PREGNANCY 1st and 2nd Trimesters

PREGNANCY 1st and 2nd Trimesters
Presentation lecture from: Orangecoastcollege

* General
o Sonography used after 4-5 weeks
o Events prior to this time:
1. Ovulation
2. Fertilization
3. Implantation
4. Placentation
5. Embryonic Development

OVULATION
A. Definition: a cyclic event controlled by two hormones (FSH and LH) that occurs monthly

1. ~ 20 ova begin maturing
2. Only one completes the maturation process
Phase??
3. After ovulation, ovum moves into uterine tube
4. If fertilized, the zygote begins to divide
5. Implantation begins in ~6 days

FERTILIZATION
A. Definition: penetration of the ovum by one spermatozooan

1. Hyaluronidase (from acrosome):enzyme that allows penetration
2. Lack of acrosome/enzyme: infertility
3. Polyspermy: More than one sperm penetrates ovum

B. Sperm and ovum are haploid (N)
C. Genetic material in nuclei fuses to form zygote (2N)
D. Zygote begins cell division (mitosis!) immediately
E. Differentiation: prior to reaching uterus, zygote has developed into morula
+ Cells continue to divide, form blastula or blastocyst
# trophoblast
# inner cell mass or blastoderm
G. Trophoblast will give rise to placenta
H. Inner cell mass will give rise to the embryo
1. Ectoderm (outer layer or “outer skin”)
2. Endoderm (inner layer or “inner skin”)
3. Mesoderm (middle layer or “middle skin”)


Primary Germ Layers

Implantation
The Uterus
Perimetrium
Myometrium
Endometrium
Placenta & Fetal Membranes
Placental formation
Chorion Frondosum
Formation of Umbilical Vessels
Fetal membranes
Umbilical Cord
Anomalies
Meckel’s Diverticulum
May indicate fetal demise, premature rupture of membranes
Omphalocele
Ectopic Pregnancy
Metastatic Carcinomas
Spread via lymph circulation
Rectouterine Pouch (of Douglas) or cul-de-sac
Hydrocephaly
Hydrocephalus
Anencephaly:
Porencephaly
Doppler U/S of the Circle of Willis in utero
Circle of Willis
Fetal circle of Willis: 3D U/S
Ultrasound-guided Prenatal Diagnosis
Amniocentesis and CVS
Pelvic masses
Uterine Anomalies
Uterus bicornis
Uterus didelphys
Uterus unicornis

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High Risk Pregnancy

High Risk Pregnancy
Presentation By:Susan Sienkiewicz

Adolescent Pregnancy: Contributing Factors
Implications of Adolescent Pregnancy
Socioeconomic:
* reliance on welfare
* cycle repeats itself

Maternal health:
* CPD
* PIH
* anemia
* nut deficits
* mortality

Fetal Health:
* LBW
* prematurity
* resp complications
* cp
* cognitive deficits
* death

Adolescent Pregnancy: Assessment
* Risks
* fundal height
* # of sexual partners
* knowledge of infant care/needs
* family unit/support system
* baseline VS/weight

IMPLICATIONS OF DELAYED PREGNANCY
* Pre-existing conditions
* Preterm labor SGA/LBW
* IUGR
* PIH Abruption
* C-section
* Uterine fibroids PP hemorrhage
* Chromosomal abnormalities


DELAYED PREGNANCY: ASSESSMENT
* Pre-existing conditions
* Fundal height
* Anxiety
* Psychosocial issues

TYPES OF SPONTANEOUS ABORTIONS
Spontaneous Abortion Management
Threatened
Inevitable
Incomplete
Missed
Post Abortion Education
SITES OF ECTOPIC PREGNANCY
S & S Ectopic Pregnancy
Surgical Management of Ectopic Pregnancy
Med Mgmt of Ectopic PG
MTX
S & S Hydatiform Mole
Therap. Mgmt: vacuum aspiration & curettage
Spontaneous Abortion Matching – Choose all that apply.
Medical Mgmt of Placenta Previa
Mom stable,fetus immature
Fetus > 36 wks
S&S Abruptio Placentae
Med Mgmt of Placental Abruption
Placental Bleeding
Thromboplastin release
Clot formation (systemic response)
clotting factors (fibrinogen, plts, PTT, FDP)
inability to form clots
profuse bleeding
Hemorrhagic Conditions: Abruption & DIC
ASSESSMENT
The Pathological Processes of Pre-eclampsia
S&S Pre-eclampsia
Treatment of Pre-eclampsia
Mild: diastolic
Severe: diastolic
S&S Eclampsia/HELLP Syndrome
* Eclampsia
* HELLP Syndrome
Treatment of Eclampsia/HELLP Syndrome
* Bedrest
* Meds
* Delivery
Assessment: Hypertensive Disorders of Pregnancy
Risk Control Strategies for Hypertensive Disorders of Pregnancy
Incompetent Cervix
Treatment
Premature Labor/Rupture of Membranes
Nursing Care for PTL/PROM
Postterm Pregnancy
Disorders of Amniotic Fluid
Risks of Multifetal Gestation
(Fetal) S&S Rh Incompatibility
Sequence of Assessments for Rh Sensitization
Blood Test for Type & Rh Factor
Management of Rh Incompatibility
Prenatal
Hyperemesis Gravidarum
Glucose Tolerance Test
Gestational Diabetes is diagnosed with FBS > 105 or with 2 of the following BS results:
Effects of Pre-Existing DM
* Maternal
* Fetal
Treatment of Pre-existing DM
Effects of Gestational Diabetes
Diabetes: Patient Education
PPCM: Manifestations
PPCM: Energy Management
PPCM: Cardiac Care
PPCM: Patient Education
Sickle Cell Disease
Systemic Lupus Erythematosis
AIDS
Treatment:
CASE STUDY

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Pelvic Masses

Pelvic Masses
Preentation by:Anna Mae Smith, MPAS, PA-C
Lock Haven University

Central Pelvic Masses
* Pregnancy
* Leiomyomata - uterine fibroids
* Endometrial malignancy or uterine sarcoma
* Ovarian or other laterally located masses may present centrally
* Bladder

Leiomyomas
* benign smooth muscle tumors of the uterus
* commonly called “fibroids”
* estrogen dependent
* rarely occur before menarche or after menopause
* grow larger during pregnancy
* rarely malignant
* most common indication for pelvic surgery in women

Leiomyomas in Pregnancy
* interfere with fetal growth and nutrition
* increase the risk of
o spontaneous abortion during the first and second trimesters
o preterm labor

Epidemiology of Leiomyomas
* develop from smooth muscle cells by means of metaplasia
* cause for growth is unknown
* occurs in 20% of women of reproductive age
o most often occurs among African American women
o nulliparous women
o women older than 35
o nonsmokers
o oral contraceptive or IUD users


Classification of Leiomyomas
* submucous - protrude into the uterine cavity
* intramural - within the myometrial wall
* subserous - growing toward the serous surface of the uterus
* intraligamentous - located in the cervix or in between the folds of the broad ligament

Leiomyomas: Symptoms
* usually asymptomatic
* symptoms increase as tumors grow
* common symptoms
o pelvic pressure
o bloating
o pelvic congestion
o feeling of “heaviness”
o urinary frequency
o dysmenorrhea
o dyspareunia
o menorrhagia
o pain - less common
* may report infertility
* pregnant women complain more of pain

Leiomyomas: Physical Exam
* absence of ascites
* normal bowel sounds
* enlarged uterus that is firm and irregular but not tender
* may be mistaken for adnexal mass if situated laterally
* if mass moves with the uterus, likely to be a leiomyoma

