Maternal

MATERNAL HEALTH
ADVANCED TRAUMA LIFE SUPPORT (ATLS) o Tissue perfusion: BP, pulse, oximetry, skin
color, temperature, capillary refill, mental
 Prevention status, urine output
o Addressing harmful behaviors, planned or o Gain vascular access, administer initial
unplanned volume (2L lactated Ringer’s)
 Goals o Responder: bleeding <20%; transient :20-
o Identify and treat threats to life, then limb, 40%, needs blood; >40%, needs blood and
then eyesight intervention to stop internal bleeding
o Prevent exacerbation of existing injuries or o Intervene to stop hidden sources of
occurrence of additional bleeding
o Return to level of function as close to pre- o Consider non-hemorrhagic sources of
injury as possible shock: tension pneumothorax, cardiac
 Principles tamponade, neurogenic shock
o Treat greatest threat to life first  Disability
o Definitive diagnosis not immediately o Brief neurologic exam: LOC, pupil
important symmetry and reaction to light, lateralizing
o Time matters (golden hour) signs
o Do no further harm o Temporize for evidence of increased ICP;
o Assess, intervene, reassess physiology elevated head of bed, mild hyperventilation
 Field triage to paCO2=35, mannitol 1 gm/kg
o Assess basic physiology  Exposure/environmental
 Systolic BP < 90 o Assess temperature
 Respiratory rate <10 or >29 o Maintain normothermia/prevent
 Glasgow Coma Scale <14 hypothermia: warm room, fluids, blankets
o Assess anatomy of injury ADJUNCTS TO PRIMARY
 Penetrating injury  Hemodynamic monitoring for BP, HR, rhythm
 Open or depressed skull fracture  Respiratory monitoring with pulse oximetry,
 Flail chest capnography, rate
 Crushed, degloved, or mangled  Arterial blood gas and lactate monitoring
extremity  CBC, electrolytes, glucose, creatinine, INR
 Paralysis  Foley placement to monitor urinary output but
o Assess mechanism of injury withhold if urethral injury
 Falls >6m adults, >3m or 2-3 times  Gastric tube placement to prevent gastric dilatation
the height in children  Assessment of intraperitoneal injury
 High-risk auto crash o Focused assessment by sonography in
o Assess special patient or system trauma
considerations o Diagnostic peritoneal lavage
 Age  Radiographs
 Anticoagulation and bleeding o AP chest, tube and line placements, and
disorders subclinical hemopneumothoraces
 Burns o Pelvis, pelvic fracture as source of hidden
 Time-sensitive extremity injury bleeding
(open fractures, vascular o Cervical spine, to assess source of
compromise) neurogenic shock
 ESRD  CT better if available
 Pregnancy >20 weeks SECONDARY SURVEY
 Initial assessment  Complete, head-to-toe physical examination to
o Primary survey  resuscitation  adjuncts identify all anatomic injuries
to primary  secondary survey  adjunct  Complete history
to secondary  ongoing post-resuscitation o Cardiac, anticoagulation, diabetic
monitoring and reevaluation  definitive medications
care  tertiary survey o Last meal eaten
PRIMARY SURVEY AND RESUSCITATION
o More detailed mechanism of injury: blunt
 Brief history: age, gender, mechanism of injury (fall, crush, motor vehicle), penetrating
 Airway with cervical spine control (gunshot, stab), environmental (burn, cold,
 Breathing with oxygenation and ventilation; chemical/radiological/biological), primary
respiratory exam pressure wave
 Circulation  Explosions combine all four and
o Stop external hemorrhage produce multi-dimensional injuries
 Head
o GCS, open skull fractures, eyes (VA< pupil o Neck: C-spine, CTA carotid and vertebral
size and reactivity, globe integrity and arteries
foreign body, extraocular muscle o CAP: blunt aortic injury, solid organ injury
movement), ears, nose (epistaxis), mouth  Interventional radiology to control arterial
 Neck hemorrhage
o Subcutaneous emphysema, cervical spine o Liver & some spleen, pelvic glutea
tenderness, paravertebral swelling EXTREMITY TRAUMA
 Chest  Reduction and splinting for bleeding and pain
o Breath sounds, hyperresonance or dullness  If pulse is lost after doing so, release and reapply
to percussion, subcutaneous emphysema traction/splint
 Abdomen  Open fractures
o Distention, tenderness o Rapid washout with Betadine solution
 Pelvis o Reduce and splint
o Bony tenderness, urethral injury o As contaminated or dirty wound, needs
(hematoma, lacerations, blood at meatus), treatment with IV antibiotics
anal tone, voluntary contraction o Operative intervention within 6 hours
 Extremities: use symmetry improves outcome
o Deformity and limb length: fracture,  Crush syndrome
dislocation o Direct muscle injury + muscle ischemia 
o Swelling: fracture, soft tissue and joint rhabdomyolysis
injury  Hypovolemia, acidemia,
o Neuromuscular function hyperkalemia, hyperphosphatemia
o Circulation: brachial, radial, femoral, and hypocalcemia, DIC
posterial tibial, dorsalis pedis o Manage with intravascular saline volume
 Back expansion to promote diuresis, goal 100
o Tenderness, deformity cc/h
o C5: shoulder abduction  Compartment syndrome
o C6: elbow flexion o Elevated pressure within osteofascial
o C7: elbow extension compartment that compromises perfusion
o C8: grip o Risks
o T1: finger spread  Tibial and forearm fractures
o T4: nipple level sensation  Crush injury
o T10: umbilical level sensation  Ischemia/reperfusion injury
o L2: hip flexion  Tight dressings or casts
 Circumferential burns
o L3,4: knee extension
o Diagnosis
o L5: big toe dorsiflexion  Pain out of proportion to injury;
o S1: ankle plantarflexion tense compartment swelling
GENERAL MANAGEMENT PRINCIPLES  Neurological and vascular
 Red flags compromise are late findings
o Hypotension o Management
o Truncal gunshot wounds  Preemptive fasciotomy for risks 1-3
o Pelvic fractures  Remove/bivalve casts
o Acidemia and hypothermia, on the way to  Escharotomy for circumferential
coagulopathy (triad of death) full-thickness burns
 Transfer to higher level/facility of care if injuries SPECIFIC TREATMENTS
exceed treatment capabilities  Cardiac tamponade:
 Clinical clearance of cervical spine o Diagnose with FAST exam with pericardial
o Awake and alert, neurologically normal, no fluid; pericardiocentesis, subxiphoid
intoxication, no distracting injuries, no neck pericardial window
pain, no midline neck tenderness, full o Relatively stable: median sternotomy
voluntary range of neck motion without o Unstable: resuscitative thoracotomy
pain  Indications for laparotomy
o When in doubt, leave collar and proceed o Blunt or penetrating abdominal trauma with
with radiological examination suspected causing hypotension
 Equivocal abdomen o Peritonitis
o Altered sensorium, distracting injuries o Evisceration
(pelvic, lower rib, lumbar spine)  requires o Free intraperitoneal air
further evaluation (FAST exam, DPL, CT o Evidence of ruptured diaphragm, GI tract,
scan) intraperitoneal bladder, and
 CT scans in stable patients, consider CT angiogram pancreaticoduodenal complex
o Head: bleeding, edema, ventricular  Contrast urography for lower urinary tract
effacement o Retrograde urethrogram for urethral
o Cystogram to define bladder injury Mechanical: intermittent pneumatic compressions,
CT or interventional diagnostic angiography graduated compression stockings, venous foot
o Penetrating zone I or III neck injuries pump
o Concern for blunt carotid or vertebral artery o Contraindications: limb ischemia due to
injury PVD, skin breakdown
o Severe fractures ORTHOPEDIC SURGERIES
o Knee dislocation (popliteal artery)  VTE risk high when undergoing major orthopedic
ONGOING ASSESSMENT surgeries such as hip and knee
 Post-resuscitation monitoring  LMWH, apixaban, and rivaroxaban preferred
o Vital signs and organ perfusion, urinary  Fondaparinux, UFH, warfarin if can’t use
output, ABG, pulse oximetry, end-tidal  Preferably 35 days from day of surgery
carbon dioxide, mentation, skin color, NON-ORTHOPEDIC
temperature, capillary refill  No DVT prophylaxis if very low-risk, mechanical if
 Assess for analgesia and comfort low risk, pharmacological with/without mechanical
o Short-acting narcotics administered IV if moderate to high-risk
o Benzodiazepines for non-hypoxic anxiety
 Repeat primary and secondary exams within 24 HYPOTHERMIA
hours as tertiary survey to prevent missed injuries
o Wrist and ankle films for falls  Core body temperature <35C/95F
o Skeletal survey in obese for subclinical ETIOLOGY
fractures  Primary (environmental exposure to cold) or
o Complete spin films in patients with one secondary (inadequate temperature regulation)
