF: prev ectopic (15% risk), tubal pathology &surgery (infection, tubal ligation, congenital anomalies – DES exposure, tumours), PID, IUD, infertility, smoking, IVF, age >35 Investigations: TV US in βhCG >1500 shows adnexal mass + empty uterus Tx: Expectant: must be stable, unruptured ectopic, and reliable Pregnancy of unknown location (βhCG below discriminatory zone): repeat βhCG in 48 h, repeat TVUS when βhCG > 1500 IU/L βhCG low and ↓, negative TVUS: weekly βhCG until 0 Medical: MTX if stable, unruptured, reliable, lives close to hospital, βhCG < 5000, ectopic size 500g if unknown GA (aka stillbirth) Causes: Fetal: chromosome abN (>50%), congenital abN, non immune hydrops, infections Placental: abruption, PPROM, fetomaternal hemorrhage, cord accident, placental insufficiency, previa, twin-twin transfusion, chorioamnionitis Maternal: uterine abN, poorly controlled DM & HTN, drugs, physical stresses (fever), env chemicals, acute infection (listeria, toxoplasmosis, parvovirus B19, HSV, CMV), endocrinopathies (thyroid, Cushing’s), antiphospholipid Ab, obesity, thrombophilias, preterm labour, uterine rupture, post term pregnancy Unexplained (15-35%) RF: LMA, obesity, smoking, drugs, prev IUFD, IUGR, post-term pregnancy, maternal disease, multifetal pregnancy, ART, no antenatal care Presentation: absent fetal mvt, ↓pregnancy-related Sx, vaginal bleeding, contractions Dx with US: no fetal cardiac activity Investigations: detailed Hx, placental and cord exam, autopsy (optional but most useful), cytogenetics (low yield, hard to obtain due to specific criteria) Bloodwork: HTN: CBC, LFT, urate DM: random glucose, HbA1C Abruption: Kleihauere Immune hydrops: T&S Infection: toxoplasmosis, CMV, herpes, HAV, HBV, VDRL, HIV, Parvovirus B19 Coagulopathy: INR, PTT, fibrinogen Thrombophilia: FVL, prothrombin, antithrombin, Protein C&S, lupus anticoagulant, anti-cardiolipin, homocysteine Autoimmune: ANA Table of Contents  FIRST TRIMESTER BLEEDING & FETAL DEMISE (4) Intrauterine Fetal Demise (cont.): Management: Expectant: 80-90% will go into labour within 2 wks, if demise > 4 wks, → risk of DIC Delivery: standard = induction of labour and vaginal delivery C-section indications: shoulder presentation, persistent transverse lie, maternal absolute contraindications to vaginal delivery D&E for smaller pregnancies 35 yrs MC condition associated with placental abruption = HTN HTN, preeclampsia, cocaine use Uterine fibroids, PPROM, chorioamnionitis, polyhydramnios Smoking, trauma (esp acceleration deceleration) Epidemiology: 1:200, most are small and not diagnosed, 1:2060 fetal death Fetal morbidity: 20% of survivors with CP (VS 1% in general pop), 20% with severe acidemia (ph12mM) Clinical presentation: clinical Dx*high yield* Vaginal bleeding (78%), uterine/back pain/period-like cramps (66%), fetal distress (60%), freq contractions, hypertonus Rare: fetal death US: -’ve findings do not exclude abruption Complications: Fetal demise, maternal death Hypovolemic shock due to maternal blood loss: liver and renal failure DIC (consumptive coagulopathy): hypofibrinogenemia, thrombocytopenia MC seen with concealed abruption since pressure of blood pushes thromboplastin into the blood Couvelaire uterus: life-threatening, bleeding that penetrates the uterine myometrium into the peritoneal cavity Table of Contents  THIRD TRIMESTER BLEEDING (2) PLACENTAL ABRUPTION (cont.) PE: vitals & orthostatic vitals, FHR (if trauma, monitor x4hrs after initial insult), abdo exam (hypertonia uterus, ↓ resting tone, low lvl contractions), speculum exam (find source) Investigations: CBC, type & screen (type & cross if acute) DIC w/u: PT, PTT, fibrinogen ?Kleihauer-Betke: 5% sensitivity, quantifies fetal Hb to guide how much Rhogam to give mom) Obstetrical US, MRI (better sensitivity than US but keep in mind abruption is a clinical Dx) Management: depends on severity of abruption No fetal distress & no evidence of hemorrhage: close monitoring, consider other factors (GA, Celestone, etc.) Hemorrhagic shock: ABCs, emergency C-section, resus with pRBC & crystalloids, treat coagulopathy (DIC: PLT, FFP – if ↑ PT or PTT, cryoprecipitate – if low fibrinogen) PLACENTA PREVIA Definition: placenta “preview” – overlying or close to cervical os, incidence 1:300 Clinical presentation: Painless bleeding from placental separation, placental hyper vascularity, and or sinus/varices in lower segment decidua Associated with morbidly adherent placenta (esp if in prev C-section scar) → PPH Poorly developed decidua that lines LUS (lower uterine segment) → vessels unable to constrict & poor myometrial dev Coagulopathies rare since blood escapes vaginally Less often associated with FHR abN RF: Prior C-section, higher order pregnancy Adv maternal age, multiparity (≥5), smoking Prev previa, prev uterine Sx, D&C, fibroids/uterine anomalies, assisted repro technology Classification: Normal: edge >2cm from cervical os Low lying: edge 100mL (takes 5), distended uterus (twins, macrosomia, poly) Protracted labour, oxytocin at inappropriately high doses connective tissue d/o Clinical Presentation: peritoneal signs (due to bleeding into abdo) → key to dif b/w uterine rupture and placental abruption Sudden onset abdo pain, peritoneal signs (guarding, rigidity), vaginal bleeding FHR abN, loss of fetal station (baby moved up), palpable fetal parts on abdo exam Signs of hemorrhagic shock (↑HR, ↓BP, ↑RR, pallor) Dx: clinical but can be seen on US, emergency – life-threatening for both mom (hemorrhagic shock) and baby (uterus disrupted) Tx: Emergency laparotomy Surgical repair of rupture Supportive Rx for hemorrhage: vitals, 2 large bore IVs, fluid bolus, CBC, type and cross, O 2, PT, PTT, INR, fibrinogen, Cr, code bleed (often transfusion 1:1:1) Massive & rapid transfusion associated with hyperkalemia and hypocalcemia Table of Contents  PRETERM LABOUR (1) Definitions: Preterm labour: regular uterine contractions with cervical effacement, dilation, or both before 37wk GA Preterm birth: live birth before 37wk GA, ~12% of all live births Late preterm = 34 to 36+6, early preterm 35 Prevention: not very successful Screening in F with RF: cervical length < 10th % (48hrs 2. Nifedipine: CCB, maternal and fetal vasodilation 3. Ritodrine: β agonist, causes myometrial relaxation and interferes with myometrial contractility Contraindications: Maternal drug contraindications (e.g., myasthenia gravis for MgSO4, aortic insufficiency for CCB) Nonreassuring fetal cardiotocography, antepartum hemorrhage with hemodynamic instability Intrauterine fetal demise, lethal fetal anomaly Chorioamnionitis Severe preeclampsia or eclampsia Abx for GBS prevention: IV ampicillin & erythromycin x48h, then PO amoxicillin & erythromycin x 5d Pediatric consultation Neuroprotection: MgSO4 for 18 hrs before onset of uterine contractions in term or preterm pregnancies RF: Prev PROM, prev preterm delivery, prev cervical surgery, antepartum bleeding, infection, cervical incompetency Uterine distension, multifetal gestation Smoking Dx: Hx: Sudden “gush” of pale yellow/clear, odourless fluid from the vagina (may also be a constant leaking sensation) PE: Sterile speculum without gel (avoid digital exam): pooling, cough test/valsalva, nitrazine (basic amniotic fluid turns nitrazine paper blue, false +’ve with blood, sperm, BV, alkaline urine), ferning (false +’ve 20% from sperm & cervical mucus, false –’ve 40%) r/o cord prolapse Maternal exam for signs of infection: temp, uterine tenderness, ↑WBC Obstetrical US: oligohydramnios FHR monitoring Complications: Maternal: infection (chorioamnionitis, endometritis, bacteremia), ↑risk C-section Fetal: infection, preterm delivery (50% will deliver in 1st 24 hrs, 70-80% in following week), cord prolapse, abruption, pulmonary hypoplasia Management: *avoid digital exam unless in labour* 1. Confirm Dx (ferning, nitrazine, cough test, pooling), Ensure maternal and fetal wellbeing (vitals q4h, daily NST, CBC to r/o infection) 2. Address underlying cause that needs Tx (abruption, chorioamnionitis) 3. GBS swab, US 4. Decide on expectant management VS induction Unstable → emergency C-section: chorioamnionitis, placental abruption, cord prolapse, non-reassuring