Leiomyomas: Diagnostic Tests
* CBC to determine if anemic
* UA to r/o urinary tract infection
* Pregnancy test
* Hemoccult
* Ultrasound
* Barium enema
* IVP
* Endometrial biopsy

Leiomyomas: Differential Diagnoses
* ovarian neoplasm
* tubo-ovarian inflammatory mass
* diverticular inflammatory mass
* pregnancy
* ectopic pregnancy
* adenomyosis
* pelvic kidney
* malignancy

Leiomyomas: Treatment
Leiomyomas: Conservative Surgery
* myomectomy
* Leiomyomas: Hysterectomy
* GI Tract

Lateral Pelvic Masses
* Ovary
* Normal premenopausal ovary - 3x2x1.5cms
* Early Menopausal ovary - 2x1.5x0.5cms
* Postmenopausal ovary - 1.5x0.75x0.5cms
* GI causes
* Pelvic kidney
* PID with tubo-ovarian abscess
* Ectopic pregnancy

Ectopic Pregnancy
* Potentially life-threatening condition in which the embryo implants outside the uterine endometrial cavity.
* Leading cause of pregnancy-related death during the first trimester
* Must be considered in all sexually active women of reproductive age who have abdominal pain or abnormal vaginal bleeding

Risk Factors for Ectopic
* current IUD use
* previous tubal surgery
* history of pelvic inflammatory disease
* history of infertility
* In-utero DES exposure
* H/o STD’s
* Smoking
* Progesterone only contraception
* Use of fertility drugs

Classic Triad of Symptoms
* Amenorrhea
* Irregular vaginal bleeding
* Pelvic pain

Physical Findings of Ectopic Pregnancy
* Prior to rupture may feel nothing…usually some form of abnormal bleeding present
* Ruptured:
o Hypovolemic/orthostatic hypotension
o Peritoneal signs
o Positive CMT & adnexal tenderness
o Bulging cul-de-sac of Douglas

Ectopic Testing
Fallopian Tube
Dermoid Cyst/Teratoma
Ovary
Laparoscopy

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Acute Abdomen in Pregnancy

Acute Abdomen in Pregnancy
Presentation by:Kate Pettit, MS III

DDx of Abdominal Pain in Pregnancy
* Divided into three categories:
1) Conditions incidental to pregnancy
2) Conditions associated with pregnancy
3) Conditions due to pregnancy

Conditions Incidental to Pregnancy

* Acute appendicitis
* Acute pancreatitis
* Peptic ulcer
* Gastroenteritis
* Hepatitis
* Bowel obstruction
* Bowel Perforation
* Herniation
* Meckel’s Diverticulitis
* Toxic megacolon
* Pancreatic pseudocyst
* Ovarian cyst rupture
* Adnexal torsion
* Ureteral calculus
* Rupture of renal pelvis
* Ureteral obstruction
* SMA syndrome
* Thrombosis/infarction
* Ruptured visceral artery aneurysm
* Pneumonia
* Pulmonary embolus
* Intraperitoneal hemorrhage
* Splenic rupture
* Abdominal trauma
* Acute intermittent porphyria
* Diabetic ketoacidosis
* Sickle Cell Disease

Conditions Associated with Pregnancy
* Acute pyelonephritis
* Acute cystitis
* Acute cholecystitis
* Acute fatty liver of pregnancy
* Rupture of rectus abdominus muscle
* Torsion of pregnant uterus

Conditions Due to Pregnancy
* Ectopic pregnancy
* Septic abortion with peritonitis
* Acute urinary retention due to retroverted uterus
* Round ligament pain
* Torsion of pedunculated myoma
* Placental abruption
* Placenta percreta
* HELLP Syndrome
* Acute Fatty Liver of Pregnancy
* Uterine rupture
* Chorioamionitis

Ectopic Pregnancy
* Classic Symptoms
o Abdominal pain
o Amennorrhea
o Vaginal Bleeding
* Diagnosis
o Transvaginal U/S (TVS)
o Serum quantitative HCG
* Management
o Option of medical vs surgical management if pt is hemodynamically stable and no rupture has occurred.
o Emergent surgical management if rupture has occurred and/or patient is hemodynamically unstable
* Prognosis
o Ruptured ectopic pregnancies account for 4- 10 percent of all pregnancy related deaths.

HELLP Syndrome
Hemolysis – Elevated Liver Enzymes – Low Platelets
Acute Fatty Liver of Pregnancy
Definition of Acute Abdomen
* Stedman's Medical Dictionary, 27th Edition defines acute abdomen as "any serious acute intra-abdominal condition attended by pain, tenderness, and muscular rigidity, and for which emergency surgery must be considered.”
Epidemiology
# 1 Acute Appendicitis
# 2 Acute Cholecystitis

Challenges of Diagnosis
* Symptoms
* Physical Exam
* Labs

Which conditions require urgent surgical management in pregnancy?
* Trauma
* Acute appendicitis
* Intestinal obstruction
* Perforated duodenal ulcer
* Spontaneous visceral rupture
* Ectopic pregnancy
* Ovarian or uterine torsion

Timing of Surgery
* 1st trimester (wks 1-12)
o 12% SAb rate
* 2nd trimester (wks 13-26)
o 0 - 5.6% SAb rate
o 5% rate of preterm labor
* 3rd trimester (wks 27-40)
o 30-40% rate of preterm labor

Imaging Options

* U/S: No known adverse effects.
* X-ray: Presence of adverse effects depends on total radiation dose.
* CT: Presence of adverse effects depends on total radiation dose.
* MRI: No known adverse effects.
* ERCP: Only recommended for therapeutic use, not for routine imaging.

Radiation during pregnancy
Use of ERCP in Pregnancy
American Society for Gastrointestinal Endoscopy Guidelines

* ERCP should only be used when therapeutic intervention is intended (usually for biliary pancreatitis, choledocholithiasis, or cholangitis).
* Several studies have confirmed the safety of ERCP in pregnancy.
* With precautions, fetal exposure is well below the 5- to 10-rad level.
o Kahaleh et al. reported an estimated fetal radiation exposure of 40 mrads (range 1-180 mrad).
* Precautions for reducing radiation exposure:
o Lead shields placed under the pelvis an

Reducing Radiation in Pregnancy
* X-ray: PA exposures lowers the radiation dose by 2 to 4 mrad compared with the traditional AP exposures because the uterus is located in an anterior pelvic position.
* CT: Narrow collimation and wide pitch (the patient moves through the scanner at a faster rate) results in a slightly reduced image quality, but provides a large reduction in radiation exposure.

Sequelae of Radiation in Pregnancy
* May cause failure of implantation, malformation, growth retardation, CNS abnormalities, or fetal loss.
* Exposure <10 rads (100 mGy) does not  the risk of fetal death, malformation, or developmental delay.*
* Highest risk of radiation damage during embryonic period of organogenesis (weeks 3-9).

*International Commission on Radiological Protection.
Childhood Leukemia and Radiation
Use of contrast in pregnancy
MRI as an imaging modality
American College of Radiology Paper on MRI Safety
MRI should only be used in pregnancy when:
o The information requested from the study cannot be obtained from nonionizing means.
o The information is needed to care for the pt and fetus during pregnancy.
o The ordering MD does not feel it is prudent to delay diagnosis until after pregnancy.

MRI in Pregnancy
* No studies have shown adverse effects on the fetus or the outcome of the pregnancy.
* However, arbitrarily MRI is NOT usually performed in the 1st trimester 2/2 to this being the period of organogenesis.
* When MRI is used, informed consent must include the possibility that a previously undiagnosed fetal abnormality may be found.