spinal fracture or calcaneal fractures  Increased heat loss: vasodilation drugs,
erythroderma (burns, psoriasis), surgery, sepsis,
multiple trauma
o Evaporation from the wound,
peripheral vasodilation
impaired sympathetic due to anesthetics,
and cold or room-temperature infusions
 Decreased heat production: endocrine
(hypopituitarism, hypoadrenalism,
hypothyroidism), severe malnutrition,
hypoglycemia, damage to posterior hypothalamic
nucleus
 Impaired thermoregulation: damage to preoptic
nucleus of hypothalamus due to CNS trauma,
strokes, toxicologic and metabolic derangements,
intracranial bleeding, PD, tumors, Wernicke, or MS
DVT PROPHYLAXIS  Other: malignancy, uremia, shock, cardiac arrest,
vascular insufficiency
 Consider DVT prophylaxis in every hospitalized PATHOPHYSIOLOGY
patient  Body loses heat through radiation (most
significant), conduction, convection
 Risk factors: elderly, immobile, history of
DVT/PE, critically ill, stroke with lower extremity  Hypothalamus maintains 36.5-37.5 by:
paralysis, advanced CHF, active cancer, acute o Conserving heat (peripheral
respiratory failure, thrombophilia, recent surgery or vasoconstriction by direct and sympathetic)
trauma, obesity, ongoing hormonal therapy o Increasing heat production (shivering
 Low-risk: young patients no risk factors increases metabolic activity and heat
o No need production)
 Moderate-risk: at least 1 risk factor  Organ effects
o Pharmacological preferred with or without o General tissue oxygen demand decreases by
mechanical prophylaxis 6% per degree below 35
 High-risk: multiple risk factors o Decreased depolarization of cardiac 
decreased CO  decreased mean arterial P
o Both pharmacological and mechanical
CLINICAL FEATURES
 LMWH preferred due to effectiveness and ease of
administration; unfractionated in low GFR  Determine core temperature with low-reading
temperature probe in bladder, rectum, or esophageal
o Contraindications: active bleeding, recent  Mild, 32-35C: confusion, amnesia, ataxia, apathy,
bleeding, high risk for bleeding, tachycardia, tachypnea, cold diuresis (fluid shifts to
coagulopathy, planned surgery in next 6-12
core from peripheral vasoconstriction, central
hours, thrombocytopenia volume receptors)
 Moderate, 28-32: worsened CNS depression,
stupor, may mimic brain death, hypoventilation,
hyporeflexia, oliguria, bradycardia, cardiac o Delirium: critical care unit for high-dose
arrhythmias IV benzodiazepines
 Severe, <28: Vfib or pulselessness, fixed pupils,  Offer treatment of alcohol use disorder
pulmonary edema, apnea, hypotension, coma
DIAGNOSIS TRAUMA-INFORMED CARE
 Mainly to assess comorbidities
 ECG: prolongation of all intervals, elevated J point PRINCIPLES
(J or Osborn wave)  1. Safety
 CXR to exclude pulmonary edema or aspiration  2. Trustworthiness and transparency
pneumonia  3. Peer support
 Complete metabolic panel, CBC, arterial blood gas  4. Collaboration and mutuality
TREATMENT  5. Empowerment, voice, and choice
 ABCDE approach; place two large (14 or 16 gauge)  6. Cultural, historical, and gender issues
peripheral IVs RE-TRAUMATIZATION
 Prevent further heat loss and begin rewarming  Touch, smell, noises
o Mild: passive external rewarming (remove  Power dynamics
wet clothes, cover blankets, warm room)  Gender of provider
o Moderate, refractory mild: active external  Loss of and lack of privacy
rewarming (warm blankets, radiant head,
forced warm air)  Look of environment
o Severe, refractory moderate: active  Specific wording or words
internal/core rewarming (IV warmed PRACTICE
crystalloid, warmed irrigation of  Culturally safe and welcoming waiting area and
peritoneum, thorax, extracorporeal blood meeting room (e.g. resources, Indigenous art)
rewarming)  Allow multiple no shows but explore barriers
 Cold-induced injuries with supportive care or  Continuous assessment of body language for stress:
surgery as needed crying, sweating, fidgeting, shaking, gripping table
CAUTIONS  Awareness of own prejudices
 Avoid rough handling and always warm trunk  Given individuals lots of options and avoid jargon
before extremities; else recirculation of cold,  Respond appropriately and apologize when needed
academic blood  Other from top to bottom:
 Cardiopulmonary resuscitation not be performed o Screening for trauma, collaboration and
until core body temperature 30-32 as may not be understanding other professionals’ roles,
responsive understanding health effects of trauma,
patient-centered communication skills
ALCOHOL WITHDRAWAL
 CIWA-Ar protocol: grades severity

o Nausea/vomiting, tremor, paroxysmal
sweats, anxiety, agitation, tactile
disturbances, auditory disturbances, visual
disturbances, headache/fullness in head,
orientation/clouding of sensorium
 Adjust pharmacotherapy according to severity
o First-line: benzodiazepines
 Short or intermediate (oxazepam,
lorazepam) in patients with slow
metabolism (elderly, liver failure)
 Longer acting (diazepam) in all
other patients
o Second-line: anticonvulsants as adjunct or
if contraindications for benzodiazepines OPEN FRACTURE CLASSIFICATION
 Supportive care  Type I: open fracture with wound less than 1 cm
long and clean
o IV fluid therapy and fluid monitoring
 Type II: open fracture with laceration greater than
o Multivitamins, folate, electrolyte repletion, 1 cm long without extensive soft tissue damage,
oral glucose, thiamine supplementation flaps, avulsions
(therapeutic dose if Wernicke, prophylactic
dose otherwise)  Type III: open segmental fracture, open fracture
with extensive soft tissue damage, or traumatic
 Manage complications amputation
o Seizures: IV benzodiazepines o A: open fractures with adequate soft tissue
o Psychotic disorder: low-dose coverage of a fractured bone despite
antipsychotics (haloperidol, risperidone) in extensive soft tissue laceration or flaps, or
combination with benzodiazepines
high-energy trauma regardless of wound
size
o B: open fractures with extensive soft tissue
injury loss with periosteal stripping and
bone exposure
o C: open fractures associated with arterial
injury requiring repair
WELL-CHILD EXAMINATION
 3-5 days after birth

 First year: 1, 2, 4, 6, 9, 12 months
PHYSICAL EXAMINATION
 Charting growth and recording of developmental
milestones
 Evaluation of resolution of primitive reflexes
SCREENING PLACENTA
 Visual development and acuity
 Physiologic red reflex evaluation; absence or  Nutrient and gas exchange between mother/fetus
leukocoria prompt further workup  Basal plate: maternal side of placenta ie in contact
 Strabismus and amblyopia screening: strabismus with uterine wall, including decidua basalis
normal in children <3 months of age  Chorionic plate: fetal side of placenta, in reference
 Hearing loss to chorion membrane
 Newborns and then 4, 5, 6, 8, 10 years DECIDUAL REACTION
 Recommended at other ages if >=1 risk factors:  Endometrium reaction at implantation  decidua
o TORCH infections, history of is altered uterine lining during pregnancy
meningitis/head trauma, recurrent or  Basalis:
persistent otitis media, NICU stay >5 days o Between embryo and uterus stratum basale
 Electric response audiometry, tympanometry, o Interacts with trophoblast and lead to
otoacoustic emissions development of placenta
 Undetected hearing loss  Capsularis:
o Can  speech, language, social delay o Surrounds embryo, faces uterine cavity
o Be mistaken for neurodevelopmental  Parietalis:
disorder, esp. communication disorders o Non-involved uterus
 Rourke baby record MEMBRANES
DEHYDRATION  Two that surround fetus in utero
 Loss of body weight, restless/irritability, less  Amnion: inner membrane
vigorous crying, sunken eyes, thirsty and drinks o Holds amniotic fluid and protects embryo
regularly, sleepy or lethargic, decreased skin turgor,  Chorion: surrounds amnion
dry mucous membranes, reduced tears and o Supports fetus and amnion
decreased urine output, rapid breathing, sunken TROPHOBLAST
anterior fontanelle, weak rapid pulse, cool or blue  Develops into placenta
extremities
BREASTFEEDING STATUS  Proliferates into two cell layers
 Track # of wet diapers and BM in 24 hour period  Outer synctiotrophoblast
 As breast milk volume increases, infan’ts urine pale o Invades endometrium with finger-like
or clear and odourless. Volume increases and wet projections villi
diapers noticeably heavier o Forms lacunae (spaces) for maternal blood
 First few stools black, tar-like meconium   Inner cytotrophoblast