fetal HR Start empiric abx: ampicillin and gentamicin Stable: ≥37wk GA (term): delivery by induction recommended, risk of fetal sepsis > RDS 34-36 wk GA (later preterm): expectant management and induction are both reasonable, risk of fetal sepsis = risk of RDS Expectant management: best rest, pelvic rest, Celestone Induction: cervical ripening, oxytocin if GBS unknown or +’ve: penicillin G, 5 million IU IV, then 2.5 million IU IV q4h until delivery Celestone < 34wk: expectant management due significant prematurity complications: Prophylactic abx (IV ampicillin & erythromycin x48h, then PO amoxicillin & erythromycin x 5d) Celestone Tocolysis (indomethacin), possible transfer to tertiary centre MgSO4 if preterm delivery < 32wk GA expected for neuroprotection Table of Contents  HTN IN PREGNANCY (1) Hemodynamics in Pregnancy: BP = (HR x SV) x SVR ↑blood V by 50% = ↑preload, ↑ CO (30-40%), ↑HR (15-20%), ↓SVR (prostaglandins) Initially effect of SVR > CO so BP ↓ (nadir at 16-20wk GA) → mask chronic HTN Postpartum: Immediate: ↑CO 80% due to autotransfusion of uterine blood and relief of IVC; counteracted by blood loss Day 1-2: initial drop in BP Days – wks: SVR normalizes, CO returns to prepregnancy lvls Day 2-7 peak in BP due to V redistribution, then starts to decline → normalize by 3mo Definitions: Chronic HTN = before 20wk GA, after 3mo postpartum Gestational HTN = after 20 wk GA without proteinuria in F known to be normotensive before pregnancy Preeclampsia: DBP ≥ 90 AND proteinuria ≥ 300 mg/24h OR ≥1 adverse condition/severe complication Pathophysiology: abN placentation (poor blood supply due to uterine spiral arteries), endothelial dysfcn (impaired relaxation) Prevalence: 2-10% all pregnancies Severe Preeclampsia: BP > 160/110, ≥1 adverse condition/severe complication, heavy proteinuria (3-5g/24 hrs), onset 160, DBP >100, HELLP, cerebral hemorrhage, oliguria (< 500mL/d), LVF, pulmonary edema, placental abruption, DIC Sx: headache, visual disturbance, RUQ pain, severe N&V, chest pain, dyspnea, edema (face/hands) Adverse Fetal Conditions – Preeclampsia IUGR, oligohydramnios, absent/reversed umbilical artery end diastolic flow Fetal disability and/or death RF for HTN in Pregnancy: High risk: prev preeclampsia, antiphospholipid Ab syndrome, pre-existing HTN/renal disease/DM, multiple gestation Other: obesity, extremes of maternal age (< 18, >35), prev stillbirth, vascular/connective tissue disease, placental abruption, fetal hydrops Clinical Evaluation: PE: Wt (mother), neuro screen (vision changes, hyperreflexia, etc.), petechiae/bleeding, abdo exam for pain, edema of face and hands Labs: ↑serum Cr, uric acid ↑AST, ALT, or LDH (liver or heme issue – e.g. DIC) with Sx, ↑bilirubin PLT37 wk, immediate delivery is recommended Severe preeclampsia: stabilize and deliver, regardless of GA Eclampsia: MgSO4, immediate delivery regardless of GA Seizure prevention: MgSO4, monitor post partum (highest risk in 1st 24 hrs), vitals q1h Table of Contents  DM IN PREGNANCY Types: Pre-existing: T1DM, T2DM Gestational Diabetes Effects of Glucose on Fetus: 1st trimester → ↑ fetal malformations 2nd and 3rd trimester: ↑ risk of macrosomia and metabolic complications Management of Pre-existing Diabetes: Attain a preconception A1C of ≤7.0% (if safe) Goal: ↓spontaneous abortion, congenital anomalies, pre-eclampsia, progression of retinopathy in pregnancy Assess for and manage any complications Switch to insulin if on oral agents Folic Acid: 3 months pre-conception to 12 weeks post-conception D/C potential embryopathic meds: ACEi & ARB (prior to or upon detection of pregnancy) Statin therapy Screen for retinopathy and nephropathy (Cr, urine ACR – if microalbuminuria or overt nephropathy → ↑risk HTN & preeclampsia) Screening: At 24-28 wks, and earlier if high risk (e.g. BMI>35) 50 g OGTT 11 mmol/l – GDM 7.8- 11 mmol/l – needs 75mg OGTT Management of Gestational Diabetes: Start with diet and lifestyle modifications Insulin Target FPG diphenoxylate (Lomotil) > codeine Mild: Sulfasalazine (5-ASA) 4-6 g/d to induce remission Mild-moderate: Budesonide PO Moderate-severe (need immunosuppressant): Prednisone 40-60 mg PO w/ taper over wks to induce remission, azathioprine/6-mercaptopurine 0.5-1 mg/kg and ↑ over wks for maintenance, methotrexate 15-25 mg IM/SC or PO q wk for maintenance Severe/ refractory disease: Anti-TNF (e.g., infliximab), colonic resection if refractory Ulcerative Colitis Definition: inflammatory disease affecting colonic mucosa anywhere from rectum (always involved) to cecum Epidemiology: 2/3 onset by age 30 (with second peak after 50); M=F, genetic (15% of cases have 1st degree relative with disease) Classification by location: proctitis (25-55%), left-sided colitis (50-70%), pancolitis (20%) Histology: superficial chronic inflammation, crypt abscesses Hx: Rectal bleeding, grossly bloody diarrhea, lower abdo cramps (especially with defecation), urgency, tenesmus, incontinence; anorexia, weight loss, fatigue if severe characteristic exacerbations and remissions; 5% of cases are fulminant PE: vitals, abdo tenderness, EIM of IBD Investigations: Bloodwork: CBC, LFTs, iron, vitamin B12, folate, vitamin D, ESR, CRP Stool: fecal calprotectin, bacterial cultures, O&P, C. difficile toxin to r/o other causes of inflammatory diarrhea Sigmoidoscopy with mucosal biopsy (to exclude self-limited colitis) without bowel prep often sufficient for Dx Colonoscopy to determine extent of disease, contraindicated in severe exacerbation CT colonography (lead pipe sign), contraindicated in severe exacerbation Tx: Mild: 5-ASA (mesalamine) to induce remission and for maintenance Mild-moderate: MMX-budesonide PO for flares Moderate-severe: Prednisone 40-60 mg PO w/ taper over wks to induce remission, azathioprine/ 6-mercaptopurine 0.5-1 mg/kg and ↑ over wks for maintenance Severe/ refractory disease: Hydrocortisone 100 mg q8h OR methylprednisolone 16-20 mg q8h to induce remission with plan to taper and switch to non-steroid maintenance If refractory to steroids, consider: Cyclosporine 2-4 mg/kg IV x7 days Anti-TNF (e.g., infliximab) if refractory to steroids Colectomy (ileal pouch-anal anastomosis (IPAA)) Common Complications: Higher incidence of liver disease (esp PSC in M), ↑colorectal cancer, toxic megacolon Table of Contents  GALL BLADDER (1) Anatomy of the Gallbladder: Gallbladder has 3 parts: neck, body, fundus Sits in gallbladder fossa on the visceral face of liver, 9th costal cartilage in midclavicular line Bile drains from common hepatic duct & joins the pancreatic duct → hepatopancreatic ampulla Sphincter of the hepatopancreatic ampullar = Sphincter of Oddi → drains to duodenum Vasculature: Arterial: cystic artery (branch of R hepatic A) Venous: neck = cystic veins → portal vein body & fundus: hepatic sinusoids Innervation: SNS: celiac plexus PSNS: hepatic branch of vagus nerve Sensory: fibres from phrenic nerve → referred pain to R shoulder (via C3 nerve fibres) Role of Gallbladder and Pancreas: Gall bladder: Stores and concentrates bile produced by liver Releases bile in response to cholecystokinin (secreted by duodenum in response to fat consumption) Pancreas: Endocrine: release of insulin, glucagon, somatostatin Exocrine: secretes HCO3- and zymogens (trypsinogen, chymotrypsinogen, pancreatic lipases & amylases, etc.) in response to food intake Types of Gallstones: Cholesterol (80%) – CaCO3 Pathophysiology: Cholesterol supersaturation, accelerated cholesterol nucleation, impaired gall bladder motility Radiolucent with radioopaque areas due to calcifications (2cm or calcified gallbladder (suggestive of carcinoma) Sickle cell disease, Pt considered for heart/lung transplant Biliary cholic: Pathophysiology: repeated minor episodes of obstruction of the cystic duct leading to inflammation & scar formation in the gallbladder Sx: Repeated episodes of constant pain (min-hrs) in RUQ & epigastrium that radiates to the back Signs: tenderness on palpation of RUQ -’ve findings: afebrile, WBC normal, -’ve Murphy’s sign DDx: MI, pneumonia, esophageal spasm, hiatal hernia, renal colic, gastric tumours, IBS, carcinoma of cecum/ascending colon Investigations: Abdo US (see stones in most cases), CXR, ECG