Appendicitis
Signs and Symptoms
* RLQ pain: Most reliable sx
* Anorexia and vomiting: Not sensitive nor specific.
* Direct RLQ tenderness: ~100%
* Rebound tenderness: 55-75% of pts
* Abdominal muscle rigidity: 50-65% of pts
* Psoas sign: Observed less frequently.
* All findings are less common in 3rd trimester due to laxity of abdominal wall muscles.

Adler Sign
Appendiceal Location
Laboratory Evaluation
1st Line Imaging for Appendicitis
2nd Line Imaging for Appendicitis
MRI
Risks for Mother and Fetus
Recommendations for Diffuse Peritonitis
Acute Cholecystitis
Pathophysiology:
Hormones and biliary disease
Epidemiology
Presentation and Diagnosis
Initial Management of Cholecystitis
* IV hydration
* Bowel rest
* Pain control
* Antibiotics
* Fetal monitoring
* Nasogastric decompression if necessary

Surgical Management of Cholecystitis
* Cholecystectomy is now recommended as the primary treatment for cholecystitis because of:
o Recurrence rate during pregnancy of 44-92%, depending on date of 1st presentation
o Reduced use of medications
o Shorter hospital stay and fewer hospitalizations
o Elimination of risk of subsequent gallstone pancreatitis
o Minimizing development of potentially life-threatening complications such as perforation, sepsis, and peritonitis

Other Indications for Cholecystectomy During pregnancy
* Choledocolithiasis (after ERCP)
* Gallstone Pancreatitis
* Recurrent symptomatic cholelithiasis

Laparotomy vs Laparoscopy?
Choosing Surgical Technique
Laparotomy
* Currently considered 1st line approach.
* Always preferred approach when diffuse peritonitis is present, as it is associated with a lower complication rate than laparoscopy in this setting.
Laparoscopy
* First offered in 1991 for pregnant patients for appendectomy and cholecystectomy.
* Many new studies show this technique to be safe in pregnancy for routine appendicitis, especially during the 2nd trimester.
Recommendations to improve safety of laparoscopy during pregnancy
* Obstetrical consultation should be obtained preoperatively.
* When possible, operative intervention should be deferred until 2nd trimester.
* Procedure should be performed with pt in supine, left lateral decubitus position and degree of reverse Trendelenburg should be minimized.
* Open Hasson technique should be used to prevent puncture of uterus.
* Pneumoperitoneum pressures should be minimized to 8-12 mm Hg with maximum 15 mm Hg.
* Administration of tocolytic agents and perioperative monitoring of fetal heart tones should be considered.
* Pneumatic compression devices should always be used as both pneumoperitoneum and the condition of pregnancy are a risk for venous stasis.

Optimizing Delivery
Use of Tocolytics for Preterm Labor
Types of Tocolytics I
Types of Tocolytics II
Use of corticosteroids to improve fetal outcomes in premature delivery
Steroids and peritonitis?
References

Acute Abdomen in Pregnancy.ppt

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Early pregnancy abnormalities

Early pregnancy abnormalities
Presentation lecture by:Angela F. Hawk

Goals of the talk:
* Differential diagnosis/work up for first trimester bleeding
* Different types of first trimester pregnancy loss
* Ectopic pregnancies: diagnosis and management
* Miscellaneous other oddities of the first trimester

First trimester bleeding
* Occurs in 20-40% women
* Etiology often unknown, goal = exclusion
* Prognosis: association b/w FTB and adverse outcome (SAB, PTD, PPROM, IUGR)
o Worse prognosis with heavier bleeding or extending into second trimester
o PTD frequency with no, light, or heavy FTB was 6, 9.1, and 13.8% respectively
o Spontaneous loss frequency prior to 24 WG was 0.4, 1.0, and 2.0 % respectively
o Vaginal bleeding in >1 trimester associated with 7 fold increased in PPROM
Evaluation – part I

* History
o Extent (amt, associated signs/sx, pain)
o Past history (previous ectopic, prior SABs, medical disorders, risk factors)
* Eval part II – physical
o Vital signs
o Tissue if available (clot vs POC)
o Abdominal exam (+/- dopplers)
o Speculum exam (external and internal) – look for lacerations, warts, vaginitis, cervical polyps, fibroids, ectropion, cervicitis, neoplastic process
o Bimanual exam – assess adnexal/cervical tenderness, adnexal masses, uterine enlargement

Ultrasound
* Cornerstone of evaluation
* Most useful with positive preg test where IUP not previously seen
* Uses: location of pregnancy (intra- or extrauterine), viability (+/- FCA), other rare findings (GTD, partial loss of multiple gestation)

Laboratory evaluation
* HCG levels – useful only with serial measurements
* No role in monitoring once viable IUP has been verified by ultrasonography
* Less useful: progesterone, estrogen, inhibin A, Papp-A)
* Always get type and screen and give rhogam if applicable

Differential diagnosis
* Abortion (threatened, inevitable, complete, incomplete, missed)
* Ectopic pregnancy
* Vanishing twin
* Trauma, wounds, vaginitis, vaginal/cervical neoplasia, warts, polyps, fibroids, ectropion
* Physiologic/implantation (diagnosis of exclusion)

Miscarriage

* SAB = most COMMON complication of early pregnancy
* 8-20% of clinically recognized pregnancies under 20 wks undergo SAB, 80% of these will be <12 wks
* Low risk of loss after 15 wks (0.6%) if fetus chromosomally normal
* Loss of unrecognized/subclinical pregnancies occurs in 13-26% of all pregs
o Unlikely to be recognized without daily UPTs

Early loss – the data
Types of miscarriage
* Threatened: closed cervix, uterus appropriately sized, FCA present if gestational age sufficiently advanced
* Inevitable: cervix dilated, increased bleeding with cramps/ctx, POC can be at os
* Complete/incomplete
* Missed: in utero death of embryo prior to 20th wk with retention of pregnancy for prolonged period of time. Cervix closed, +/- bleeding
* Septic abortion: rare with SABs, foreign bodies ie IUDs, invasive procedures, legal EABs; common complication of illegal EABs.

Ultrasound and SABs
* Definitive diagnosis of SAB when:
o Absence of FCA with CRL >5mm
o Absence of fetal pole when mean sac diameter >25 mm (TAUS) or >18 mm (TVUS)
o Absence of yolk sac 32 days post IVF
* Promising findings for lack of SAB
o Yolk sac b/w 22-32 days from IVF associated with +FCA in 94% pregs
o Positive FCA…. But age matters! Women <36 +FCA associated with SAB in only 4.5% pregs. 36-39 y/o SAB rate 10%, women >40 y/o SAB rate 29%.

You might worry when…
* YS abnormal (irregular, LGA, free floating)
* Slow fetal heart rate (ie HR <85 bmp at 6-8 wks associated with 0% survival)
* Small sac (MSS-CRL <5 mm)
* Subchorionic hematoma (ie double SAB rate with women with large -- >25% of gest sac volume -- subchorionic hematomas in study of first trimester bleeders)
* Management
* Threatened: expectant
* Complete: ideally nothing, but difficult to distinguish clinically/ radiologically so consider D&C
* Septic: stabilize pt, obtain blood and endometrial cultures, broad spectrum Abx (gent + clinda +/- amp), D&C
* 3 options for incomplete, inevitable, and missed ABs
* Surgical: D&C – use this if bleeding heavy, suction curettage is best. Data on Abx (doxycycline) post SABs limited. Has shown 42% decrease in infection with EABs
* Medical: Miso (some studies show expulsion in 71% by day 3, 84% by day 8)
* Expectant: use if stable vital signs, no evidence of infection. Can be used for up to one month

Ectopic pregnancy
* 3 classic symptoms: abdominal pain (99%), amenorrhea (74%), vaginal bleeding (56%)
* Occur with both ruptured and unruptured cases
* Clinical manifestations often appear 6-8 wks after LMP but can appear later
* Often see above symptoms with breast tenderness, frequency urination, and nausea
* Shoulder pain (blood irritating diaphragm), urge to defecate (blood pooling in cul-de-sac) can also be seen with ruptured ectopic pregnancies
* 50% women asymptomatic before rupture with no identifiable risk factors

Differential diagnosis abdominal pain (a very limited list)
* UTIs
* Nephrolithiasis
* Diverticulitis
* Appendicitis
* Ovarian neoplasms
* Endometriosis
* Endometritis
* PID
* IBS
* Fibroids
* Gastroenteritis
* Interstitial cystitis
* Pregnancy miscellaneous!