greenish brown within first few days  three or o Constantly proliferating  cells migrate
more stools a day by day three  transition to loose into synctiotrophoblast
yellow stools that may or may not be seedy by day o Secretes proteolytic enzymes to aid
5 invasion of endometrium
o Delayed transition to light-colored stools or CHORIONIC VILLI
lack of stooling may be sign of ineffective  Projections of both layers chorionic villi
milk intake o Contact maternal blood for nutrient/gas
 Fetal mesoderm invades villi  grow branches of
umbilical artery/vein grow  eventually connects
to umbilical cord
o Trophoblast cells do not express many
MHC class I antigens
o Placenta secretions block immune response
PREGNANCY
DATING
 Embryonic age: dated to time of fertilization
 Gestational age: age dated to last menstrual period
PLACENTAL CIRCULATION o ~Embryonic age + 2 weeks because
 Maternal side fertilization usually ~1 day of ovulation
o Endometrial (spiral) arteries  villous o Used more in clinical practice
spaces/lacunae  endometrial vein  ~38 weeks from last ovulation, ~40 weeks from
 Fetal side onset of LMP
o Two umbilical arteries deliver HUMAN CHORIONIC GONADOTROPIN
deoxygenated  chorionic arteries   Similar structure to LH
capillaries that fill villi  single umbilical o Two glycoprotein subunits, a and B
vein o Alpha subunit same as in LH, FSH, TSH
 No direct mixing of maternal/fetal blood  Binds to LH receptors in corpus luteum 
o Oxygen and CO2 diffuse maintains corpus luteum  continues progesterone
o Facilitated transport of glucose o Prevents menstruation
o Active transport of amino acids o Maintains pregnancy for first 10 weeks at
o IgG antibodies can cross but not IgM which time placenta makes progesterone
o Some nutrients, drugs, infectious agents  Test:
(some drugs and conditions are harmful in o Antibody-based ELISA variants detect B
pregnancy but others not) subunit of HcG
UMBILICAL CORD o Serum tests:
 Connection between embryo and placenta  Most sensitive, can detect very low
 Derived completely from fetus: 1-2mIU/mL
 Yolk sac: cavity  May be positive <1 week
 Allantois: outpouching of hindgut conception
o Walls form umbilical blood vessels o Urine tests:
o Lumen occludes in development  20-50mIU/mL
o Becomes urachus: fibrous remnant  May not positive until >=2 weeks
connecting bladder to umbilicus HUMAN PLACENTAL LACTOGEN
o In adult: median umbilical ligament may  Chorionic somatomammotropin
cause adenocarcinoma of bladder  Protein hormone produced by syncytiotrophoblast
 Components: o Increasing levels as placenta grows
o Two arteries, one vein  Blocks effects of insulin
o Wharton jelly: contains o Raises blood glucose, good for baby
mucopolysaccharadies, similar to vitreous o Promotes breakdown of FAs and proteins
humor by mother for fuel
o Allantoic duct: connects fetal bladder to DIABETES IN PREGNANCY
umbilical cord  Decreased maternal response to insulin when
SINGLE UMBILICAL ARTERY pregnant  worsened DM or gestational DM
 Abnormal variant often identified on prenatal US  Screening:
 Associated with fetal anomalies o Serum glucose testing
o Aneuoploidy, congenital malformations o Glycosuria occurs in normal pregnancy
URACHUS ANOMALIES EVENTS OF PREGNANCY
 Patent urachus  Levels of estrogen and progesterone increase
o Urine discharge from umbilicus steadily
 Vesicourachal diverticulum  Source is corpus luteum in first trimester, placenta
o Diverticulum of bladder in second and third trimesters
EARLY
 Urachal cyst
 Trophoblast which become the placenta begins
o Partial obliteration  fluid-filled cavity  secreting
may become infected
IMMUNOLOGY OF PREGNANCY  Secretion of hCG by trophoblast ~8 days after
fertilization  informs corpus luteum that
 Fetus contains foreign HLA antigens compared to fertilization has occurred  continues to synthesize
mother because half of genes from father estrogen and progesterone
 Protected from maternal immunity by placenta by o Maintain endometrium for implantation
several mechanisms
o Suppress development of ovarian follicles
FIRST TRIMESTER
 hCG begin at day 8 after ovulation (~3 weeks o Uncoordinated Braxton Hicks contractions
gestation) begin ~1 month before parturition
 Levels maximal at ~gestational week 9  2. Near term, fetal HPA axis activated and fetal
SECOND AND THIRD TRIMESTERS adrenal cortex produces significant cortisol
 Progesterone: cholesterol  placenta from  3. Cortisol increases estrogen/progesterone ratio 
maternal circulation  pregnenolone  increases sensitivity of uterus to contractile stimuli
progesterone  4. Estrogen stimulates (progesterone decreases)
 Estradiol: pregnenolone as before  fetal local production of prostaglandins PGE2 and
circulation  DHEA in fetal adrenal cortex  PGF2a
hydroxylated to 16-OH DHEA-sulfate in fetal liver o 1) increase intracellular Ca of uterine
 crosses back to placenta  sulfatase enzyme smooth muscle to increase contractility
removes sulfate  aromatase converts to estradiol o 2) gap junction formation between uterine
PHYSIOLOGIC CHANGES smooth muscle cells to permit synchronous
 Plasma volume: total body volume expands contraction
o Blood fills placenta  diverted from o 3) softening, thinning (effacement), and
mom’s circulation  salt/water retention dilation of cervix in early labor
via RAAS  Oxytocin ambiguous
 Red cell mass: red cell mass expands o Uterine oxytocin receptors upregulated
o Increased maternal EPO toward end of gestation
o However, rise in volume > rise in RBCs  o Dilation of cervix stimulates oxytocin
dilutional anemia  lower HCT secretion
 Hemodynamics: CO output rises  After stage III (delivery of placenta):
o Preload increased by rise in blood volume o All hormones back to prepregnant levels
o Afterload reduced because fall in SVR except prolactin which remains high if
o Maternal HR raises slightly mother breast feeds
 SVR falls  BP falls MANAGEMENT OF EARLY CONTRACTIONS
o Placenta is 1) low resistance system placed  Before baby is thought to be ready
2) in parallel with rest of body  Terbutaline/ritodrine
o Maternal vasodilation o B-2 agonists  raise cAMP in uterine
o Removal raises BP in mother and newborn smooth muscle  relaxation and inhibition
after birth of contractions
 Coagulation: hypercoagulable state APGAR SCORE
o Probably evolved to protect against blood  Assess newborn immediately after birth
loss at delivery  10 point score at 1 and 5 minutes after birth
o Increased concentration in all vitamin K o Value of 0, 1, or 2 for five categories:
procoagulant factors, increased fibrinogen, o HR, RR, muscle tone, reflex irritability,
decreased protein S and AT activity skin colour (pink, blue)
 Fetus also obstructs venous return  DVTs  If score low, then reassessed at 5-min
common o If score remains <=3 associated with
 Pulmonary: ventilation increases mostly due to neurologic damage
increased tidal volumes; RR minimal change o Indicator of major CNS dysfunction
o More CO2 to exhale because metabolism PREGNANCY TERMINATION
occurring in baby AND hormone-related  Mifepristone
 Immune: slightly compromised o Anti-progesterone prevents implantation
o Suppressed Th1 response to accommodate and causes shedding of uterine lining
semi-allogenic “fetal-graft” AND impaired  Misoprostol
PMN leukocyte chemotaxis and adhesion o Synthetic prostaglandin E1 analog induces
o 1/3 rule for autoimmune disease: 1/3 uterine contractions
worsen, 1/3 worsen, 1/3 unchanged  Combination = abortion in >90% of women
o Contribute to more susceptible to infection  MTX used only in ectopic pregnancy since drugs
SUPINE HYPERTENSION that target uterus useless
 Later stages of pregnancy
 Large baby compresses IVC when lying flat  LABOR
decreased venous return/preload  CO decreases
 reflex tachycardia may produce symptoms Onset weeks 37-42
PARTURITION Regular uterine contractions
 Regular uterine contractions  progressive dilation Cervical changes: cervical effacement (thinning and
of cervix  descent and expulsion of fetus dilation)
 Normally 40 weeks STAGE 1
 Preterm labor <37 weeks  Uterine contractions from fundus sweep down 
HORMONES OF PARTURITION move fetal head toward cervix and progressively
 1. Once fetus reaches critical size, distention of widens (to 10cm) and thins the cervix
uterus increases contractility
Latent: 0-4cm abdominal muscles, extension and
o <20 hours in primiparas (first birth) straightening of fetal body
o <14 hours in multiparas (birth before)  3. Flexion
 Active: dilates to 10cm o Chin is brought toward chest