Management: elective laparoscopic cholecystectomy Table of Contents  GALL BLADDER (2) Acute cholecystitis: Pathophysiology: obstruction of the cystic duct that causes distention and inflammation of the gallbladder Subserosal edema → subserosal hemorrhage → patchy mucosal necrosis → fibrosis → gangrene and perforation Sx: acute RUQ pain, N&V (50%), similar episodes of past pain Signs: RUQ pain, palpable gallbladder, +’ve Murphy sign, fever Investigations: Leukocytosis US: gallstones, sludge, thickening of gallbladder wall, pericholecystic fluid or edema, sonographic Murphy’s sign DDx: PUD, acute pancreatitis, acute appendicitis in Pt with high cecum, acute hepatitis Tx: IV fluids, abx (ciprofloxacin + metronidazole), analgesics, monitor for signs of perforation Surgical management: early laparascopic cholecystectomy preferred If critically ill or general anesthetic contraindications: percutaneous cholecystostomy tube Expectant: elective cholecystectomy after Sx improve is sometimes an option Choledocholithiasis: Pathophysiology: presence of stones in the CBD causing obstruction Sx: sometimes aSx, pain in the RUQ, hyperbilirubinemia → dark urine, pale stools, jaundice/icterus -’ve findings: no signs of sepsis (↑HR, ↓BP, ↓mental status, fever) – concerning for cholangitis Investigations: Labs: ↑bilirubin, mildly ↑ ALT & AST (N in 1/3 of Pt) Abdo x-ray, CT: can visualize radioopaque stones US: ID stones in gallbladder and dilation of CBD, but not good for seeing stones in the duct MRCP used to better delineate biliary tree Tx: ① observation, ② ERCP (clears stones in CBD), ③ cholecystectomy If Pt passes stone, they should later receive elective cholecystectomy to prevent recurrence Acute cholangitis: Pathophysiology: choledocholithiasis leading to bacterial infection of the biliary tract S&S: Charcot’s triad: fever, RUQ pain, jaundice Reynold’s pentad (severe suppurative acute cholangitis): confusion, hypotension, fever, RUQ, pain, jaundice Labs: leukocytosis, ↑bilirubin, mildly ↑LFT, ↑amylase Tx: ① observation & broad spectrum abx (ceftriaxone + metronidazole), ② ERCP (clears stones in CBD), ③ cholecystectomy after recovery to prevent recurrence Table of Contents  GALL BLADDER (3) Gallstone Pancreatitis: Pathophysiology: obstruction of hepatopancreatic ampulla leading to backflow of bile into pancreatic duct and edema in pancreas due to backpressure of stone Epidemiology: M>F, 2nd MC cause of pancreatitis, after EtOH abuse Sx: acute epigastric abdo pain, N&V, dyspnea if severe (due to diaphragmatic irritation or pleural effusion) Signs: tenderness in epigastric area, distended abdomen, hypoactive bowel sounds, icterus, jaundice, fever, ↑HR, hypoxemia, ↓BP Investigations: ↑lipase, ↑amylase, US to look for gallstones Tx: Conservative: analgesia ± fluids ERCP and sphincterotomy for Pt with worsening pancreatitis or evidence of choledocholithiasis (in most cases of gallstone pancreatitis, stone has already passed) Avoid if possible since s/e of ERCP is pancreatitis Elective cholecystectomy to prevent recurrence Rare Complications: Mirizzi syndrome: extra0luminal compression fo CBD or common hepatic duct due to large stone in cystic duct or Hartmann’s pouch Sx: fever, RUQ pain, jaundice Gallstone ileus: gallstone causing intestinal obstruction Acalculous cholecystitis Table of Contents  PERIANAL DISEASE Hemorrhoids Pockets of blood vessels; outpouching related to weakness and exertion Internal hemorrhoids: above dentate line; generally not painful; presents with bleeding and prolapse External hemorrhoids: below dentate line; somatic innervation = tender; sudden severe pain can indicate thrombosed external hemorrhoid Investigations: anoscopy for internal hemorrhoids Tx: Generally supportive + ↓ constipation Typically, 6 week trial of Metamucil & ++ water before reassessment Venixxa Internal: Rubber band ligations, sclerotherapy, cryotherapy, excision hemorrhoidectomy, staples Thrombosed external: excision under local anesthesia Anal Fissure small ulceration/treat associated with constipation and exertion; painful Tx: generally supportive + ↓ constipation Perianal Abscess Arises from glands within anal canal Presentation: painful swelling Tx: incision and drainage, no abx Complications: fistula (connection b/w canal and skin), recurrent abscesses IBD is a big RF for perianal fistula Anal Cancer 2.7% of all GI malignancies Squamous cell carcinoma MC, less common = adenocarcinomas Biggest RF = HPV, receptive anal sex Perianal Crohn’s Disease Affects 1/3 ppl with CD Epidemiology: bimodal presenting at 15-30y and 50-70y, M=F, most common in Caucasians, risk in Asians ↑with move to Western counties Transmural inflammation Complications: fistula, rectal strictures, skin tags, fissures Management: Lifestyle: smoking cessation, fluids only in acute exacerbation, supplements (Vit D, Ca, Mg, Zn, Fe, B12) Antidiarrheal agents (↓ small bowel motility): loperamide (Imodium) > diphenoxylate (Lomotil) > codeine Mild: Sulfasalazine (5-ASA) 4-6 g/d to induce remission Mild-moderate: Budesonide PO Moderate-severe (need immunosuppressant): Prednisone 40-60 mg PO w/ taper over wks to induce remission, azathioprine/6-mercaptopurine 0.5-1 mg/kg and ↑ over wks for maintenance, methotrexate 15-25 mg IM/SC or PO q wk for maintenance Severe/ refractory disease: Anti-TNF (e.g., infliximab), colonic resection if refractory Table of Contents  COLORECTAL CANCER RF (94% sporadic) Diet: high fat, low fibre Genetics: familial adenomatous polyposis (100% risk by age 40), HNPCC (Lynch), 1st degree relative Crohn’s Adenomatous polyps: villous > tubulous, sessile > pedunculated Presentation Right sided lesions: anemia from chronic occult blood loss, wt loss, anorexia, weakness, vague abdo pain Left sided lesions: typically “apple core” obstructive lesions, Δ bowel habits (constipation, obstipation), blood streaking Rectal lesions: tenesmus (feeling of needing to have a BM), bright red blood per rectum, -’ve FOBT insufficient to rule out CRC Pathology Adenoma → high grade dysplasia → carcinoma → invasion → LN mets Investigations Annual FOBT: good for screening, not diagnostic DRE Barium enema Colonoscopy: 1st test if Pt is symptomatic CT/MRI CRC screening: Avg risk: FIT test q2 yr 1˚ relative with CRC: colonoscopy q5yr at age 40 of 10 yrs before age of affected family member IBD with pancolitis/extensive colitis: colonoscopy 8-10 yr after Dx, then q3 yrs IBD with distal colitis: colonoscopy 15 yrs after Dx, then q3 yrs Lynch: colonoscopy q 1-2 yrs starting at age 25 FAP: sigmoidoscopy q1yr starting at age 12 Previous large adenomatous polyps: 1-2: q5 yr ≥3: q3yr Tx Surgical resection of tumour (anastomosis, stoma/Hartman’s, palliative – intestinal bypass) Chemo-radiation: adjuvant & neo-adjuvant Radiation: good for rectal cancer but not other locations Chemo given in both Can monitor CEA to detect recurrence, repeat colonoscopy, abdo CT to screen for mets, LFTs Table of Contents  DIVERTICULAR DISEASE Definitions: Diverticula: outpouching of mucosa and submucosa (false diverticula) that herniate through colonic muscle layers in areas of ↑ intraluminal pressure; MC in sigmoid colon Diverticulosis: multiple diverticula; MC cause of acute LGIB in Pt >40 yrs Diverticulitis: inflammation and generally microperforation of diverticulum secondary to fecalith impaction RF: Low fibre (#1), high fat, older age (70% occur in ≥ 80yr), obesity, genetics, connective tissue d/o Presentation Diverticulosis: painless bleeding (MC cause of LGIB) , anemia, chronic constipation Diverticulitis: LLQ pain, fever, N&V Complications: perforation (abscess, bleeding), obstruction (due to strictures when healing), fistulas to adj organs (vaginal, urinary, bladder) 30% recurrence after 1st attack 1st attack usually worst and MC attack to have complications Management: Uncomplicated diverticulosis: high fibre diet or Metamucil, routine f/u Diverticular bleeding: bleed usually stops spontaneously; transfuse and hydrate prn If bleed doesn’t stop: colonoscopy Diverticulitis: CT abdo pelvis Admit patient, IV broad spectrum abx (e.g. ceftriaxone & metronidazole), analgesia, NPO If abscess ≥2cm, percutaneous drainage 4-6 post d/c: barium