Risk factors - high
Risk factors – moderate
Risk factors - low

Initial evaluation
Ectopic preg: ultrasound pics
hCG monitoring
Discriminatory zone
Management – above the DZ
Management: below DZ
Uncommon ectopic cases
Cervical pregnancy
Natural history
Management
Gestational trophoblastic disease
Epidemiology
Clinical manifestations
* Vaginal bleeding
* Enlarged uterus
* Pelvic pressure/pain
* Theca lutein cysts
* Anemia
* Hyperemesis gravidarum
* Hyperthyroidism
* Preeclampsia prior to 20 wks gestation
* Vaginal passage of hydropic vesicles
Complete moles
Partial moles
Management
References

Early pregnancy abnormalities.ppt

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Management of Pancreatic Cystic Lesions

Evaluation and Management of Pancreatic Cystic Lesions with Endoscopic Ultrasound and Fine Needle Aspiration.
Presentation by:Praveen Sateesh, M.D., M.H.S.A.
Georgetown Internal Medicine,

Differential Diagnosis of Pancreatic Cystic Lesion.
* Congenital cysts
* Acquired cysts
* Extrapancreatic cysts
* Cystic Pancreatic Tumors
* Serous Cystadenoma
* Mucinous Cystic Neoplasm
* Intraductal Papillary Mucinous Neoplasm

Role of EUS
* Identify architecture of cystic lesion
* Ease of FNA
* Determine type of CPT and malignant potential
* Examination of pancreatic ducts and parenchyma
* Guide surgery

Cystic Fluid Analysis
* Cytology
* Tumor markers
* Amylase

EUS FNA characteristics of certain pancreatic cystic lesions
Retrospective Study
* Preoperative diagnosis of pancreatic cystic lesions remains difficult and no established guidelines for evaluation and management of these lesions.
* Identify cases of cystic pancreatic lesions identified by CT or MR undergone EUS FNA with fluid sent for amylase, CEA, and cytology
* Evaluate performance of EUS findings and FNA findings (cytology, amylase, CEA) as compared to surgical pathology and/or clinical follow up (final diagnosis)
* Number of cases
* Differentiating cysts based on size, location, and EUS characteristics
* Obtaining data including amylase, CEA, cytology, surgical pathology, and 6 month clinical follow up after EUS FNA.

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CT Imaging of Acute Pancreatitis

CT Imaging of Acute Pancreatitis
Presentation by:Erin Rikard

Outline
* Definition
* Epidemiology
* Causal Factors
* Pathophysiology
* CT Evaluation and Findings – Normal and abnormal
* Complications
* Management
* Prognosis

Definition
Acute Pancreatitis - Inflammation of pancreas with potential for complete healing
Epidemiology
Causal Factors
Incidence
Cholelithiasis
Trauma/Surgery
Metabolic Disorders
Viral Infection
Pathophysiology
* Pancreatic autodigestion, with activated pancreatic enzymes escaping the ductal system and lysing tissue of pancreas and adjacent structures
* Lack of capsule facilitates spread
Normal CT Findings
Normal Anatomy by CT
* Pancreas arcing anteriorly over spine
* Head adjacent to duodenum
* Tail extending toward spleen
* Splenic vein posterior to body and tail
* Portal vein confluence immediately posterior & left of pancreatic neck

Normal Morphology by CT
Evaluation by CT
Evaluation of Acute Pancreatitis
* Contrast-enhanced CT is imaging modality of choice
* Oral and IV contrast differentiate pancreatic tissue from adjacent blood vessels and duodenum
Recommendations for Contrast-Enhanced CT
* Clinical diagnosis in doubt
* Severe clinical pancreatitis
* Ranson score > 3
* APACHE score > 8
* Failure to rapidly improve within 72 hours of beginning conservative medical therapy
* Initial improvement with later deterioration

Ranson Criteria
Abnormal CT Findings
* Peripancreatic inflammation
* Diffuse or focal pancreatic edema
* Poor definition and heterogeneity of gland
* Fluid collections
* Necrosis
* Thickening of pararenal fascia

Spectrum of Disease
* Mild Cases
* Severe Cases
Peripancreatic Inflammation/ Pancreatic Edema/Fluid Collections
Infection?
Necrosis
Complications
* Pancreatic Pseudocysts
* Abscess
* Hemorrhagic Pancreatitis
* Splenic Artery Pseudoaneurysm formation or rupture/ Splenic Venous Thrombosis

Pancreatic Pseudocyst
* Fluid collection surrounded by fibrous capsule but not lined by epithelium
* Occurs in 10% of cases
* Significant % will not resolve spontaneously
* Seen within pancreas and potential spaces with which gland is continuous (lesser sac and left pararenal space)
Abscess
Hemorrhagic Pancreatitis
Splenic Artery Pseudoaneurysm
Management
Prognosis
Reasons for Reduced Mortality
Resources

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Recurrent Idiopathic Pancreatitis

Recurrent Idiopathic Pancreatitis
Presentation lecture by:Rebecca Byers, MD
Primary Care Conference

Objectives
* Review the common clinical presentation of chronic pancreatitis.
* Describe the natural course of chronic pancreatitis.
* Discuss the various types of cystic lesions in the pancreas.
* Describe the diagnostic and treatment recommendations
* Disclaimer - I have not received any outside funding in regards to this presentation.

Clinical Cases
Hospitalization
* Stopped Lasix, Lisinopril, Cozaar.
* Renal arteriogram – normal.
* Echo – normal.
* +H. pylori – treated with 2 weeks Biaxin, Flagyl, Prevacid.
* Discharged on Amlodipine and Atenolol.
* BPs never high since.

GI Clinic Follow-up
* Diagnosis of Recurrent Idiopathic Pancreatitis and a mature pancreatic pseudocyst.
* Need to assess for structural abnormality
* Plan for repeat CT in 6 weeks and ERCP and/or endoscopic ultrasound.
* 8/4/03 – Abd CT without change. 4 non-specific pulm nodules, 6-7 mm. Endless f/u.

Surgical Consult
* Diagnosis of acute relapsing pancreatitis.
* Recommendation for resective drainage operation and definitive treatment.

ERPC

* Impression: (1)Recurrent pancreatitis (2) Improved pancreatogram with diffuse pancreatic ductal irregularities less prominent on this exam (3) No definite pancreatic duct stricture(s) visualized (4) s/p 5 mm pancreatic sphincterotomy with prompt drainage of contrast.

Endoscopic Ultrasound
* Impression: 1) Pancreatic tail solid-cystic lesion 2) FNA consistent with a mucinous neoplasm.
* FNA Report - Cytologic Exam: Positive, compatible with a mucinous neoplasm.


Surgery
* Surg Path Report – Predominantly intracystic mucinous adenocarcinoma, with focal infiltrating adenocarcinoma, in a background of chronic pancreatitis.
* Surgical margins were negative for carcinoma.
* Ten out of ten resected lymph nodes were negative for carcinoma. Adrenal gland and spleen also negative for carcinoma.