o <5-6 hours in primiparas, at rate of 1- (occipitofrontal diameter shifts to
1.2cm/h suboccipitobregmatic diameter)
o <4-5 hours in multiparas, at rate of 1.2- o Due to resistance from cervix, pelvic walls,
1.5cm/h or pelvic floor
 Starting from active, 3 obstetrical Ps important for  4. Internal rotation
labor to progress normally o Move occiput away from transverse axis
o Passenger: fetus o OA more common than OP
o Pelvis: bony pelvis anatomy  Crowning
o Power: power of uterine contractions  5. Extension
o Psyche: psychological support for mom o Delivery of head
 Force of uterine contractions with intrauterine o Due to resultant vector in direction of
pressure catheter, expressed in Montevideo units introitus
o 200 MVU adequate for labor progression  Force from uterus posteriorly
STAGE 2  Force from pelvic floor and pubic
 Fetus passes through birthing canal symphysis acting anteriorly
 <3 hours in primiparas o Chin drops downward to lie over maternal
 <2 hours in multiparas anus
CARDINAL MOVEMENTS  6. External rotation/restitution
 Positional changes of presenting part required to o Occiput and fetal body rotate into
navigate the pelvic canal transverse position based on original
 Fetus straightens (back loses convexity, extremities direction
brought closer to body)  ovoid becomes o If ROA then towards R ischial tuberosity
cylindrical shape  smallest possible cross-section o Brought on by same pelvic factors that
passing through pelvic canal produced internal rotation
 Movements are sequential and may overlap  7. Expulsion
 Head is floating o Delivery of anterior and posterior shoulders
 1. Engagement o Rest of body passes through quickly
o Biparietal diameter (diameter of baby’s
head) enters pelvic inlet
o Leading edge of spine is at or below station
0
o Presentation: occiput transverse or oblique
(right occiput anterior, left occiput anterior)
 Direct OP/OA does not make use
of larger transverse axis of pelvic
inlet
STAGE 3
 Delivery of placenta
 2. Descent  Contractions of uterus constrict uterine blood vessel
o During 2nd stage for nulliparas, begins with and limit postpartum bleeding
engagement for multiparas  <30 minutes in both primiparas and multiparas
o Due to pressure of amniotic fluid, direct
pressure on breech by fundus during FETAL MONITORING DURING LABOR
contractions, bearing-down of maternal  Check heart rate
 External (most women), low risk pregnancy o 20-30mm: cervicovaginal discharge sample
 Continuous: one sensor records baby’s heart rate, tested for fetal fibronectin
other how long contractions  If positive, risk of delivery in next
o Can be assuring and show problem right 7 days high  same as <20mm
away  If negative  same as >30mm
o Increase in C-sections and use of vacuum o >30mm: risk of delivery in 7 days low
or forceps during delivery even when one is  Observed 4-6 hours and
not needed (changes in heartbeat not reevaluated in two weeks
necessarily indicative of problem)  >34 weeks: 1) monitor cervical changes, fetal well-
 Intermittent: hand-held device being observed for 4-6 hours, obstetric
o Can walk around complications
 Internal (thin wire from sensor placed through o If no abnormalities  discharged and
cervix into uterus onto baby’s scalp), high risk reevaluated in two weeks
pregnancy (e.g. preeclampsia, baby has health o Otherwise delivery:
problem)  Cervical changes, fetal distress,
complications
ABNORMAL LABOR  Vaginal bleeding, decreased fetal
activity
 1) abnormal onset of labor COMPLICATIONS
 2) abnormal duration of stages of labor  Neonatal respiratory distress syndrome,
bronchopulmonary dysplasia, patent ductus
PRETERM LABOR arteriosus, retinopathy of prematurity, necrotizing
 Before 20-24 weeks gestation, delivery is abortion enterocolitis, periventricular leukomalacia,
(hasn’t developed enough to survive) neurological disorders (cerebral palsy, learning
 After 20-24 weeks before 37 weeks, preterm labor disabilities, developmental delays, ADHD), anemia
RISK FACTORS of prematurity, intraventricular hemorrhage (birth
 Lifestyle: smoking, alcohol, illicit drug use, age weight <1500g and delivery <32w, maternal
<=18;>35 chorioamnionitis, hypoxia during or after birth)
 Obstetric: prior preterm labor, multiple gestation
(i.e. twins or more), short cervical length (<25mm
on U/S before 24 weeks gestation), prior cervical
surgery
 Conditions: UTI or genital infections,
preeclampsia, HELLP syndrome, placenta praevia
(close proximity of cervix or covers altogether), POSTTERM PREGNANCIES
placental abruption (premature detachment from  Considered “late term” starting from week 41
uterine wall)  Strongest risk factor is prior postterm pregnancy
CLINICAL PRESENTATION MANAGEMENT
 Preterm ROM, regular uterine contractions and  1) Expectant management with regular fetal
associated symptoms of labor monitoring
CLINICAL DIAGNOSIS  Monitoring required because high risk of
 Based on preterm contractions and cervical changes macrosomia and intrauterine fetal death
 Cervicovaginal fetal fibronectin (fFN) detection test o 2x/week starting from week 41
o Elevated fFN levels support diagnosis o Includes U/S of fetal size and amniotic
o Primarily used in patients with symptoms to fluid level, NST, and BPP
differentiate true and false labor  NST: 20 minute recording of fetal HR using
TREATMENT cardiotocograph
 Prophylaxis: intravaginal progesterone o Fetal HR varies 110-160 bpm and at least 2
o Patients with previous preterm or short accelerations – 15bpm lasting more than 15
cervical length seconds in pregnancies beyond 32 weeks,
 <34 weeks: depends on cervical length 10bmp lasting more than 10 seconds in
o <20mm: risk of delivery in 7 days high pregnancies below 32 weeks
 Antenatal corticosteroids to help o Lower HR or fewer/shorter accelerations =
fetal lungs mature NST non-reactive = potential fetal distress
 Tocolytic medications (e.g.  BPP: NST, fetal breathing movement, fetal torso
nifedipine, NSAIDs, terbutaline) and limb movements, muscle tone, and amount of
given to suppress uterine amniotic fluid (these four on U/S)
contractions o Two points per criteria
 Antibiotics (ampicillin + o 6/10 considered good score
gentamicin) to prevent intrauterine  Options:
infection with group B strep in
vaginal flora o 1) spontaneous labor
 Magnesium sulfate to protect fetal o 2) if fetus doing well, postpone induction of
nervous system labor until 42 weeks and 6 days
o 3) If oligohydramnios or evidence of fetal  2) Controlled cord traction (hand on abdomen to
distress, then induction of labor secure uterine fundus, other gently tugs at umbilical
 Induction of labor: cord)  gently or uterine inversion
o Amniotomy: fetal head against cervix, fetal  3) Manual extraction (hand secures uterine fundus,
membranes cut through cervix other goes into uterus and separates placenta from
o Cervical ripening agent: prostaglandin or wall with side-to-side motion of fingers)
balloon catheter o Stop if abnormally adherent
o IV oxytocin if previous two not enough  Placenta accreta spectrum of conditions: burrowed
given at 1mL/hour more deeply than should be
PROLONGED LATENT PHASE o May cause life-threatening postpartum
 Risk factors: early analgesia (namely epidural), hemorrhage
abnormal fetal position (transverse lie)  Definitive treatment requires hysterectomy
 Management: therapeutic rest, morphine sedation
both IM and IV HYPERTENSIVE ORDERS OF PREGNANCY
o Later stages of labor require effort
 If false labor, contractions stop and no cervical  Systolic >140 or diastolic >90
changes  Before 20 weeks
 If true labor, cervical changes o Chronic HTN (not due to pregnancy)
 Other options: oxytocin, amniotomy if fetal  After 20 weeks, with no proteinuria or damage to
membranes haven’t ruptured other organs
o C-section should not be performed because o Gestational HTN
previous options usually effective  After 20 weeks, with proteinuria or other organ
PROLONGED ACTIVE PHASE dysfunction
 If cervix dilates <1cm over 2 hours, oxytocin o Preeclampsia
started and amniotomy if membranes haven’t  Severe: >160 and/or >110 can lead to organ
ruptured damage, proteinuria is marker
 Active phase arrest: 1) after 4 hours of adequate PREECLAMPSIA
uterine contractions; 2) after 6 hours without  Risk factors:
adequate uterine contractions and no cervical o First pregnancy, multiple gestations, 35+
changes during the active phase years
o C-section indicated and performed ½ ways: o Pre-existing HTN
o If not: compression, fetal stress hypoxia o DM, CKD, autoimmune disorders (e.g.