enema, colonoscopy Surgery: if chronic pain (primary anastomosis), perforation (surgical resection with temporary colostomy = Hartmann’s) Table of Contents  BREAST DISEASE (1) BREAST LUMP Hx & Px of breast lump: Hx: onset, change, tenderness, Hx of lumps & breast disease, FHx of breast or ovarian cancer, HRT/OCP, BSx Px: size, contour, tenderness, other lumps, nipple abnormalities (retraction, erythema), skin abN (dimpling, erythema), axillary or cervical nodes Malignant features: peau d’orange, skin tethering, nipple retraction DDx: Benign: F 30-50, rare after menopause, MC in upper out quadrant, mobile, varies with menstrual cycle, nipple d/c (straw-like, brown, green) #1 = Cyst: no Tx needed, consider aspiration if Sx bothersome Fibroadenoma: single well circumscribed nodule Benign phyllodes Fat necrosis: radiographically presents like breast CA but biopsy shows fat globules; often 2˚ to breast trauma; Tx = analgesia Lipoma Intraductal papilloma, galactocele, duct ectasia, ductal/lobular hyperplasia Neurofibroma Granulomatous mastitis (TB, sarcoid), abscess Sclerosing adenosis & radial scar Malignant: carcinoma, malignant phyllodes, angiosarcoma (rare) Investigations: 1st line US: good for Pt < 40 when breast it too dense for screening/diagnostic mammography Mammogram: generally used in F ≥40 FNAC 1st line after imaging; other options: core biopsy, excisional biopsu MRI BIRADS: BIRADS 0 – insufficient or incomplete study BIRADS 1 – normal study BIRADS 2 – benign features BIRADS 3 – probably benign (95% chance of malignancy) BIRADS 6 – malignant (proven malignant on tissue biopsy) Table of Contents  BREAST DISEASE (2) BREAST CANCER RF: Excess exposure to estrogen: early menarche, late 1st age of pregnancy, nulliparity, OCP/HRT Histologic RF: lobular carcinoma in situ, proliferative changes with atypia Genetic: BRCA1, BRCA2, FHx of ovarian or breast cancer Males: prev hormonal Tx for prostate cancer, use of finasteride or testosterone, episodes of orchitis/epididymitis, Klinefelter syndrome Other: excess EtOH intake and obesity → ↑endogenous estrogens Clinical Presentation: Early findings: single, nontender, immobile, firm/hard mass Locally advanced: axillary lymphadenopathy, breast enlargement, pain, peau d’orange, dimpling, skin tethering Late findings: ulcerations, supraclavicular lymphadenopathy, arm edema, eczematous rash of the nipple spreading to areola ± discharge (Paget’s disease – specific for ductal carcinoma) Metastatic disease: bone (pain), lung (dyspnea, cough), liver (abdo pain, nausea, jaundice), firm ≥1cm fixed axillary LN Screening, Diagnostic Imaging: ASx & avg risk: mammography at 50-74 yo q 2-3 yrs If Pt has higher risk (e.g. 1st degree relative), Pt in ON can get mammography at 40 with MD referral For younger Pt with Sx or abnormal mammogram → US → FNA if suspicious US If lifetime risk ≥25% (referral to genetics at CHEO), then screen with mammography and MRI Genetic testing for BRCA if: trachea during inhalation → tension pneumo Most common cause = penetrating trauma such as gun shot wounds and stabbings Tx: 3-sided occlusive dressing, then chest tube at 5th ICS anterior axillary line Massive pneumothorax: blood in the pleural space which makes it hard for affected lung to expand; also source of significant blood loss Tx: chest tube at 5th ICS posterior axillary line (Pt supine → blood pooling in back) Flail chest: ≥ 2 fractures (per rib) in ≥ 2 ribs → flail section of chest moves opposite to the resp of the chest during ventilation = inefficient P/E: asymmetric chest rise during breathing Tx: early intubation and ventilation control Circulation: control active hemorrhage, replace blood loss P/E: vitals signs and LOC Class I (< 15% blood loss): ↑HR, normal BP, Tx = crystalloid fluids (NS, RL) Class II (15-30%): ↑HR, ↓BP and ↓pulse pressure (dif b/w SBP and DBP), Tx = crystalloid fluids (NS, RL) Class III (30-40%): ↑↑HR, ↓↓ BP, ΔLOC (agitation, confusion), Tx = blood pdt + crystalloid fluids (NS, RL) Class IV shock (>40% blood loss): ↑↑HR, ↓↓ BP, obtunded, Tx = blood pdt + crystalloid fluids (NS, RL) TXA: improved survival when TXA 1g given over 8 hrs in the hospital Disability: Neuro status, AVPU/GCS, gross motor/sensory of extremities, pupils (size, symmetry, rxn to light) Exposure: remove all clothing, use blankets to prevent hypothermia Table of Contents  TRAUMA (2) Secondary Survey: Head to Toe HEENT: ecchymosis around eyes and behind the ears, tenderness of facial bones/nasal bones/jaw, visual acuity, look for injuries near eyelids/globe oral cavity (tongue laceration, missing teeth) ear canal (blood behind TM, foreign bodies) scalp (skull factures, swelling, lacerations) palpate C-spine for tenderness/swelling while keeping Pt immobile, anterior neck (swelling deformity, laceration) Chest: tenderness, swelling, SC emphysema, bruising, seat belt sign, listen to heart and breath sounds, palpate clavicle/sternum/ribs Abdo: P/E: swelling, tenderness, bruising deformity POCUS: free fluid in abdomen Pelvis: Look for ecchymosis, swelling deformity palpate for tenderness, deformity, asymmetry, instability (avoid opening and closing pelvis because blood loss every time it moves) Perineum: lacerations, hematoma, blood in urethra (avoid catheter if blood in tip of urethra due to potentially undiagnosed urethral injury) Extremity: pulse, motor, sensation, check jts for swelling/deformity, note any lacerations that need suturing Log roll: (1 person leading, 3-person roll – 1 stabilizing C spine, 2 crossing arms to stabilize torso) palpate spine, observe for swelling, tenderness, step deformities Sides of the spine: lacerations, bruising Rectal exam: high riding prostate suggestive of posterior urethral disruption, ↓tone, blood Table of Contents  CANADIAN CT HEAD AND C-SPINE RULE Canadian CT Head Rule Inclusion criteria: GCS 13-15 and ≥ 1 of: loss of consciousness, amnesia to the head injury event, witnessed disorientation. Exclusion criteria: age < 16, blood thinners, seizure after injury High Risk: CT & may need neurosurgical intervention GCS 3ft or >5 stairs Canadian C-Spine Rule: Used to safely rule out cervical spine injury (CSI) in alert, stable trauma patients without the need to obtain radiographic images. Exclusion criteria: non-trauma Pt, GCS 8wk pre-op Post op: chest physio, intermittent positive pressure breathing, selective NGT decompression after abdo surgery, short-acting neuromuscular blocking agents, appropriate pain control, early ambulation, ↓resp depressing drugs Urinary Retention More common with spinal anesthesia, older M with Hx of BPH, and Pt on anticholinergics Presentation: abdo pain, palpable bladder, overflow incontinence, PVR >100mL Tx: Foley catheter, then TOV; can also try tamsulosin Oliguria/Anuria Most common post-op cause is prerenal +/- ischemic ATN Eternal fluid loss: hemorrhage, dehydration, diarrhea Internal fluid loss: 3rd spacing due to bowel obstruction and pancreatitis Urine output 12hrs?), amount, association with feeds, bilious, projectile, hematemesis Associated Sx: inconsolable crying, irritability, anorexia, abdo distension/tenderness, fever, diarrhea, meconium passage, # wet diapers (dehydration) Trauma, abN ingestions (toxins, foreign bodies) PE: vital signs to determine clinical status and hydration state Investigations: CBC, electrolytes, BUN, Cr, amylase, lipase, glucose done routinely in sick child, add: ESR, venous blood gases, C&S (blood, urine, stool), AXR, abdo US, UGI series for anatomy abN of bilious vomiting GERD: Most common cause of vomiting in the infant age group, becomes less common in babies when they start to sit up Effortless spit up (no contraction of abdo muscles), emesis is milky, worse with supine position & better when positioned upright, arches back during feeds, wheeze (emesis drips into trachea, causing a reactive airway), fussy Due to poor developmental coordination and strength of LES fcn Tx: resolves with time, upright positioning, thickening feeds, smaller volume of feeds, ±PPI (treats esophagitis but not GERD) Table of Contents  INFANTILE VOMITING (2) Bilious vomiting: congenital obstructive GI malformations, such as duodenal/jejunal atresia, malrotation with