Surgical Follow-up

* Dilemma – If there was no invasive cancer, her treatment would now be complete; the finding of invasive cancer, along with some previously elevated tumor makers and pulmonary nodules, are concerning.
* Plan – redo all scans and serum markers, discuss at hepatobiliary conference, refer to medical oncologists.

Chronic Pancreatitis
* Chronic pancreatitis is an inflammatory condition that results in permanent structural changes in the pancreas which lead to impairment of exocrine and endocrine function.
* Can be asymptomatic over long periods of time, or can present as recurrent postprandial epigastric pain.

Clinical Features
* The two primary clinical manifestations are abdominal pain and pancreatic insufficiency.
* Pain is typically epigastric, often radiates to the back, often worse 15 to 30 minutes after eating, as the condition progresses, the pain tends to become more continuous.
* Problems digesting food/absorption, fat malabsorption, glucose intolerance/diabetes.
Etiology 1
Etiology 2
Pathogenesis
Diagnosis 1
Diagnosis 2
Complications
* Pseudocysts (10% of patients)
* Mechanical obstruction of the duodenum and common bile duct
* Pancreatic ascites
* Pleural effusion
* Splenic vein thrombosis with portal hypertension
* Pseudoaneurysm formation (e.g., splenic artery)

Cystic Lesions of the Pancreas
* Retention cysts
* Pseudocysts
* Cystic neoplasms.

Pseudocysts

* Result of pancreatic inflammation and necrosis.
* Single or multiple, small or large, located either in or outside of the pancreas.
* Most communicate with pancreatic ductal system, high concentrations of enzymes.
* Walls formed by adjacent structures; fibrous lining; lack an epithelial lining seen in true cystic lesions.

Cystic Neoplasms
* Mucinous cystadenoma/cystadenocarcinoma
* Mucinous duct ectasia (intraductal papillary mucinous neopplasm)
* Serous cystadenoma
* Papillary cystic neoplasm

Mucinous cystadenoma
* Most common cystic neoplasm.
* Typically in middle-aged women.
* Usually a mass lesion composed of one or more macrocystic spaces lined by mucous-secreting cells.
* Most are malignant at time of diagnosis. High potential for malignant change.

Management
Uncertain Etiology
References

Recurrent Idiopathic Pancreatitis.ppt

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Pancreatitis

Pancreatitis
Presentation lecture by:Brad Brough, DO

Acute pancreatitis
* Pathophys- insult leads to leakage of pancreatic enzymes into pancreatic and peripancreatic tissue leading to acute inflammatory reaction
* Etiologies
o Idiopathic
o Gallstones (or other obstructive lesions)
o EtOH
o Trauma
o Steroids
o Mumps (& other viruses: CMV, EBV)
o Autoimmune (SLE, polyarteritis nodosa)
o Scorpion sting
o Hyper Ca, TG
o ERCP (5-10% of pts undergoing procedure)
o Drugs (thiazides, sulfonamides, ACE-I, NSAIDS, azathioprine)

“Less Common” causes
* Pancreas divisum
* Chinese liver fluke
* Ischemia (bypass surgery)
* Cystic fibrosis

Trivia
Signs & Symptoms
* Grey Turner sign
* Cullen’s sign
Differential
* Not all inclusive, but may include:
o Biliary disease
o Intestinal obstruction
o Mesenteric Ischemia
o MI (inferior)
o AAA
o Distal aortic dissection
o PUD
Evaluation

* amylase…Nonspecific
* lipase
* Other inflammatory markers will be elevated
* Depending on severity may see:

Radiographic Evaluation

* AXR - “sentinel loop” or small bowel ileus
* US or CT may show enlarged pancreas with stranding, abscess, fluid collections, hemorrhage, necrosis or pseudocyst
* MRI/MRCP newest “fad”
o Decreased nephrotoxicity from gadolinium
o Better visualization of fluid collections
o MRCP allows visualization of bile ducts for stones
# Does not allow stone extraction or stent insertion
* Endoscopic US (even newer but used less)
o Useful in obese patients

CT Scan of acute pancreatitis
Gall stone pancreatitis by ERCP
Prognosis
Ranson Criteria
CT Severity Index
* CT Grade
* Necrosis score)
* TOTAL SCORE
Therapy
Complications
Prognosis
Chronic pancreatitis
* Pathophys - irreversible parenchymal destruction leading to pancreatic dysfunction
* Persistent, recurrent episodes of severe pain
* Anorexia, nausea
* Constipation, flatulence
* Steatorrhea
* Diabetes

Evaluation
CT - chronic pancreatitis
Complications
Conclusion
References

Pancreatitis.ppt

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Neurology & NeuroSurgery Grand Rounds 2005 videos