 cerebral palsy, anoxic brain injury APS)
 Transverse incision/bikini cut: 2-3cm above  Pathophysiology:
symphysis pubis o Normally spiral arteries dilate 5-10x size
o In planned and most urgent cases and develop into uteroplacental arteries
o Better cosmetic appearance and less o Preeclampsia  uteroplacental arteries
postoperative pain/risk of hernia undergo fibrosis  hypoperfused placenta
 Vertical incision: midline and can up to belly  release proinflammatory proteins 
button mother’s endothelial cells dysfunction 
o Emergency or transverse not adequate vasoconstriction and kidneys retain more
PROLONGED SECOND STAGE salt  HTN
 Management depends on uterine contractions and  Vasoconstriction  reduced blood
whether fetal head is engaged flow to kidneys  ischemia 
 If uterine contractions occur less than every 3 glomerular damage  proteinuria
minutes, or if significantly lower than 200 MVU   Complications:
increase oxytocin o HTN  risk of placental abruption
 If doesn’t help and fetal head is not engaged (i.e. (detaches from uterine wall)
not reached inlet of pelvic brim)  emergency C- o HELLP: hemolysis, elevated liver
section enzymes, low platelets
 If fetal head is engaged, no disproportion with o HTN  endothelial injury  tiny thrombi
pelvis  operative vaginal delivery with vacuum in vasculature  1) uses platelets so
or forceps increased risk of bleeding and 2) large
o Vacuum: ‘easy extraction’, cup on baby’s rocks in river, damages RBCs moving past,
head and suction extrinsic hemolytic anemia and 3) block
o Forceps: difficult or signs of fetal distress, blood flow to liver, elevation in liver
two arms locked around baby’s head, pull enzymes
o If unsuccessful after 15-20 minutes   RBCs split into schistocytes,
emergency C-section visible on peripheral blood smear
PROLONGED THIRD STAGE/RETAINED  Damaged liver swells, in some
PLACENTA cases capsule can rupture 
 Management: subcapsular hematoma
 1) Increase oxytocin dose  RUQ pain
 Or severe hypotension diffuse and circumferential proliferation of
o DIC large trophoblast cells
o Damage to endothelium  release TF   Cytotrophoblasts: central nuclei
triggers coagulation cascade (DIC)  and pale cytoplasm
depletes coagulation factors  Syncytiotrophoblasts: multiple
 Bleeding from mucosal surfaces, nuclei and darker cytoplasm
IV lines, incision sites o Stain for p57 protein: produced by gene
 Decreased platelets and coagulation only in maternal cells, so complete will be
factors (-)
 Schistocytes on peripheral smear  Incomplete mole  also secrete hCG but not as
 Prolonged PT and PTT high
 Elevated D-dimer from clot lysis o Missed periods and vaginal bleeding
o Endothelial injury  increased vascular o Uterus not larger than expected
permeability, in addition to loss of protein: o No 4 symptoms of hCG hyperstimulation
 Generalized edema (legs, face, o Transvaginal U/S will show fetal parts
hands) o Histologically some chorionic villi
 Pulmonary edema (cough, SOB) hydropic
 Cerebral edema (headache, o P57 staining (+)
confusion, seizure)  Treatment
 Preeclampsia + seizures = eclampsia o Uterine evacuation through suction
 Treatment: curettage and MTX
o Chronic HTN or gestational HTN o MTX is antimetabolite medication similar
 Hydralazine, methyldopa, labetalol, to folic acid that is toxic to rapidly diving
nifedipine cells of embryo
o Preeclampsia and eclampsia o Monitor hCG levels  if do not return to
 + IV Mg Sulfate to prevent or treat normal  suspect invasive mole or
seizures choriocarcinoma
 Definitive = delivery of fetus &  Course
placenta o Complete and incomplete are benign
(hytadiform) but can develop into
GESTATIONAL TROPHOBLASTIC DISEASE malignant: invasive moles and rarely
choriocarcinomas
 Moles from error in normal fertilization   Invasive mole: villi invade into myometrium
abnormal proliferation of trophoblast cells o Complete risk 15-20%
o Complete ‘classic’: chromosome empty egg o Incomplete <5%
fuses with sperm  sperm genetic material  Choriocarcinoma: most during or after non-molar
duplicates so 46 chromosomes  develops pregnancy
into mass instead of fetus o Most are small
o Incomplete ‘partial’: normal egg fuses with o Secrete hCG: hyperthyroidism and bilateral
two sperm  69 chromosomes  non- theca lutein cysts
viable fetal parts o Large  abdominal pain/pressure
 Complete mole  placenta secretes excess hCG o Extremely aggressive. Common metastasis
o Signs of pregnancy is lungs “cannonball metastases”. Also to
o Vaginal bleeding brain: headache, dizziness, nausea, slurred
o Parts of mole may be eliminated: grapes or speech, visual disturbances
cherry clusters o Histologically similar to moles BUT no
o Can lead to early preeclampsia (<20w) villi
o Hyperemesis gravidarum and potential o Treatment: MTX
severe dehydration
o hCG has subunit similar to TSH  ECTOPIC PREGNANCY
hyperthyroidism
o Theca lutein cysts  pelvic pain or  Normally fertilized egg implants in uterus but
pressure on affected side somewhere else, most common ampulla of fallopian
o Physical exam shows uterus too big for tube
gestational age  Risk factors:
o Transvaginal U/S will show no fetal parts, o PID: scarring and adhesions particularly in
but diffuse ‘snowstorm pattern’, cluster of fallopian tube
grapes o Prior ectopic pregnancy
 Abnormal placental villi and blood
clots that accumulate in uterus o Previous surgery of tubes
o Histologically chorionic villi will mostly o Endometriosis
be hydropic (swollen and edematous) AND o Advanced age
o Smoking (epithelial lining damage to  Diagnosis:
fallopian tube) o Fetal bradycardia (<110) and diminished or
 Presentation: absent fetal movement
o Signs of pregnancy (missed menstrual o U/S
period, nausea, fullness of breasts)  Treatment:
 Complications: o If hemorrhage severe or evidence of fetal
o Fear that runs out of space and ruptures compromise, emergency C-section
o Presents with sudden onset severe lower
abdominal pain occasionally light vaginal VASA PREVIA
bleeding
o If massive hemorrhage, then hemodynamic  Two umbilical arteries and umbilical vein run over
instability or hemorrhagic shock or close to cervical os
 Diagnosis:  Risk factors
o If hemodynamically unstable, immediate o Velamentous umbilical cord insertion
surgery to diagnose/treat ectopic o Normally inserts into middle of placenta.
o If stable, then serial measurements of hCG However may insert in fetal or
 If not normal (intrauterine hCG chorioamniotic membranes and then travel
levels double every 48 hours) then within membranes to placenta  not
suspect ectopic pregnancy protected by Wharton’s jelly  along with
o Transvaginal U/S detect intrauterine by vasa previa vulnerable to rupture
week 5 or 6  Presentation:
o If uterine curettage or scraping, changes in o Triad of membrane rupture, painless
endometrium due to progesterone secretion vaginal bleeding, and fetal bradycardia or
but no embryonic or trophoblastic tissue death (from hypoxia)
 Treatment: o Hemorrhagic shock and Sheehan syndrome
o Hemodynamically stable, termination with  Diagnosis:
MTX o Transvaginal U/S before rupture of
o Hemodynamically unstable, salpingostomy membranes occurs
(open, take out, close) or salpingectomy  Treatment:
o C-section
PLACENTAL ABRUPTION
PLACENTA PREVIA
 Partial or complete separation of uterine wall and
decidua basalis  Normally placenta in upper uterus but here in lower
 Risk factors uterus
o Acute blunt trauma (car crash, fall,  Complete, partial, or marginal (edge of placenta
domestic violence) because placenta less extends to within 2 cm of cervical os)
elastic than uterus  Risk factors:
o Smoking or chronic HTN results in o Upper uterus not well vascularized
degeneration of uterine arteries supplying  Endometrial damage e.g. previous
placenta C-section, abortion, uterine
o Severe preeclampsia surgery, multiparity, advanced
o Drugs (cocaine, meth) vasoconstrict maternal age, smoking
placental blood vessels and abrupt increase o Multiple placentas
in BP o Placenta with larger SA
o Multiparity  Presentation:
o Maternal age > 35 o Sudden onset painless bright bleeding that
 Presentation: typically begins in third trimester, after 20
o Usually happens in third trimester weeks gestation
o Abrupt onset abdominal pain  Intermittent or continuous
o If marginal separation, then continuous o As pregnancy progresses lower uterine
vaginal bleeding (apparent abruption) segment grows  disrupts placental blood
o If central separation, then no bleeding but vessels
pocket of blood between basalis and uterine  Complications
wall (concealed abruption) o Hemorrhagic shock (hypotension,
 Complications: tachycardia, or syncope) and Sheehan
o Hemorrhagic shock syndrome + fetal hypoxia
o Sheehan’s syndrome: perinatal pituitary  Treatment:
necrosis from hypovolemia o Severe or fetal compromise then emergency
 Agalactorrhea C-section
o DIC because releases large quantities of TF
from decidua basalis layer MORBIDLY ADHERENT PLACENTA
 Two independent measurements of
 Abnormal attachment of placenta to uterine wall >=126 mg/dL for DM and 92-125
 If decidua basalis too thin, goes deeper and attach to mg/dL for gestational DM
myometrium without penetrating (placenta o Third (24-28 weeks)
accrete)  Recommended in all pregnancies
 If penetrate but not fully (placenta increta)  50g, one-hour oral glucose
 If all the way through into uterine serosa and even challenge test. Blood glucose
neighboring organs, bladder or rectum, (placenta should <135 mg/dL
percreta)  Confirmation with 100g, 3h oral
 Risk factors: glucose challenge test if screening
o Prior C-section or uterine surgery, esp. 50g positive. Blood glucose should
when implants near scar <140 mg/dL
o Multiparity  Treatment
o Advanced maternal age o Glycemic control
 Dietary modifications and regular
 Presentation: exercise