volvulus, meconium ileus or plugs, and Hirschsprung disease. Duodenal atresia/stenosis: Dx as a neonate, associated with DS, polyhydramnios during pregnancy S&S: bilious emesis, gastric distension Most commonly affects ileum and jejunum AXR: double bubble sign Tx = surgical excision of the undeveloped section of bowel, ampicillin & gentamycin prophylaxis Pyloric stenosis: Normal abdo US findings for pylorus = 3.14 → 3mm thick and 14mm long; width 6mm, wall enhancement, appendicolith, and inflammatory changes Overall accuracy 94-100%, optimal investigation Lifetime risk of fatal radiation included malignancy is 1.8% for a 1 yo child Tx: IV fluids, correct lyte abN, NPO, analgesia, fever Rx, appendectomy (gold standard), perioperative abx: Cefazolin + metronidazole if uncomplicated peri-operative dose is adequate Abx only Tx reasonable for delayed presentation >5 d, uncomplicated appendicitis 10-20% recurrence rates Meckel’s diverticulum: displaced gastric mucosa in an abN portion of bowel → acid in an area not designed to withstand acid Rule of 2: 2% population (usually aSx), 2% symptomatic, present ~ age 2, 2M;F, 2 inches long, 2 feet from terminal ileum, 2cm wide, 2 blood supplies, 2 types ectopic mucosa S&S: Hematochezia (60%): due to ulcer formation in ileum from acid, 90% +’ve technetium 99 (concentrated by gastric mucosa) Bowel obstruction (25%): intussusception, volvulus with malrotation, mechanical Inflammation (15%) Tx: IV hydration, acid blockade IV, surgical resection Incarcerated Inguinal Hernia: Incarcerated hernia: irreducible hernia, normal overlying skin Obstructed hernia: Sx of mechanical bowel obstruction (sudden onset abdo pain, N&V, abdo distension, constipation, obstipation) Strangulated hernia: Sudden severe groin pain caused of ischemia of hernial contents, signs of sepsis or shock Overlying skin: erythema, tender Management: emergency surgical reduction of hernia Table of Contents  PEDIATRIC FLUID RESUS (1) Causes of Dehydration: (most common in blue) ↓ intake: poor feeding, unable to convey thirst, lethargy, refusal, neglect ↑losses: vomiting, diarrhea, ↑ insensible losses (fever, resp distress, burns) ↑urine output (DM, DI, adrenal insufficiency), post op (NG tubes, drains, 3 rd spacing) Hx: Intake: amount, type of fluid (breast milk, milk, Pedialyte, water, etc.) Losses (*need to be specific): what, frequency, urine output Insensible losses: fever, resp distress Mental status: irritability, lethargy (↓LOC, difficult to rouse, falling asleep) PE: Hydration Assessment LOC vitals (↑HR = 1st physical sign of dehydration) Perfusion (cap refill, mottling), (playful, lethargic, coma), mucous membranes, fontanelles (sunken), sunken eyes/tears, ↓ skin turgor Urine output (diapers) Investigations: (Hx and PE are most important) urine: specific gravity, ketones Blood: urea, Cr, lytes, venous gas (abN in resp distress and DKA), glucose Total fluid intake = maintenance + deficits + ongoing losses NS is used in fluid bolus, then D5NS +20mEq/L KCl is used in kids as a maintenance fluid Maintenance fluids: replaces normal insensible and sensible losses, function of energy expenditure, calculated using 4:2:1 rule (if > 20kg → 60+ #kg over 20) 4 cc/kg/hr for the first 10 kg, 2 cc/kg/hr for the second 10 kg, and 1 cc/kg/hr for every kg above 20kg Deficits: (% = % total BW) Mild Moderate Severe Direct: exact, based on ins and outs & exact wt loss < 1 year 5% 10% 15% Indirect: estimate, based on clinical assessment > 1 year 3% 6% 9% Mild (most info on Hx): thirsty, ↑losses, ↓ intake, ↓UO, ↓tearing, ↑HR Moderate (most info on PE): dry mucous membranes, sunken fontanelles/eyes, ↓↓UO, CRT delayed, irritable Severe: ↓BP, ↓LOC Take BP with a grain of salt: ↓CO = ↑ HR x ↓↓ SV; BP ↓CO x ↑ SVR = → Hypotension in children is a late and often sudden sign of CV decompensation ↓BP @ 25% volume loss (normal BV = 80mL/kg) – i.e in a 10kg child, 25% is 250mL or 1 cup Minimal acceptable SBP (5th percentile) = 70mmHg + (2 x age in yrs); at age 1 = 70, age 60 with osteoporosis Tx: closed reduction + long arm cast; open reduction if # is intra-articular Table of Contents  FRACTURES (4) UPPER EXTREMITY # (cont.) Scaphoid Fracture Most common fractured carpal bone, due to FOOSH Tx: thump spica cast Complication = avascular necrosis of the proximal pole Humerus Fracture (pictured) Due to direct trauma Radial nerve injury may result in wrist drop and loss of thumb extension Tx: hanging arm cast VS coaptation splint and sling; functional bracing “Nightstick” Fracture Ulnar shaft # from direct trauma, often in self defense against a blunt object Tx: ORIF if significantly displaced Galeazzi Fracture (pictured) Diaphyseal fracture of the radius with dislocation of the distal radioulnar joint from direct blow to radius Tx: ORIP of radius and casting of fractured forearm in supination to reduce distal radioulnar jt Boxer’s Fracture # of the 5th metacarpal neck from forward trauma of a closed first Tx: closed reduction and ulnar gutter splint, percutaneous pinning of # excessively angulated Table of Contents  BONE NEOPLASMS (1) BONE METASTASES Lytic: Blastic: Lung Prostate Colon Thyroid Renal Breast General Management of Bone Mets: Tx needed if: Require fixation to prevent # if there are large >1/3 diameter or lytic Produce pain on wt bearing in lower limb If survival >3mo, consider prophylactic fixation and radiation therapy 2 weeks after fixation Tx = protect, radiation, surgery OSTEOSARCOMA Most common primary bone malignancy in kids and teens Adults: often is a transformation of other benign tumours, including Paget’s disease Usually in metaphyseal distal femur, proximal tibia, and proximal humerus Often metastasizes to lungs Arises from osteoblasts in periosteum Presentation: Progressive pain that worsens at night, B Sx, erythema and enlargement over site of tumour, limping, pathologic # Management: XR is the best initial test: sunburst appearance of lytic bone and/or Codman triangles, osteolysis adjacent to osteosclerosis (moth eaten appearance) Biopsy = most accurate Dx Neoadjuvant and adjuvant chemo: methotrexate, doxorubicin, cisplatin, ifosfamide Surgical resection Usually resistant to radiation therapy Prognosis: if primary osteosarcoma, 5 yr survival is 70%; if secondary osteosarcoma, the prognosis is poor due to low response rate to Tx EWING SARCOMA Presentation: Peak incidence at 10-20yrs, mainly affects Caucasians, M>F Localized progressive pain, worse at night, fever, swelling, tenderness on palpation, erythema Primary tumour often affects diaphysis of long bones; mets: lung, skeletal system, bone marrow Management: XR: lytic lesion, classic onion skin appearance of periosteum Biopsy Surgical resection, plus neoadjuvant and adjuvant polychemotherapy Additionally: radiation therapy (usually responsive) 80% 5 yr survival for localized dz Table of Contents  BONE NEOPLASMS (2) CHRONDROSARCOMA Malignant tumour from mesenchymal cells that produce cartilage Etiology of secondary chondrosarcoma: osteochondroma, Paget disease of the bone, radiation Presentation: Insidious onset, dull, progressive pain, worse at night, local swelling Pathologic #, neurovascular damage, limited ROM Most commonly seen in the medullary cavity of pelvis, ribs, proximal femur, and proximal humerus Management: XR: osteolysis with moth eaten appearance, ring arc calcifications, popcorn calcification, endosteal scalloping and cortical breach with infiltration of soft tissue Biopsy for Dx Definitive surgical resection, chemo and radiation therapy as adjuvant therapy or palliative Tx Table of Contents  DISLOCATIONS Patterns: Shoulder, elbow, finger, ankle: mobile jts, isolated injuries, few associated # Shoulders > PIP > elbows > ankles Hip, knee: stable jts, combined injuries, associated injuries Shoulder Dislocations 95% anterior, 5% posterior (more commonly seen with seizures) Mechanism: abduction and external rotation Empty deltoid convexity Tx: conscious sedation, traction, reduction, immobilization Complications after shoulder dislocation: Brachial plexus palsy Axillary artery injury Associated # Recurrent dislocation Frozen shoulder Rotator cuff tear Elbow Dislocations Posterolateral dislocation