Neurology & NeuroSurgery Grand Rounds videos - 2005
from University of Arizona

December 16, 2005 NEUROLOGY	Benefits & Risks of Immunomodulation in Multiple Sclerosis Therapy Olaf Stüve, MD Assistant Professor Department of Neurology, University of Texas, Southwest Medical Center at Dallas Disclosure: Nothing to disclose.
December 9, 2005 NEUROLOGY	GRAND ROUNDS NOT AVAILABLE AT REQUEST OF PRESENTER Amir Akhter , MD, Assistant Professor, Clinical Neurology, VA Hospital
December 2, 2005 NEUROSURGERY	Management of Malignant Skull Base Tumors Involving the Carotid Artery Iman Feiz-Erfan, MD Neurosurgery Resident, Barrow Neurological Institute, St Joseph's Hospital and Medical Center Phoenix, Az Disclosure: Nothing to disclose.
October 21, 2005 NEUROLOGY	Lysosomal Storage Disorders Tim Miller, M.D. Neurosurgery Resident UA College of Medicine, Dept. of Neurosurgery Disclosure: Presenter is a consultant for Genzyone.
October 14, 2005 NEUROLOGY	Neurotube 2005 A. Lee Dellon, MD, Professor of Plastic Surgery and Neurosurgery, John Hopkins University Baltimore, Maryland, The University of Arizona Disclosure: Presenter has relationship with commercial products or devices included in discussion.
October 7, 2005 NEUROSURGERY	Surgical Treatment of the Peripheral Entrapment Neuropathy of the Lower Extremities: 158 consecutive surgical cases Juan Valdivia-Valdivia, M.D. Neurosurgery Resident UA College of Medicine, Dept. of Neurosurgery Disclosure: Nothing to disclose.
September 30, 2005 NEUROLOGY	Drug-Induced Movement Disorders Holly Shill, M.D. Director, Muhammad Ali Parkinson Research Center, Barrow Neurological Institute Disclosure: Presentation will include discussion of unlabeled/investigational drug use.
September 23, 2005 NEUROLOGY	Telemedicine and it's use in Acute Stroke: The Stroke DOC Clinical Trial Brett Meyer, M.D. Assistant Professor, Neurology; USCD Stroke Center San Diego, CA Disclosure: Nothing to disclose.
September 16, 2005 NEUROLOGY	Neurologic Treatment of Status Epilepticus Yu-Tze Ng, MD, FRACP; UA Asst. Professor, Clinical Pediatrics & Neurology; Pediatric Neurologist/Epileptologist, Division of Child Neurology, Children's Health Center, Barrow Neurologic Institute Disclosure: Presenter in on the speakers bureau for Novartis, GSK, Ortho-McNeil, and Cyberonics
September 9, 2005 NEUROLOGY	Tourette Syndrome: An Integrative Approach SLIDES Evan S. Trost, MD; Troon Family and Preventative Care, PLLC Disclosure: Nothing to disclose.
September 2, 2005 NEUROSURGERY	Stereotactic Radiotherapy of Central Nervous System and Head and Neck Lesions using a Conformal Intensity Modulated Radiotherapy System: The PEACOCK System Mario Ammirati, MD Adjunct Professor, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA Disclosure: Nothing to disclose.
August 26, 2005 NEUROLOGY	The Search for Neuroprotection in Parkinson's Disease Richard B. Dewey, Jr., MD Associate of Professor of Neurology, Department of Neurology The University of Texas Southwestern Medical Center at Dallas Disclosure: Nothing to disclose.
August 19, 2005 NEUROLOGY	Physicians, Stress and Optimal Performance: How to Perform Optimally in Today's Healthcare Environment Larry G. Oñate, M.D. House Staff Counselor,The University of Arizona College of Medicine, Chair, UMC Physician Well-being Committee Disclosure: Nothing to disclose.
August 12, 2005 NEUROLOGY	Health Consequences of Sleep Disordered Breathing Stuart F. Quan, M.D. Professor, Medicine, Anesthesiology, Public Health; Director, Sleep Disorders Center, The University of Arizona Disclosure: Nothing to disclose.
August 5, 2005 NEUROSURGERY	Lower Extremity Nerve Pathology Jerome K. Steck, D.P.M UA Clinical Assist. Professor, Surgery Institute for Plastic Surgery and Peripheral Nerve Surgery, Foot & Ankle Institute of Arizona. Disclosure: Nothing to disclose.
July 29, 2005 NEUROLOGY	Epilepsy and Depression David M. Labiner, M.D. Professor of Neurology, Pharmacy Practice & Science. Disclosure: Nothing to disclose.
July 22, 2005 NEUROLOGY	Temporolimbic Epilepsy and Behavior SLIDES Geoffrey L. Ahern, M.D., PhD Professor of Neurology, Psychology, and Psychiatry. Director, Behavioral Neuroscience & Alzheimer's Clinic, The University of Arizona Health Sciences Center Disclosure: Nothing to disclose.
July 15, 2005 NEUROLOGY	The Hospitalists in Neurology SLIDES Marc Malkoff, M.D. Director Neurocritical and Neurovascular Service, Barrow Neurological Institute Disclosure: Nothing to disclose.
July 8, 2005 NEUROSURGERY	Safety and Effectiveness of Cortical Stimulation in Patients with Hemiparetic Stroke, The Baker Study Martin E. Weinand, M.D. Disclosure: Nothing to disclose.
July 1, 2005 NEUROLOGY	Systemic Thrombolysis for Stroke Andrei V. Alexandrov , M.D. Assoc. Professor, Director, Cerebrovascular Ultrasound, Dept. of Neurology, University of Texas, Houston Disclosure: Presenter recieves grant/research support. Presenter is a consultant for IMARX and is on the speakers' bureau for Genentech.
June 24, 2005 NEUROLOGY	Neuronal Migration Disorders Dinesh Talwar , M.D. Pediatric Neurology Associates Disclosure: Nothing to disclose.
June 17, 2005 NEUROLOGY	Does Prolonged Status Epilepticus Produce a Model of Temporal Lobe Epilepsy with Hippocampal Sclerosis? Hemant Kudrimoti, M.D., Ph.D. Assistant Professor, Department of Neurology, The University of Arizona Disclosure: Nothing to disclose.
June 10, 2005 NEUROLOGY	Disturbing Sleep: Dreams, Violence and REM Behavior Disorder Pedram Navab, D.O. Neurology Resident, The University of Arizona Disclosure: Nothing to disclose.
June 3, 2005 NEUROSURGERY	Not available due to privacy concerns
May 27, 2005 NEUROLOGY	Technical Advances in the Treatment of Brain Tumors Baldassarre 'Dino' Stea, M.D., Ph.D. Disclosure: Nothing to disclose
May 20, 2005 NEUROLOGY	Cortico-Hippocampal Interactions and Memory Consolidation: Insights From Neural Ensemble Recording and Immediate-Early Gene Activation Studies Bruce L. McNaughton Ph.D. Disclosure: Nothing to disclose
May 13, 2005 NEUROLOGY	Cancelled
May 6, 2005 NEUROSURGERY	Hyperglycemia During Acute Cerebral Infarction: Does it Matter?/New Concept in the Neurovascular Unit Askiel Bruno, M.D./ Gregory del Zoppo, M.D.
April 29, 2005 NEUROLOGY	A Deadly Cross-Talk Between Mitochondria and Nuclei in Neuronal Apoptosis & Neurogeneration Seong-Woon Yu, Ph.D. Disclosure: Nothing to disclose
April 22, 2005 NEUROLOGY	Dr. Alzheimer Goes Molecular: Recent Developments in Diagnosis and Treatment Earl Zimmerman, M.D. Disclsoure: Presenter recieves grant/research support from Pfizer, General Electric. He is on the speakers bureau for Pfizer, Forest Labs and Novartis
April 8, 2005 NEUROLOGY	The Physiology of Emotion: A Non-Human Primitive Model Katalin Gothard, M.D. Disclosure: Nothing to disclose
April 1, 2005 NEUROSURGERY	Dynamic Cerebral Blood Flow Phillip Carter, M.D. Disclosure: Presenter has relationship with commercial products or devices included in discussion.
March 18, 2005 NEUROLOGY	Automatic Tracking of Body Movement, Gait & Gestures Jay Nunamaker, M.D. Disclosure: Nothing to disclose.
March 4, 2005 NEUROSURGERY	Advances in Endovascular Neurosurgery Eric Eskioglu, M.D. Disclosure: Presentation includes discussion of unlabeled or investigational drug use.
February 25, 2005 NEUROLOGY	Genetic Disorders and Epilepsy David King-Stephans, M.D. Disclosure: Presenter is on the speakers bureau for UCB Pharma, Novartis , and GlaxoSmithKline
February 11, 2005 NEUROLOGY	Recent Advances in Vestibular Testing Terry D. Fife, M.D. Disclosure: Presenter has a financial interest, arrangement or affiliation with GlaxoSmithKline.
February 4, 2005 NEUROSURGERY	Localizing and False Localizing Signs in Neurosurgery Patients Charles W. Needham, M.D. Disclosure: Nothing to disclose
January 21, 2005 NEUROLOGY	Treatment of Ischemic Stroke Adhan Qureshi, M.D. Disclosure: Presenter has a financial interest, arrangement or affiliation with corporate organizations.
December 3, 2004 NEUROSURGERY	Arachnoid Cysts: To Treat or Not to Treat and How to Treat When Treating David H. Shafron, M.D. Disclosure: Nothing to disclose.

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Tourette Syndrome

Tourette Syndrome
Presentation by:Samuel H. Zinner, M.D.

Overview
Take Home Points:
* TS is not rare
* Tics are usually mild, not catastrophic
* In most people with TS, tics are one of many related complications
* Address main problems, often not tics

Who cares about Tourette syndrome?
* TS is:
o common
o under-diagnosed
o misunderstood
o ripe with opportunity for management (and mismanagement)& research

Tic Disorders: Characteristics
* Tic Definition
o motor or phonic
o involuntary (unvoluntary?)
o sudden and rapid
o recurrent
o non-rhythmic and stereotyped

Tourette’s Disorder
* DSM-IV-TRTM Criteria
o Multiple motor + 1 or more vocal
o Many times/day & at least 1 year
o Onset before 18 years
o Not due to substance or medical condition

Epidemiology
Etiology
Differential Diagnosis of tics
* Compulsions
* Habits
* Stereotypies
* Allergies
* Sydenham chorea
* Various involuntary neuromuscular
Genetics
Genetics barriers to identifying genes
* Diagnosis based on behaviors
* Defining the TS phenotypic spectrum
o “endophenotypes”
* Family pedigree problems
* Environmental influences
* Combinations of genes may be involved
* Symptoms decrease with age
* Transient tics