o Difficulty delivery of the placenta (tears  Strict glucose monitoring 4x daily
from uterine wall and leaves some behind  Insulin therapy if glycemic control
 placental vessels  postpartum is insufficient with diet
hemorrhage)  Metformin and glyburide in
o 4 Ts: tone (uterine atony), trauma patients who refuse insulin therapy
(lacerations, incisions, uterine rupture), o Regular U/S to assess fetal development
thrombin (coagulopathies), and tissue o Consider inducing delivery at week 39-40 if
(morbidly adherent placenta) glycemic control poor or complications
 Complications: occur
o Hemorrhagic shock and Sheehan’s but no  Complications
fetal hypoxia because postpartum o Increased risk of maternal and fetal
o All forms of adherent placenta are morbidity
associated with placenta previa for o Maternal: gestational HTN, preeclampsia,
unknown reasons eclampsia, and HELLP, UTI
 Diagnosis:  In most cases resolves. Increased
o U/S risk of T2DM (up to 50% over 10
 Treatment: years); screen for DM 6-12 weeks
o Uterine massage and utertonic medications postpartum (75g 2h GTT) and
(oxytocin) to help uterus contract and repeat every 3 years
constrict arteries o Fetal: diabetic fetopathy
o If doesn’t work than bilateral ligation of DIABETIC FETOPATHY
internal iliac artery  Onset second and third trimester
o If doesn’t work then hysterectomy  Pathophys: chronic fetal hyperglycemia  fetal
hyperinsulinemia, islet cell hyperplasia  increased
GESTATIONAL DIABETES insulin-like growth factor and growth hormones 
increased metabolic effects and oxygen demand 
 Occurs in 5-7% of all pregnancies, usually in fetal hypoxia
second and third trimesters  Effects: macrosomia, polycythemia (increased risk
 Pathophysiology: insulin requirement varies hyperviscosity syndrome and hyperbilirubinemia),
during pregnancy neonatal hypoglycemia, electrolyte imbalances
o First trimester, insulin sensitivity increases (hypo calcemia and magnesemia), respiratory
and tendency toward hypoglycemia distress, hypertrophic cardiomyopathy
o In second and third, hormonal changes
trigger progressive insulin resistance that AMNIOTIC FLUID ABNORMALITIES
results in hyperglycemia
 Risk factors:  Volume of fluid determined by that moving in and
o Gestational DM in prior pregnancy, out of amniotic sac
recurrent pregnancy loss, at least one birth  In second half pregnancy, much of fluid from fetus’
of child diagnosed with fetal macrosomia urine with small contributions from placenta 
 Clinical features reabsorbed as fetus continuously swallows
o Mothers usually asymptomatic  Polyhydramnios
o May present with edema o Excessive amniotic fluid volume expected
o Warning signs: polylhydramnios or large- for gestational age
for-gestational age infants (>90 percentile) o Can’t swallow: mostly esophageal or
 Screening and diagnostics duodenal atresia/stenosis, rarely
o First and second (0-24 weeks) anencephaly (brain controlling swallowing)
o Increased urine production: multiple complications (early or delayed), umbilical cord
gestation, fetal anemia (increased CO), prolapse, compression, or entanglement, abnormal
maternal diabetes (fetal hyperglycemia) positioning of baby, anemia, macrosomia,
o Other: cystic lung malformations; Rh meconium in amniotic fluid, placental abruptio,
incompatibility uterine rupture
o Diagnostics: abdominal girth and uterine SIGNS
size large for gestational age; U/S (amniotic  Decreased movement of baby
fluid index >=25, assess fetal anomalies),  Cramping
Rh screen  Vaginal bleeding
o Complications: fetal malposition,  Excessive or inadequate weight gain
umbilical cord prolapse, premature birth  Abnormal FH rate or rhythm, abnormal amniotic
o Treatment: mild no treatment; U/S for fluid levels, abnormal biophysical profile, high BP,
growth and fetal assessment and deteremine failure to progress/thrive
delivery timing; reductive amniocentesis if FETAL HEART RATE
significant respiratory complaints  Procedure
associated with restricted diaphragm o During birth, monitored internally via
movement; electrode attached to fetal head (scal
 Oligohydramnios electrode monitoring) but ROM has to be
o Amniotic fluid less than expected for have occurred
gestational age o Used when external monitoring is difficult
o Inadequate urine excretion: bilateral renal (e.g. maternal obesity, polyhydramnios,
agenesis or posterior urethral valves (and multiple gestations)
other forms of urethral excretion),  Accleration
autosomal recessive polycystic kidney o Normal temporal increase from baseline by
disease >15bpm for more than 15 seconds but less
o Maternal conditions: placental insufficiency 10 minutes
(still inadequate urine production), late or  Decelearotin
postterm pregnancies (>42 weeks), o Temporary decline >15bmp for maximum
premature ROM duration of 3 minutes
o Diagnostics: U/S to determine amniotic  Characteristic changes in response to fetal hypoxia
fluid and assess fetal anomalies; AFI < 5 and metabolic acidosis
(normal range 8-18cm) o Tachycardia, 160-180/min
o Complications: intrauterine growth o Bradycardia, <110/min
restriction, birth complications (e.g. o Loss of baseline variability
umbilical cord compression) o Recurrent variable deceleartions and/or late
o Treatment: underlying cause, weekly decelartions
maximum vertical pocket measurements  Reassuring fetal status
and nonstress tests, fetal growth o Good beat to beat variability (>6bmp), >2
assessment, delivery at 37 weeks gestation accelerations within 20 minute period, no
assuming membranes intact evidence of fetal distress
o Any cause  intrauterine compression and  Management
decreased amniotic fluid ingestions  o Repositioning of mother, administer O2,
Potter sequence because fetus pressed and possibly fluids
against membrane of sac + decreased space  Fetus pushed back uterus
for fetal development  internal and
external developmental abnormalities o If unsuccessful, consider
(flattened face, widely separated eyes with  Amnioinfusion: instillation of
saline into amniotic cavity after
epicanthal folds, low-set ears, clubbed feet) artificial ROM
o Clinical features: pulmonary hypoplasia  If uterine tachysystole present (>5
(cause of death due to neonatal respiratory contractions in period of 10
insufficiency), craniofacial abnormalities minutes) reduce uterine cavity w/
(above), wrinkingling of skin, limb tocolytics
anomalies (bowed legs, clubbed feat)  Emergency C-section
 POTTER: pulmonary hypoplasia (lethal),
oligohydramnios (origin), twisted facies, twisted
skin, extremity deformations, renal agenesis (classic NEONATAL HYPOGLYCEMIA
form)
 Drop in blood glucose expeted following birth;
FETAL DISTRESS continuous supply of exogenous IV glucose from
placenta suddenly ceases; declines in first few hours
of life; asymptomatic and brief/transient
 Causes: IUGR, preeclampsia, placental abruption,  Underlying mechanisms:
uncontrolled diabetes, polyhydramnios or
oligohydramnios, pregnancy >40 weeks, labor
o Insufficient glucose supply, with low
glycogen or fat stores or poor mechanisms Inborn errors: http://www.perinatalservicesbc.ca/our-
of glucose production services/screening-programs/newborn-screening-program/
o Increased glucose utilization caused by disorders-screened
excessive insulin production or increased
metabolic demand IMMUNIZATION SCHEDULE
o Failure of counter-regulatory mechanisms
(e.g. pituitary or adrenal failure)  https://www.canada.ca/en/public-health/services/
 Groups of infants publications/healthy-living/canadian-immunization-
o IUGR or small compared to gestational gea guide-part-1-key-immunization-information/page-
o Infants of diabetic mothers or lage for 13-recommended-immunization-schedules.html
gestational age iinfants
o Late-preterm infants (34-36.6 weeks) DEVELOPMENTAL MILESTONES
 Preterm, IUGR, and small  decreased glycogen
stores, decreased apidose tissue, increased
metabolic demands because relatively large brain
size
o In V. low birth weight (<1000g), enzymes
involved in GNG expressed low levels;
produce endogenous glucose poor
 Gestational DM and large for gestational age: fetal
hyperinsulinism and increased peripheral glucose
utilization
o Facilitated diffusion in utero so fetal
glucose proportional to maternal levels 
prolonged = fetal hyperglycemia and
pancreatic overstimuilaton to increase fetal
endogenous insulin production
o Gestational diabetes decreased ability to
mobilize glycogen stores after birth and
relative adrenal insufficiency with
decreased catecholamines, further
contributing
 Infants experiencing perinatal stress (fetal distress,
perinatal ischemia, preclampsia/eclampsia, sepsis,
hypothermia) or those with congenital heart disease
 increased metabolic energy reuqirements
 Iatrogenic causes of transient neonatal
hypgolycemia = intrapatum administration of
maternal medication (beta-adrenergic tocolytics, AUTISM SPECTRUM DISORDER
valproic acid, propranolol, conduction anesthetics),
delayed feeding, and exogenous insulin  Encompasses previously separate
administration neurodevelopmental dx of autistic disorder,
 Low glucose concentrations beyond first 48 hours Asperger disorder, childhood disintegrative
of life  concern underlying disorder disorder, and pervasive developmental disorder-not
o Hyperinsulinism (congenital other specified
hyperinsulinism, Beckwith-Wiemann EPIDEMIOLOGY
syndrome, Soto syndrome)  Males:females 4:1
o Insufficient energy supply (inborn errors of ETIOLOGY
metabolim resulting in difieicinies of  Multifactorial, strong underlying genetic
glycogen, amino acids, FFAs) predisposition
o Deficiency in cortisol or growth hormone  Childhood disintegrative disorder associated with:
(Costello syndrome, hypopituitarism, o Subacute sclerosing panencephalitis
congenital adrenal hyperplasia, (chronic infection by form of measles virus)