most common Associated injuries: median N, ulnar N, vascular injury Knee Dislocations Usually anterior (tibia in relation to femur, as pictured) Vascular injury common, sometimes nerve injury Multiple ligaments injured Tx: conscious sedation and immediate reduction (knee extension) due to injury to popliteal artery Posterior Hip Dislocations Presentation: hip flexion adduction, internal rotation, limb shortening Mechanism of injury: usually from posteriorly directed force directed on internally rotated, adducted hip (dashboard injury) XR: L femoral neck looks a bit smaller than R Often associated with sciatic nerve injury and AVN Other common injuries seen from dashboard injury: PCL tear, proximal tibia #, patella #, femur # Tx: immediate closed reduction (with Pt supine, press down on flexed hip and lift flexed knee upwards), then abduction pillow/bracing; eval with CT after reduction Table of Contents  UPPER LIMB PAIN (1) CERVICAL SPINE STENOSIS Definition: Narrowing of the cervical spinal canal and compression of SC and arterial/venous blood supply to SC, most freq due to aging Often caused by cervical spondylosis Progressive degeneration of cervical vertebral bodies and intervertebral discs Leads to disc herniation, facet/uncovertebral/vertebral body osteophytes, ossification and hypertrophy of the posterior longitudinal ligament/ligament flava Sx: variable; due to compression and damage to spinal nerve roots and SC Pain in neck, subscapular region, shoulder, often radiation to arms Dermatomal parasthesias or numbness in arms; loss of sensation in lower limbs Sx exacerbated by neck flexion and extension Loss of fine motor control in hands, UE weakness, spastic gait UMN: ↑reflexes, +’ve Babinski UE LMN in myotomal distribution: weakness, atrophy, ↓reflexes → C5-7 MC affected Sx often insidious W/u: CT or MRI spine; EMG usually not needed unless trying to r/o other Dx (e.g. ALS, GBS, NPH) Tx: Non-surgical: activity modification, NSAIDs, muscle relaxants, amitriptyline, pregabalin Surgical decompression: cervical discectomy and corpectomy, laminectomy, laminoplasty, etc. PANCOAST TUMOUR Definition: Superior pulmonary sulcus tumours arising from the apical pleuro-pulmonary groove superior to the 1st rib 3-5% of all lung cancers, almost all are NSCLC (squamous cell carcinoma = MC histologic Dx) Causes Pancoast syndrome when they invade surrounding structures brachial plexus compression, parietal pleura/rib/vertebral invasion, sympathetic chain invasion, etc. Presentation: Brachial plexus palsy (MC C8 and T1 nerve roots): shoulder/arm pain associated with paresthesias along medial 4 th and 5th fingers and medial side of arm If affects the sympathetic trunk and cervical ganglion can cause ipsilateral facial flushing and sweating Horner’s syndrome (myosis, anhidrosis, ptosis) & SOB are late findings W/u: CXR = good initial investigation CT for staging: extent of tumour, satellite nodules, mediastinal adenopathy CT guided core biopsy Before surgery, often need MRI check, chest, upper abdo to determine extent of vascular and brachial plexus involvement Tx: chemoradiation, then surgical resection Table of Contents  UPPER LIMB PAIN (2) THORACIC OUTLET SYNDROME Definition: Nonspecific Dx that represents many conditions that involve compression of NV structures passing through the thoracic outlet Due to space occupying lesions (tumour, cyst), fibrous muscle bands, trauma, abN neck position 2˚ causes: clavicle #, trapezius muscle abN (leads to shoulder depression) Common in swimmers, tennis players, water polo athletes, and baseball players Presentation: very variable Venous obstruction: UE swelling, venous distension, pain in hand and/or forearm, DVT Arterial obstruction: UE colour change, ↓pulses Neurogenic: MC presentation, vague pain, atrophy of intrinsic muscles of the hands, sensory deficits Spurling test to recreate radicular pain W/u: CXR & C-spine XR, venous dopplers Tx: Conservative: lifestyle modifications (no overhead arm sleeping, posture correction), PT Surgical: rarely needed (indication = muscle atrophy of hand) and success rate is 50-75% SUBACROMIAL BURSITIS Definition: Bursa = fluid filled sac served to lubricate joints Common etiologies: subacromial impingement, repetitive overhead activities, direct trauma, crystal deposition, infection, autoimmune Chronic bursitis often co-exists with tendonitis Presentation: Anterolateral shoulder pain, no radiation Pain on resisted arm abduction beyond ~75 degrees (painful arc) W/u: XR shoulder to r/o other pathologies), US shoulder Tx: rest, NSAIDs, PT, CS injections, surgical if not responsive to conservative Tx Table of Contents  ROTATOR CUFF TENDINOPATHY UPPER LIMB PAIN (3) Most common cause of shoulder pain that is a combination of tendonitis, tendinosis, and tendon rupture Presentation: Repetition/overuse, especially with overhead activity (swimmer, pitcher, wheelchair); occasionally due to single event May be associated with laxity or instability Pain with overhead activity, pain to sleep on, inability to lift arm in a complete tear Subacromial Impingement: Rotator cuff tendons (usually supraspinatus) are impinged when they pass through the subacromial space Subacromial space ↓ if lateral scapula is translated anteriorly or humerus is internally rotated. Common culprit = weak posterior musculature (scapular stabilizers: rhomboids, trapezius), tight internal rotators (pecs, lats), weak external rotators (infraspinatus, teres minor) → Commonly seen in body builders Signs: Inspection: wasting and weakness of rotator cuff muscles Palpation: painful subacromial space and bursa Active ROM: painful arc (60 ˚- 120˚) → occurs because not enough space for soft tissues to fit as the greater tuberosity of the humerus passes under acromion mild ↓ROM (pain), pain with combined abduction and internal rotation, pain with resisted rotation cuff muscle testing Special Tests: positive impingement signs Neer’s test (all 4 rotator cuff tendons): +’ve = pain doing a “gymnast’s salute” → thumbs down in full elbow extension then raise arms Empty can/Jobe test (supraspinatus): +’ve = pain or weakness “emptying a can” while resisting downwards pressure Drop arm test (during active ROM) = tear in supraspinatus tendon Push off test (subscapularis): +’ve = pain/weakness when Pt has arms behind back and pushing against pressure Cups test (infraspinatus and teres minor): +’ve = pain/weakness “holding cups” with elbows tucked in at waist and resisting inwards pressure applied against the outside of their forearms Tx: PRiceM → protect, rest, medications Physiotherapy to strengthen scapular and GH stabilizers, pecs stretching Corticosteroid injection Surgery if full thickness muscle tear (avoid in elderly because will result in bad quality muscle) SLAP Lesion (Superior Labral Anterior to Posterior) Labral tear where long head of biceps inserts @ supraglenoid tuberosity of scapula due to repetitive overhead throw or excessive inferior traction (ex: carrying or catching a heavy object) S&S: poorly localized shoulder pain, worse with overhead activity Special tests: O’Brien: +’ve = pain worse when Pt resists downward pressure in internal rotation compared to external rotation with arms fully extended Dx: initially with MR arthropathy with dye to visualize labrum, but definitive Dx is with surgical exploration Tx: surgery Biceps rupture: Usually detachment of long head of biceps (elbow flexor) Presentation: usually older athlete or older person, “Popeye’s sign” Often accompanied by acute pain which then goes away, little loss of strength because there are lots of biceps flexors Investigation: US then MRI if needed Tx: usually conservative (ROM + strengthening), surgery if distal tear (@radius, both heads) or athlete Table of Contents  BACK PAIN (1) 70% are idiopathic (lumbar sprain/strain) → typically moderate Sx that worsens with mvt or cough 27% mechanical: fracture (osteoporotic, traumatic, neoplasms, inflammatory, Paget’s), facet arthritis, degenerative discs, herniated discs, spinal stenosis 2% referred: AAA, GI, GU (pyelonephritis, kidney stone), pelvic 1% non-mechanical: neoplasm (multiple myeloma, metastasis, SC tumour, etc), inflammatory