Differential Diagnosis of tics
* Sydenham’s chorea
* Compulsions
* Blepharospasm
* Other hyperkinetic disorders
* Stereotypies
* Allergies

Diagnostic Pitfalls 101
Diagnostic Pitfalls 102
Assessment: co-morbid conditions
Clinical Course
Quality of Life?
Management
Identification
Identification – comorbid conditions
KEY POINT!
Always assess for non-tic comorbidity
Identification – comorbid conditions
TRICHOTILLOMANIA: moth-eaten appearance to hair and scalp excoriations
Clinical Course
A common sense guide to complementary/alternative medicine
Integrative Medicine websites

National Center for Complementary and Alternative Medicine
http://nccam.nih.gov
Consortium of Academic Health Centers for Integrative Medicine
www.imconsortium.org
Management: Advocacy and Legal Rights
Pharmacotherapy for Comorbid Conditions
KEY POINT!
Target the most troubling symptoms
Pharmacotherapy
KEY POINTS!
Take Home Points: Clarifying Common Misconceptions

Tourette Syndrome.ppt

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Human Anatomy and Physiology ppt lectures

Human Anatomy and Physiology
Presentation lectures by:R. Adam Franssen, PhD
Roane State Community College

• Muscle Tissue Lectures week 1
• Muscle Tissue Lectures weeks 2 and 3
• Blood Lectures weeks 4 and 5
• Heart Lectures weeks 5 and 6
• Blood Vessels week 7
• Lymphatic System weeks 9 and 10
• Respiratory System weeks 11 and 12
• Digestive System weeks 12 and 13
• Urinary System week 14

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Spasmodic Dysphonia

Spasmodic Dysphonia (SD)
Presentation by:Robin Bohot

Voice Disorders
Definition

* a central nervous system voice disorder caused by involuntary movements of one or more muscles of the larynx
* tight, strained or strangled voice quality

Causes of SD
* Damage to the Basal Ganglia
* Lack of any structural abnormality in the larynx
* Damage to the RLN?

Types of SD
* Adductor Spasmodic Dysphonia
* Mixed Spasmodic Dysphonia
* Variants-
http://www.youtube.com/watch?v=3m21wKQJwcU

Co-Occurring Disorders
* Blepharospasm (excessive eye blinking and involuntary forced eye closure)
* Tardive dyskinesia (involuntary and repetitious movement of muscles of the face, body, arms and legs)
* Oromandibular dystonia (involuntary movements of the jaw muscles, lips and tongue)
* Torticollis (involuntary movements of the neck muscles)
* Tremor (rhythmic, quivering muscle movements)

Treatments
Sources
* National Institute of Deafness and Other Communication Disorders
* http://www.dysphonia.org/
* http://www.asha.org/public/speech/disorders/SpasmodicDysphonia.htm

Spasmodic Dysphonia.ppt

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Management of Pediatric Neck masses

Evaluation and Management of Pediatric Neck masses
Presentation by:Steven T. Wright, M.D.
Ronald Deskin, M.D.

Pediatric Neck Masses
* Congenital masses
* Benign lesions
* Vascular and lymphatic malformations
* Infectious and inflammatory conditions
* Malignant lesions

Embryology and Anatomy
* Branchial System- 6 pairs of pharyngeal arches separated by endodermally lined pouches and ectodermally lined clefts.
* Each arch consists of a nerve, artery, and cartilaginous structures.
* The remaining neck musculature gains contributions from cervical somites.

Branchial system
* First Branchial arch
* Second Branchial Arch
* Third Branchial Arch

Branchial system
* Third Branchial Pouch
* Fourth and Sixth Branchial arches fuse to form the laryngeal cartilages.
* Fourth Arch
* Fourth Pouch- superior parathyroid glands and parafollicular thyroid cells
* Sixth Branchial Arch
* Epipericardial ridge
* Cervical Sinus of His

Thyroid Gland
First Branchial Cleft Cysts
* Type I
* Type II
Second Branchial Cleft Cysts
Fourth Branchial Cleft Cysts
Thyroglossal Duct Cyst
Cervical Thymic Cysts
Dermoid and Teratoid Cysts
Dermoid Cysts
Teratoid Cysts and Teratomas
Laryngoceles
Laryngoceles
Vascular Lesions
Lymphangiomas
Plunging Ranula
Sternomastoid Tumor of Infancy (Pseudotumor)
Infectious and Inflammatory Lesions
Bacterial Cervical Adenitis
Deep Space Neck Abscess
Tuberculous Mycobacteria
Nontuberculous Mycobacteria
Cat Scratch Disease
Viral Adenitis
Infectious Mononucleosis
Kawasaki Syndrome

Pediatric Neck masses.ppt

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Otitis Media

Otitis Media
Presentation by:Rick Newton, MD

Definition:inflammation of the middle ear

Why the Worry?
* Ear Pain
* Possible Complications
o Hearing Loss (esp. conductive)
+ Leading to speech, language, and cognitive abilities
o Ruptured TM
o Mastoiditis
o Meningitis
o Labyrinthitis
o Brain Abcess
o Lemierre’s Syndrome - anaerobic suppurative thrombophlebitis involving the internal jugular vein

Epidemiology
Risk Factors
Pathogenesis
* Typically follows URI or Allergy
* Congestion obstructs eustachian tube @ isthmus.
* Middle ear secretions accumulate
* Normal flora or new infections in upper respiratory tract to middle ear.

Bacteriology
3 bacteria remain most common isolates even in post-PCV7 & HIB vaccine era
Strep. pneumoniae
Haemophilus Influenzae
Moraxella catarrhalis


Symptoms/Signs
Otalgia
Otorrhea
Non-specific

o Fever
o Irritability
o HA
o Apathy
o Anorexia
o Vomiting
o diarrhea

Syndromes: Otitis-Conjunctivitis

* Symptom complex of otitis media and purulent conjunctivitis
* Classically nontypable H. influenzae (54% of all cases)
* inflammation of the TM in which bullae are present on the tympanic membrane
* occurs in ~ 5 percent of cases of AOM in children younger than 2 years
* Characterized by increased pain

Syndromes: Bullous Myringitis
Virology
* RSV
* Rhinoviruses
* Influenza

Other Microbes
* Mycoplasma pneumonniae
* Chlamydia trachomatis
* Tuberculous
* Ascaris lumbricoides
* Blastomyces dermatitidis
* Candida
* Aspergillus

Diagnosis

* Two diagnostic criteria for AOM
o Inflammation
o Fluid in middle ear
* Otoscopy
o TM erythematous, bulging, and immobile
* Techniques to Confirm Dx
o Pneumatic Otoscopy
o Culture

AAP Consensus Dx Criteria:
Nature of the Illness
Antibiotics & Otitis Media
The Controversy
Treatment Options
When to Consider Tympanostomy Tubes or Chemoprophylaxis
Tympanostomy Tubes
Complications of Tympanostomy Tubes
To Swim or Not to Swim
Management of Patients with Tympanostomy Tubes
* Otorrhea
* Tube Extrusion
* Cholesteatoma
* Persistent TM Perforation
* Tympanosclerosis

Otitis Media.ppt

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Cervical Rib Resection Procedure

Cervical Rib Resection Procedure
Presentation by:April Carter RN,MSN,CNOR
NorthWest Florida State College

Objectives

* Assess the related terminology and pathophysiology of the lungs.
* Analyze the diagnostic interventions for a patient undergoing a cervical rib resection
* Plan the intraoperative course for a patient undergoing
* Assemble supplies, equipment, and instrumentation needed for the procedure.
* Choose the appropriate patient position
* Identify the incision used for the procedure
* Analyze the procedural steps for cervical rib resection.
* Describe the care of the specimen