hypothyroidism) o Tuberous sclerosis: genetic disorder
 Inborn errors of metabolism: maple syrup urine o Leukodystrophy: maldevelopment of
disease, glycogen storage disease, hereditary myelin sheath causing white matter to
fructose intolerance, galactosemia, FA oxidation disintegrate
disorders o Lipid storage disease: toxic accumulation
 Treatment: breastfeeding, infant formula, dextrose of excessive lipids in brain and NS
gel 200mg/kg massaged into buccal mucosa, IV  Associated with
glucose if < 40mg/dL or symptomatic; second-line o Neurodevelopmental and psychiatric
include corticosteroids or glucagon for persistent disorders
o Higher head circumference:brain V ratio subacute sclerosing panencephalitis, tuberous
 Higher risk of sclerosis
o Epilepsy, sleep disorders, digestive issues, TREATMENT
uncommon responses to pain, metabolism  Early behavioral and educational management
problems o Behavioral: reinforce acceptable and
PATHOPHYSIOLOGY discourage undesired with rewards
 Not clear-cut o Educational: school planning and IEP
 Different populations for different subtypes of ASD (therapies, student-to-teacher ratio, peer
o E.g. CDD in children with normal interaction opportunities)
developmental milestones o Social and communication skills, speech
CLINICAL FEATURES and language, occupational
 Symptoms evident before 2-3 years of age  Occupational: daily life skills
 Core o Family counselling (self-injury,
o Persistent impairment in communication communicate, recognize triggers, learn
and social interaction supportive routines and behaviors)
o Restricted, stereotyped patterns of behavior,  Additional supports
interests, and activities o Early childhood, entering school, becoming
 Additional adult, getting job, transitioning living alone
o Intellectual and/or language impairment o Government and community programs for
o Emotional dysregulation respite care, financial aid, parenting support
DIAGNOSIS  Medical treatment
 Comprehensive evaluation of o SSRIs: repetitive stereotyped behavior,
o Social interaction and communication skills anxiety
o Cognitive development o Antipsychotic drugs: aggression, self-injury
 Exclude reversible causes of condition o Methylphenidate: ADHD
o Hearing and vision testing  Indicators of poor prognosis
o CBC, urea and electrolytes/glucose, heavy o Severe core symptoms
metals o Cognitive impairment
o LFTs and thyroid function test o Poor or absent language skills
o HIV testing
o Urine screening for aminoaciduria CHILD MALTREATMENT: WHAT TO DO GUIDE FOR
o Neuroimaging studies and EEG PROFESSIONALS WHO WORK WITH CHILDREN
o Genetic for fragile X syndrome and
tuberous sclerosis DIAGNOSING
 DSM V criteria  Physical abuse: bruising of soft tissue, bruises at
o Deficits in social interaction and different stages of healing, burns, inadequately
communication explained bone fractures, X-ray evidence of
o Restricted interests, repetitive behavior, and multiple fractures, head injuries, retinal bleeding
activities  Emotional abuse: speech problems, developmental
o Impaired everyday functioning delay
DIFFERENTIAL DIAGNOSES  Neglect: medical needs not met, abandonment,
untidy appearance/poor hygiene, malnutrition, poor
growth
 Sexual abuse: trauma to genital or anal area,
unexplained STI or vaginal/urethral infection,
pregnancy
 Exposure to family violence: increased risk of
physical harm or injury due to proximity
 All forms beget behavioral signs: anxiety,
depression, low-self-esteem, disruptive or
aggressive behavior, hyperactivity, sleep disorders
or nightmares, loss of skills, unusual fear of
physical contact with others, lack of emotional
expression when hurt, unusual passivity or
withdrawal, sucking/rocking/biting, poor social
skills or relationships, school absenteeism, running
away
PROCESS OF REPORTING
 Legal obligation when ‘reasonable grounds to
suspect child has or is suffering from abuse’
 Heavy metal poisoning, aminoaciduria, o If made in good faith protected from any
hypothyroidism, brain tumor, organophosphate legal proceedings
exposure, HIV infection, childhood schizophrenia,
o Most penalties are from failing to report
 Consult local child maltreatment experts or make
anonymous call to local CPS
 For First Nations communities, delegated to First
Nations Child and Family Service Agencies
(FNCFSAs)
 1. Act on suspicion quickly – contact local CPS and
report situation
 2. Write down what you have been told and by
whom, your observations, what you did
 3. Try to learn as much about situation and context
and find out if currently at risk (ongoing exposure
to perpetrator), but do not interview about details.
Responsibility of CPS
o Not trained. Kid not guilty. Parents don’t
know exactly what was discussed.
 4. Immediate medical assessment/treatment of
physical problems and referral to ED
 5. Consider referral to mental health professional
for psychological or psychiatric problems MULTIDISCIPLINARY GUIDELINES ON
 6. Short-term and long-term safety plans prepared IDENTIFICATION, INVESTIGATION, MANAGEMENT
in collaboration with CPS OF SUSPECTED ABUSIVE HEAD TRAUMA 2008
 7. Afterwards, reassure child and that it was right
for them to disclose situation and allow child to Abuse head trauma (AHT) specific form of TBI
express feelings and thoughts Constellation of findings consequence of violent
o Monitor long-term physical and shaking, impact, or combination of two
psychosocial health o Intracranial hemorrhage, retinal
MANAGEMENT hemorrhage, and brain injury
OVERALL o Skull, rib, long bone fractures may also be
 Immediate safety ensured and urgent health present
concerns o Consider in any child with altered level of
 Next physical and psychosocial health and responsiveness not due to obvious cause
development assessed in detail  Forensic and psychosocial info through
 Management and referral to appropriate services – investigations important in clarifying circumstances
evidence-based treatments available to varying – physical and psychosocial environment
degrees, if not available, seek best available  Investigative process in entirety which may include
 If no signs and symptoms of maltreatment, regular court deliberation will determine whether events
assessment of health and development and monitor were abusive
child’s safety on daily basis  Legally, mandatory when suspected to report to
PREVENTION CPS so begin investigation
 Physical abuse: home visitation by nurses or o Be cautious of giving potential mechanism
paraprofessionals as may influence investigations. Say
 Sexual abuse: education about sexual abuse in ‘trauma’
primary schools  self-protection IDENTIFICATION
 Neglect: nurse home visitation  Any of the following symptoms: lethargy,
INTERVENTIONS decreased feeding, irritability, vomiting, respiratory
 Physical abuse: parent-child interaction therapy, distress, apnea, seizures, or altered LOC
resilient peer-mediated treatment, CBT, family  Full assessment esp in:
therapy o Acute or chronic injury with adequate,
 Sexual abuse: trauma-focused CBT inconsistent, evolving, or no explanation
 Neglect: Group play training, resilient peer- o Severe head injury allegedly short fall or
mediated treatment for withdrawal preschoolers; minor trauma
therapeutic day treatment; multisystemic therapy o Unexplained symptomatic head injury who
and parent training was well when last seen
o Subdural hemorrhage, retinal hemorrhage,
rib, skull, or metaphyseal fractures
 Absence of external injuries common
 Caregiver may have no knowledge of cause or may
not give accurate history
ASSESSMENT
 Complete physical exam with special attention to
nervous system and eyes (retinal findings)
 Labwork
o CBC, platelets, coagulation studies
o Additional to rule out other diagnoses: ALZHEIMER
glucose and electrolytes, metabolic screen,
toxicology, microbiology
 Early neuroimaging
o CT for acute, MRI for additional
information on presence and location
o May include intracranial bleeding and/or
cerebral edema
 Skeletal survey (series of X-rays for entire
skeleton), and another in 10-14 days
o Subtle and acute bony injuries with nuclear
medicine bone scan
REFERRALS
 Expertise in maltreatment
 Ophthalmologist, preferable with pediatric expertise
 Neurologist/radiologist preferably with pediatric
MEDICAL MANAGEMENT
 Level of care determined by severity of brain injury
o Mild: rest and observation
o Moderate (GCS 9-12): neuroprotective
measures, normoxia, normocapnia,  Chronic neurodegenerative disease
normotension, normothermia (or, in some ETIOLOGY
cases controlled hypothermia), and  Amyloid precursor protein (APP) gene
euglycemia, and ICP management to o 10-15% of early-onset familial AD
prevent secondary brain injury o Since APP gene located on chromosome
 Neurosurgery indicated 21, trisomy 21 increases risk of early-onset
 FU neuroimaging 12-24 hours or APP
before discharge o Onset usually resembles parental age (~49
o Severe: similar to moderate but tranexamic years)
acid unlikely benefit and FU neuroimaging  Apo E
6h o Late-onset increases risk with increased
 Indications for inpatient observation number of Apo E4 alleles
o Skull fracture >3 mm separation or o Apo E2 alleles may be protective
depressed, signs of raised ICP, suspected  Presenilin-1
abuse, neurological deficits o Early onset compared to AD due to
 Evaluation of siblings: eye examination, mutations of other genes (median 43 years)
neuroimaging, and skeletal survey even if initial  Presenilin-2
physical exam normal o Later onset (average 54 years)
 Communication with family and investigators RISK FACTORS
o Physician’s responsibility to ensure all  Females over males
information are made available to  Age is strongest predisposing for regular AD
authorities  Family history of dementia strongest for early-onset
 Discharge planning with CPS  African American or Hispanic descent