arthritis (ankylosing spondylitis, psoriatic spondylitis), infection (osteomyelitis, septic diskitis, shingles, etc) Hx: OPQRST, mechanism of injury, location, Hx of trauma AAA risk factors (smoking, older age, M, Caucasian, CVD, atherosclerosis, HTN), infection (fever, chills, STIs, IV drug use), B Sx, Degenerative conditions (older age , FHx, previous imaging, smoking, steroid), autoimmune (younger age, insidious onset, >3mo, ++AM stiffness, worse with rest, SI joint involvement, IBD presentation), GI, GU, pelvis R/O cauda equina (see below) PE: Vitals, abdominal exam (AAA), neurological (inspection, tone, power, sensation, reflexes, gait, DRE) MSK: inspection, palpation, ROM, Straight leg test (herniated risk if Pt experiences sciatic pain), Schober (mark 5cm above and below PSIS, +’ve test for ankylosing spondylitis if distance 1 yr; no difference in 3yr prognosis), referral to spine center Medications: Tylenol, NSAIDs, narcotics (20% develop abuse or dependency), steroids, colchicine (used in disc /d/o), allopurinol (↓uric acid in blood) Encourage wt loss (obesity can worsen Sx) Vitamin D and Ca CAUDA EQUINA Etiology: spinal lesion/tumour/inflammation/infection, lumbar spine stenosis, trauma to lower back (gunshot, fall, MVA), AVMs, spinal hemorrhages (SAH, subdural, epidural), post-op lumbar spine complications, spinal anesthesia Presentation: Urinary retention, urinary or fecal incontinence Saddle anesthesia, weakness in lower extremities, sciatica, sexual dysfcn ↓ or absent lower extremity reflexes Management: MRI may be helpful in Dx Urgent surgery after Dx → decompression of S1-3 nerve roots to prevent permanent paralysis and incontinence Table of Contents  BACK PAIN (2) SPINAL STENOSIS Usually due to degenerative changes causing narrowing of lumbar or cervical spinal canal causing nerve root compression Seen in middle age and elderly adults Presentation: Unilateral radicular pain ± neck pain and/or back, bilateral claudication Better with forward flexion of trunk/walking uphill (relieves pressure on nerves) Rare bowel/bladder involvement Px: usually no neuro signs, look for pulses Dx: XR, MRI Tx: Mild-mod: NSAIDs, wt loss, abdominal muscle strengthening Advanced: epidural CS injections Refractory: surgical laminectomy needed in 75% of Pt DISC HERNIATION Common causes: degenerative changes, trauma, neck/back strain or strain 95% in L5-S1 (most common) and L4-L5 Common in middle age + older men Presentation: sudden onset severe electricity-like LBP, usually preceded with several months aching pain; exacerbated by coughing and Valsava, associated with sciatica, paresthesia, muscle weakness, atrophy, contractions, or spasms L5-S1 (S1 distribution): absent Achilles reflex, lateral foot numbness L4/L5 (L5 distribution): extensor hallicus longus weakness Dx: straight leg raise (sensitive not specific) and contralateral straight leg raise (specific not sensitive), MRI Tx: 1st line: NSAIDs, physiotherapy, local heat, continue to exercise (no bed rest); 2nd line: epidural steroid injection or nerve block SPINAL CORD COMPRESSION Sx: pain and stiffness in neck or back, burning pain that radiates to the limbs, numbness, cramping, weakness in limbs, loss of sensation in feet, trouble with hand coordination RF: osteoporosis, cancer Dx: urgent MRI Tx: pain management (usually needing narcotics), immediate IV high dose dexamethasone, surgery, external beam radiotherapy and stereotactic body radiotherapy if SCC caused by cancer SPINAL EPIDURAL ABSCESS Sx: severe sharp back pain, localized, worse w/ physical activity/at night/with palpation, reduced back ROM, fever in 45% of Pt, ± motor weakness/sensory weakness/meningitis Dx: ESR, CRP, 2x blood culture, MRI spine; consider nuclear medicine scan or CT guided aspiration biopsy if initial investigations –’ve but suspicion is high Tx: empiric abx (vancomycin, ceftriaxone), analgesia, CT guided drainage, debridement Table of Contents  JOINT PAIN – ORTHO Disease Path & RF Hx PE Findings Diagnosis + Management OA Degradation of Progression over years XR: narrow jt space, marginal osteophytes, subchondral cartilage and Gradual, pain worse with sclerosis, cysts degeneration of activity, better with rest Tx: Tylenol, NSAIDs, wt loss (8% BW), intra-articular steroid surrounding soft DIP, PIP, 1st MCP, large injection or hyaluronic acid infections, jt replacement, tissues joints physiotherapy Morning stiffness 50 000 = Strep; Gonococcal, G – Recent infections Urethral d/c, penile ulcers, pelvic diagnostic and PMNs >50%), Culture & Gram stain, Crystals ’ve rods (young, Cervical/urethral discharge exam (presence doesn’t r/o septic arthritis) elderly, Recent STI: 50% of sexually Imaging immunocompromised) active cases due to G&C testing: Swab or urine Viral (HIV, HBV, gonococcal infection Blood culture parvovirus, Shoulder, hip, knee, ankle Tx: Sx control: NSAIDs/opioids; IV antibiotic (ceftriaxone) enterovirus) most common affected area therapeutic arthrocentesis, arthroscopic or surgical drainage Fungal, TB S. aureus RF: endocarditis, (indications: joint inaccessible to needle drainage, Abx STI, DM, CKD, cancer, OA, RA resistance, no improvement in 3-4 days; contraindication: skin immunosuppressed, N. gonorrhea RF: migratory infection over the joint prosthetic jt polyarthritis, sexually active, Complications: pustural rash osteomyelitis (30%), Kleb pneumo: alcoholics permanent jt damage, Pseudomonas: IVDU sepsis Table of Contents  PEDS ORTHO (1) LIMP Developmental Dysplasia of the Hip (DDH): Presentation: 0-18months, limb length discrepancy, ↓abduction (most sensitive after 3-6mo), asymmetric skin folds, 50% bilateral, 8F:1M Exam: Barlow (+’ve for dislocatable hip), Ortolani (+’ve for dislocated hip), Galeazzi sign (inequality in knee height with knee + hips flexed when child is supine) W/u: 6mo: XR showing dislocated femoral head, acetabular dysplasia, break in Shenton’s line, smaller femoral ossification Tx: 0-6mo: Pavlik harness, double diaper 6-18 mo & dislocated hip: closed reduction & spica cast >12mo & dislocated hip that cannot reduce closed: open reduction ± femoral osteotomy ± pelvis osteotomy, spica cast Perthes: Presentation: hip concern in kids 4-8, can present with knee-only pain, painless limp, ↓abduction & internal rotation Workup: XR showing unilateral or mixed stage bilateral epiphyseal ossification abnormalities Tx: maintain ROM, self-limiting Slipped capital femoral epiphysis (SCFE): Presentation: MC hip problem in teens Sx spectrum: mild pain → unable to walk even with crutches Obligatory hip external rotation with flexion Obesity = #1 RF In young teens consider DDx: endocrine d/o, renal disease W/u: hip XR showing slipped ice cream cone Tx: all need to avoid wt bearing, urgent surgical internal fixation with pinning of femoral head Monitor for hip avascular necrosis (common complication) Table of Contents  PEDS ORTHO (2) SCOLIOSIS Definition: abN spine curvature, 3D deformity, Cobb angle > 10˚ Types: congenital, syndromic, neuromuscular, early onset, adolescent idiopathic scoliosis Presentation: Can be aSx, obvious spine curve Exam: look for difference in shoulder height when Pt is in hip forward flexion Management: If scoliosis suspected, order 3’ standing PA/LAT XR Small: Cobb 50˚ Only bracing and surgery influence outcome: Bracing: >20-25˚ to 45˚ and still growing Surgery: >50-55˚ LIMB LENGTH DISCREPENCY Common presentation; main issue is LLD at maturity Presentation: Most proportional If 10% less at a certain age, will be same percentage at later age (ie. 10% shorter in 15 cm femur is 1.5 cm, same child at maturity with 40 cm femur it’s a 4 cm LLD) Causes include: hemihypertrophy, fibular hemimelia Half deformity present at 3yrs (girls), 4yrs (boys) Some are dynamic Growth arrest after trauma → e.g. 10yr old boy (16yrs mature) with distal femur arrest will get (6yrs growth x 9 mm/yr = 5.4cm LLD) Growth femur: 30% proximal; 70% distal (9mm/year) Growth tibia: 60% proximal (6mm/year); 40% distal Management: In general: worries about discrepancy at maturity; length and angulation in both planes clinically relevant If growing, consider using growth arrest If done growing, consider lengthening