Terms and Definitions
* Thoracic outlet: formed by the first ribs, spine, and sternum
Definition/Purpose of Procedure

* Decompression of the thoracic outlet through partial or entire removal of the rib
* Surgical Goal: release compression of the neurovascular tissue and restore neurovascular function to the affected upper extremity, neck, or shoulder

Pathophysiology
* Thoracic Outlet Syndrome
o Compression of the subclavian vessels and the brachial plexus at the apex of the thorax.
o Other names: cervical rib syndrome, first thoracic rib syndrome, costoclavicular syndrome, hyperabduction syndrome
o Classifications
+ Arterial thoracic (result compression of subclavian artery and results in severe ischemia of arm)
+ Neurological
+ Venous thoracic

Surgical Intervention:
Special Considerations
Surgical Intervention: Positioning
* Position during procedure
Surgical Intervention: Special Considerations/Incision
Surgical Intervention: Supplies
Surgical Intervention: Instruments
Thoracic Instrumentation
Surgical Intervention: Equipment
Surgical Intervention: Procedure Steps
Surgical Intervention:
Procedure Steps
Specimen & Care
Resources
For visualization of the pleurae, lower and middle mediastinum, and pericardium, the surgeon would need a:

* Thorascope
* Mediastinoscope
* Bronchoscope
* Laryngoscope
As the STSR, with which of the following procedures would you anticipate the use of chest tubes and a water-seal drainage system?
* Lobectomy
* Scalene Node Biopsy
* Percutaneous Transluminal Coronary Angioplasty
* Cardiac Pacemaker Insertion

Which of the following retractors would be most useful in a posteriolateral Thoracotomy?
* Balfour
* O’Sullivan-O’Connor
* Davidson scapula
* Weitlaner

With which of the following procedures would you expect the greatest amount of bleeding?
* Wedge Resection of the Lung
* Decortication of the Lung
* Open Thoracotomy fro Closure of a Ruptured Bulla
* Closure of a Patent Ductus Arteriosus

The removal of a lung is referred to as a/an:
* Pneumonectomy
* Endarterectomy
* Blalock-Hanlon operation
* Cryoablation

Cervical Rib Resection is performed to relieve:
* Thoracic Inlet Syndrome
* Thoracic Outlet Syndrome
* Adult Respiratory Distress Syndrome
* pneumothorax

The procedure performed to remove a fibrous covering from the lung following empyema formation is:
* Aneurysmectomy
* Thoracostomy
* Thymectomy
* Pulmonary Decortication

When two chest tubes are placed into the pleural space, the uppermost tube is used to:
* Evacuate air/re-establish negative pressure
* Evaluate blood/re-establish positive pressure
* Evacuate serous fluid/re-establish positive pressure
* Evacuate pus/re-establish negative pressure

When a rib is removed, the remaining bone edges are trimmed with a:
* Doyen raspatory
* Bethune shear
* Lebsche knife
* Stille-Luer rongeur

When transporting a patient with a closed water-seal drainage:
* The bottle should be kept at or above the height of the patient’s chest
* The chest tube should always be clamped
* Chest tube clamps should accompany the patient at all times
* The patient should be placed in Trendelenburg position

Mediastinoscopy is usually performed with the patient in what position?
* Lateral
* Sims
* Dorsal recumbent
* prone

Removal of air or fluid from the pleural cavity via needle aspiration is:
* Thoracoscopy
* Thoracotomy
* Hemocentesis
* Thoracentesis

Cervical Rib Resection Procedure.ppt

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Infections of the Central Nervous System

Infections of the Central Nervous System
Presentation by:Charles S. Bryan, M.D.

* Pleocytosis: increased WBCs in the CSF
* Hypoglycorrhachia: low CSF glucose
* Meningitis: inflammation of meninges
* Encephalitis: inflammation of the brain
* Meningoencephalitis: both of the above
* Myelitis: inflammation of the spinal cord
* Encephalomyelitis: encephalitis + myelitis
* Parameningeal infection: localized infection “beside the meninges”, e.g. brain abscess, subdural empyema, epidural abscess,suppurative intracranial thrombophlebitis, mycotic aneurysm

The CSF formula
* Red cells (normally 0)
* WBCs (normally < 5/cmm)
* Differential (normally all mononuclear cells)
* Protein (normally 15 to 45 mg/dL)
* Glucose (normally 40 to 70 mg/dL or about 2/3 of simultaneous blood glucose)

Some pointers on the LP
* If you think of it, it’s generally best to do it!
* In chronic problems, rule out localized intracranial pathology; for acute problems, don’t delay if there are no localizing signs!
* Save an extra tube (the Golden Rule)!

Acute bacterial meningitis
* A MEDICAL EMERGENCY
* Consider in every patient with a history of URI interrupted by one of the “meningeal symptoms”: vomiting, headache, lethargy, confusion, stiff neck
* Clinical picture is often unimpressive when the patient is first seen

Triad of acute bacterial meningitis
* Fever (bacterial invasion of blood & CSF)
* Stiff neck (nuchal rigidity due to protective reflexes from inflammation of the subarachnoid space)
* Brain dysfunction (nausea/vomiting, headache, irritability/excitability; obtundation)

Kernig’ sign
Brudzinski’s sign
LP in acute bacterial meningitis
Gram’s stain of CSF in meningitis
Pathogenesis of meningitis
* Mucosal colonization
* Mucosal invasion
* Bacteremia
* Meningeal invasion
* Bacterial replication in CSF
* Host response to bacterial antigens
* Subarachnoid space inflammation

Pathogen offensive strategies in acute bacterial meningitis
* IgA protease secretion
* Ciliostasis
* Adhesive pili
* Evasion of alternative complement pathway by polysaccharide capsule

Host defensive strategies in acute bacterial meningitis
* Secretory IgA
* Ciliary activity
* Mucosal epithelium
* Complement (serum bactericidal system)
* Cerebral endothelium: Blood-brain barrier

The blood-brain barrier in meningitis
* 99% of bacteremic adults do not develop meningitis
* However, 1/3 of bacteremic infants develop meningitis suggesting immaturity of blood-brain barrier
* Barrier seems to function unidirectionally (inoculation of subarachnoid space causes bacteremia 1/3 of the time)
* Normal functions: active transport, facilitated diffusion, aqueous secretion of CSF, homeostasis
* Major sites: arachnoid membrane, choroid plexus, and endothelial cells of cerebral microvascular
* Meningitis: cytokines (especially interleukin-1) increase permeability

Cytokines in meningitis
Why is bacterial meningitis so devastating?
Complications of meningitis
Causes of bacterial meningitis by age
“The big three” of bacterial meningitis
Haemophilus influenzae meningitis
H. influenzae meningitis: current issues
Invasive meningococcal disease
Epidemiology of meningococcal disease
Meningococcal disease: indications for preventive
Pneumococcal meningitis
Neonatal meningitis due to gram-negative bacilli
Listeria monocytogenes meningitis
Epidemiology of bacterial meningitis: some associations
Aseptic meningitis: etiology of the term
Aseptic meningitis: current operational definition
Causes of viral meningitis
Pearls on viral meningitis
Other causes of aseptic meningitis syndrome
* Partially-treated bacterial meningitis
* Tuberculous or fungal meningitis
* Parameningeal infection
* Syphilis or leptospirosis
* Toxoplasmosis, amebiasis
* Sarcoidosis
* Drug reactions
The syndrome of chronic meningitis
Causes of chronic meningitis
Tuberculous meningitis
Cryptococcal meningitis
Syphilitic meningitis
Herpes simplex encephalitis
Brain abscess
Subdural empyema
Cavernous sinus thrombosis
Spinal epidural abscess

Infections of the Central Nervous System.ppt

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