or shortening Projected Discrepancy Treatment 0-2cm Observation, shoe lift 2-5cm Epiphysiodesis 5-7cm Bone shortening vs lengthening 7-15cm Lengthening +/- Epiphysiodesis >15cm Amputation +/- Prothesis Table of Contents  PEDS ORTHO (3) INFECTION Presentation: Walking painless limp to bedridden and ++ pain Workup Inflammatory: benign picture, little systemic evidence of infection, recent illness (URTI) common Management: watch for worsening, w/u to r/o other issues, arrange close f/u Infection (septic joint): w/u suggestive but not localization, systemic Sx If jt fluid → obligated to sample If no fluid → bone scan to r/o osteomyelitis Abx therapy only after samples and Tx (if surgery) carried out W/u: best to r/o DDx of infective VS inflammatory Sensitive, not specific: physical exam, labs, XR U/S of joints, bone scans Osteomyelitis: If near joint can mimic septic arthritis (especially acetabular osteomyelitis) Pain, fever, minor guarding if at all of joints Blood cultures, radiographs, then IV Tx before getting bone scan Weird things such as salmonella common in sickle cell disease, but S. aureus still most common in this population CLUB FOOT Background Talipes equinovarus is a congenital deformity of the foot 2/1000 live births, 50% bilateral, 2M:1F Presentation: Forefoot adduction, varus of the calcaneum, talus, and midfoot Foot is not flexible Management: Serial corrective casts at birth Surgery if resistant after 3-6mo Early Tx needed SPINA BIFIDA Background Defect of neural tube closure, usually affects the lower lumbar spine, myelodysplasia 2/1000 Presentation: Mild to complete paraplegia (if Pt has a L5 spina bifida, L5 is the last functioning level → need ankle braces to ambulate) Bladder and bowel dysfcn Occulta, meningocele, myelomeningocele Table of Contents  PEDS ORTHO (4) FRACTURES Salter Harris Classification for long bone epiphyseal #: in relation to the growth plate II: MC II-IV: intra-articular requiring anatomy reduction V: diagnosed after growth arrest Presentation: Often associated of trauma Pain, bleeding, anxiety Open #: infection risk (give Ancef), biologic compromise, higher soft tissue injury) In immature bone, bone fails in compression first – buckle fractures Management: Initial: look for open wounds, NV status If closed → splint, XR, control swelling (ice, NSAIDs) If open → eliminate gross contamination, sterile dressing, splint, XR, tetanus, Keflex (or another 1st gen cephalosporin), add G- coverage for high risk wounds If displaced and healing: accept up to 20-30˚ angulation in plane of joint in young child (6mo age: open or laparoscopic orchidopexy Complications Testicular cancer (germ cell tumors): The risk of testicular cancer is not eliminated by surgery. Infertility: higher temperature of the abdominal cavity is suboptimal for spermatogenesis → oligospermia → infertility Testicular torsion Inguinal hernia Saphenous Varix: Dilated, saccular swelling of the great saphenous vein Psoas Abscess Rare; collection of pus in the iliopsoas muscle compartment caused by hematogenous of lymphatic spread of a pathogen from a distant source S aureus = most common E coli = 2nd most common Sx: antalgic gait, flank pain, fever, mass in the inguinal/iliac region w/u: CBC, urinalysis, CT abdo Tx: 3.5cm or septic Pt Table of Contents  PROSTATIC DISEASE (1) Prostate anatomy: 3 anatomical lobes in adult: 1 anterior (to urethra) lobe, 2 lateral lobes posterior to urethra and adjacent to rectum 3 clinically described zones in adult peripheral zone ~70% of volume and typical site of cancer central zone ~25% of volume and surround the ejaculatory ducts peri-urethral transitional zone ~5% of gland and surrounds the urethra, which is typical site of BPH Prostate physiology: seminal vesicles, prostate gland and bulbourethral glands all contribute to semen prostate gland secrete a thin, milky fluid, which make up 20% of semen volume prostate secretion is important for sperm viability and motility prostatic secretion contains citric acid, zinc, acid phosphatase, clotting enzyme and fibrinolysin fibrinolysin to help break clotted ejaculate, so that sperm can swim away epithelial cells of prostate gland secrete prostate-specific antigen (PSA), which liquefies semen in seminal coagulum and allow sperm to swim freely PSA is elevated in setting of prostate cancer, benign prostate hyperplasia, prostatitis, trauma from DRE / catheterization, ejaculation prostate cancer cells growth is stimulated by androgens (mainly testosterone and dihydrotestosterone (DHT) secreted by testicles) PROSTATITIS Background: Inflammation of the prostate Chronic prostatitis, aSx inflammatory prostatitis: etiology unknown Acute and chronic bacterial prostatitis: bimodal distribution in younger and older M RF: bladder outlet obstruction, immunosuppression, phimosis, intraprostatic ductal reflux, unprotected intercourse, UTI, indwelling catheter, instrumentation, congenital ureter abN, sexual abuse Organisms: Klebsiella, E. coli (most common), Enterobacter, proteus, Serratia, pseudomonas, staph, Neisseria gonorrhea, chlamydia trachomatis Presentation: Chronic prostatitis: pain lasting ≥3mo in lower abdo/penis/scrotum/lower back/ between scrotum and anus Pain after ejaculation Pain in urethra after urination, urinary frequency and urgency, weak stream Acute bacterial prostatitis: sudden onset + severe pain in groin/scrotum area, urinary freq & urgency, dysuria, urinary retention, fever, chills Chronic bacterial prostatitis: ≥3mo of Sx similar to acute bacterial prostatitis but less severe Px & W/u: DRE Investigations: Urinalysis, urine culture, urodynamic tests, cystoscopy, transrectal US PSA will be elevated Tx: Chronic prostatitis: finasteride, NSAIDs, amitriptyline, Lyrica Acute bacterial prostatitis: PO Septra or ciprofloxacin, may benefit from α blocker if BOO (terazosin), drink lots of fluid Chronic bacterial prostatitis: 6mo course of low dose abx to prevent recurrent infection, α blockers, increase fluid intake Table of Contents  PROSTATIC DISEASE (2) BENIGN PROSTATIC HYPERPLASIA Background: Pathophysiology: benign glandular and stromal hyperplasia of the transitional zone of the prostate, causing a firm hyperplastic nodule → prostatic urethral compression → bladder outlet obstruction (BOO), leading to: Detrusor overactivity (involuntary detrusor contractions during bladder filling) → irritative Sx of BPH Weakening of bladder wall → incomplete voiding → urinary stasis → predisposition to UTI, acute/chronic urinary retention, formation of bladder stones ↑ intracystic pressure while voiding → detrusor muscle hypertrophy → bladder trabeculation and pseudodiverticula formation Epidemiology: ↑age, present in 50% of M>50, and 80% M>80 S&S: Irritative Sx of LUTS: urinary frequency, urgency/urge incontinence, nocturia, occasionally dysuria Obstruction Sx of LUTS: hesitancy, straining to urinate, weak stream, prolonged terminal dribbling, sensation of incomplete voiding, acute urinary retention Other: gross hematuria DRE: symmetrically enlarged, smooth (no nodules), firm, nontender, rubbery Investigations: voiding diary (esp for storage Sx – nocturia) Urinalysis to r/o UTI PSA: > 1.5 ng/mL: suggests an enlarged prostate > 4 ng/mL: increased likelihood of prostate cancer If BOO is suspected: renal US to r/o hydronephrosis, PVR If prostate cancer suspected: transrectal US guided prostate biopsy Tx: Sx not bothering Pt: watchful waiting, non-pharmacological management Review meds: stop/↓ non-essential meds that can contribute to LUTS (opioids, TCA, antihistamines, decongestants) Diet: avoid excess fluids at night/leaving house, limit caffeine & EtOH Bladder emptying technique bladder retraining (resist urge to void), double voiding, urethral milking (squeeze base of penis to prevent prolonged terminal dribbling) Bothersome Sx: ① pharmacological, ② surgical Pharmacologic: α blockers: Tamsulosin, Doxazosin, Alfuzosin, Terazosin MOA: inhibits α 1 receptors in bladder neck and prostatic urethra → smooth muscle relaxation – 1st line in BOO Tx outcome: Sx control 5-α-reductase inhibitor: finasteride, dutasteride; 2nd line to α blockers MOA: inhibition of 5-α-reductase → ↓T to DHT conversion → ↓pr