 Ongoing follow-up  Diabetes, obesity, dyslipidemia
 HTN, peripheral atherosclerosis, cerebrovascular dx
 Low SES and/or educational status
DIFFERENTIAL DIAGNOSIS
 Early-onset (<65) familial AD ~10% all cases
 Alzheimer’s and vascular > 90% of cases
 AD: slow and progressive, episodic impairment of
memory
 VD: stepwise deterioration due to vascular
events/infarction, sudden onset
 Dementia with Lewy bodies (protein misfolds):
visual hallucinations, features of parkinsonism
 Frontotemporal dementia: early changes in
personality, inappropriate social behavior
Altered mental  Normal pressure hydrocephalus: triad of gait
disorder, dementia, urinary incontinence
 Wernicke encephalopathy: triad of confusion,
ataxia, ophthalmoplegia
 Late neurosyphilis
PATHOPHYSIOLOGY  Symptoms
 Senile/neuritic plaques o Insidious onset (relatives)
o Extracellular in grey matter o Objectively confirmed progressive loss of
o AB protein main component function in 2 or more cognitive domains
o Enzymatic cleavage of transmembranous (usually including memory)
APP by B-secretase and y-secretase  AB  Neuropsychological testing
peptide aggregation  formation of o Cognitive testing: MMSE, MoCa, Mini-
insoluble plaques with tau protein and cog
microglia  neurotoxic effect o Functional testing: FAQ, PSMS
 Neurofibrillary tangles o Global testing: GDS
o Intracellular  Neuroimaging
o Hyperphosphorylated tau protein main o CT/MRI
component  Generalized or focal cerebral
o Hyperphosphorylation of tau  formation atrophy: enlarged ventricles,
of insoluble intracellular fibrils  narrowing of gyri, prominent
neurotoxic cerebral sulci
 Culminate in degeneration of cholinergic neurons  Disproportionate atrophy of
 role in declining cognitive abilities hippocampus and/or medial
o Hippocampus usually first  memory temporal lobe
CLINICAL FEATURES o PET
 Common symptoms of cognitive impairment  Temporoparietal hypometabolism
o Short-term memory impairment  Increased amyloid uptake signal
 Insidious onset  EEG
 Slow progression o Slower basic rhythm, long evoked potential
 Episodic memory affected first latency
o Language impairment  CSF
 Impaired naming, then o Increased phosphor-tau protein, decreased
comprehension, then fluency B-amyloid proteins AB1-42
o Temporal and spatial disorientation HISTOPATHOLOGY
(person, place, time, events)  Macroscopic
o Impairment of executive functions and o Cerebral atrophy
judgement o Damage to hippocampus and
 Less common symptoms parahippocampal cortex (medial temporal
o Primary progressive aphasia lobe) is earliest change
o Apraxia (inability coordinated, learned o Diffuse cortical atrophy as disease
movements) progresses
o Acalculia (inability mathematical tasks) o Axonal and neuronal loss
o Alexia (inability to read)  Microscopic
o Agnosia (inability to process sensory o Amyloid beta: stains with Congo red under
information  cannot identify persons, polarization
sounds, objects, etc.) o Tau protein: intracellular neurofibrillary
 Noncognitive symptoms tangles that stain with Gallyas silver
o Behavioral changes o Hirano bodies: intracellular rod-shaped
 Apathy eosinophilic aggregates of actin and actin-
 Irritability, aggression associated proteins in neurons, especially
o Mood disorders (e.g. depression) hippocampus
o Urinary incontinence TREATMENT
o Hyposmia  Cholinesterase inhibitors
DIAGNOSIS o First-line for Alzheimer and vascular
 Use neuropsychological testing (MMSE, MOCA) to o Donepezil, rivastigmine, galantamine
diagnose dementia in patients with memory loss, o Increased ACh concentration and can
cognitive, and/or functional decline improve some symptoms
 Rule out reversible causes o Adverse: nausea, dizziness, insomnia
o 1. Review medications, substance use o Contraindications: cardiac conditions
o 2. Sensory loss (presbycusis, presbyopia)  **anticholinergics, e.g. tricyclic antidepressants,
o 3. Depression (generalized depression should be avoided
scale, diagnosis with PHQ-9)  Memantine
o 4. Metabolic (TSH, Ca, vitamin B12) o Moderate to advanced cases of Alzheimer
o 5. Neuroimaging (vascular, hydrocephalus, and vascular
tumors, signs of Alzheimer) o NMDA-receptor antagonism  decreased
 AD can only be confirmed via glutamate-induced calcium-mediated
neurohistopathological examination post-mortem excitotoxicity
CLINICAL DIAGNOSIS
o Adverse: headaches and dizziness, o Endocrinopathies – hypo/hypercortisol,
confusion, hallucinations hypoglycemia
 Low number needed to harm (many side effects) o Acute vascular – hypertensive
with minimal benefit from trials = cautious encephalopathy, septic hypotension
prescription o Toxin and drugs – esp. anti-cholinergics,
 Memory training opioids, benzodiazepines
PREVENTION o Heavy metals
 Modulate risk factors
 Physically active – depression, DM, HTN,
cholesterol, obesity
 Socially active – depression, social isolation
 Cognitive stimulation – depression, low levels
formal education, social isolation
 Healthy diet – DM, high alcohol, cholesterol,
obesity, poor diet
 Conscious and safe choices – head injuries,
hearing loss, high alcohol, living near busy roads,
smoking RISK FACTORS
 Manage stress – depression, HTN  Elderly (>65 years) and hospitalized patients are
particularly susceptible
DELIRIUM  Multiple medical problems: especially constipation,
pneumonia, UTI
 A syndrome of acute confusion characterized by PATHOPHYSIOLOGY
fluctuations in awareness, cognition, and attention  Multiple neurotransmitter abnormalities, especially
ETIOLOGY cholinergic deficiency
 Metabolic encephalopathy most common cause  Generation of inflammatory markers, including
o Liver or kidney failure cytokines (IL-1b and IL-6, CRP, TFN-a)
o DM (diabetic ketoacidosis)  Reversible impairment of cerebral oxidative
o Hyper or hypothyroidism metabolism
o Vitamin deficiencies (vitamin B12, folic  Neuronal membrane may not be able to depolarize
acid, thiamine) properly and cannot transmit AP
o Electrolyte abnormalities  Stress of any kind can upregulate sympathetic and
 Infections such as UTI (most common cause in downregulate parasympathetic, impairing
elderly), pneumonia, cellulitis cholinergic function. Older people particularly
 Toxin/drug encephalopathy vulnerable to reduced cholinergic transmission
o Anticholinergics   cerebral hemispheres or arousal mechanisms of
o Benzodiazepines, barbituates thalamus and RAS become impaired
o Antihistamines CLINICAL PRESENTATION
o Opioids  Acute (hours to days) alteration in level of
awareness and attention
o Alcohol use disorder and alcohol
withdrawal  Other features
o Heavy metals (arsenic, lead, mercury) o Disorganized thinking
o Recreational drugs or withdrawal o Delusions
 Recent surgery o Illusions
 Hypoxia (anemia, cardiac failure, COPD, o Hallucinations (mostly visual)
pulmonary embolism) o Emotional lability
 Acute vascular: MI, shock, vasculitis o Agitation, combativeness
 CNS pathology (stroke, brain tumor) o Cognitive deficits (e.g. memory)
 Losing sleep can worsen symptoms  Mixed type: psychomotor activity fluctuates or
 I WATCH DEATH stays at baseline; most common in general pop.
o Infections – pneumonia, urinary, skin/soft  Hypoactive: decreased; most common type in
tissue, CNS elderly
o Withdrawal – alcohol, sedatives,  Hyperactive: increased; most commonly delirium
barbiturates due to substance use or withdrawal
o Acute metabolic changes – altered pH,  Severity of symptoms fluctuates throughout day and
hypo/hyper Na+ Ca++, acute liver or renal worsens in the evening (sundowning)
failure  Usually temporary and resolves when underlying
o Trauma – brain injury, subdural hematoma cause is addressed
DIFFERENTIATE WITH DEMENTIA
o CNS pathology – post-ictal, stroke, tumour,
brain mets  Sudden onset, rapid and fluctuating course,
disorganized thought, impaired attention, decreased
o Hypoxia – CHF, anemia LOC, reversible
o Deficiencies – thiamine, niacin, B12
o + hallucinations (often visual or tactile), o Depression screening
increased or decreased psychomotor DIFFERENTIAL DIAGNOSIS
activity, abnormal EEG findings  Hydrocephalus
 Insidious, slowly progressive course, impoverished  Hypertensive encephalopathy
thought, intact attention, intact LOC, irreversible  Chronic subdural hematoma
DIAGNOSIS WITH DSM-V  Osmotic demyelination syndrome
 Disturbance in attention (focus, maintain attention) MANAGEMENT
and awareness  Treatment of underlying condition
 Additional disturbance in cognition (memory o Discontinue or reduce causative
deficit, disorientation, language, visuospatial medications
ability, perception)  Supportive care based on clinical manifestations
 Over short period of time, change from baseline, o Fever control and pain management,
tends to fluctuate during course of day preferably with nonopioid medications
 Disturbances are not better explained by preexisting o Maintain adequate hydration and nutrition
neurocognitive disorder o Reorient patient to time, place, and person
 Evidence from history, physical exam, or lab at least three times a day
findings that disturbance is caused by medical o Initiate cognitive stimulation therapy to
condition, medication side effect, or substance improve cognitive function
intoxication or withdrawal  Prevent decubitus (pressure) ulcers, aspiration, falls
WORKUP TREATMENT OF AGITATION
 CBC  Initially manage with nonpharmacologic
o Low Hb in anemia o Family member remain with patient at all
o WBC elevated or low in infection times
 Basic metabolic panel (BMP) o Use de-escalation techniques
o Glucose for hypo or hyperglycemia  Medications reserved for severe agitation or
o Urea and creatinine, elevated in renal refractory agitation
failure and uremia o First-line antipsychotics
o Electrolytes, elevated or low K, Na, Ca  Haloperidol, D2 antagonist,
o Magnesium, elevated or low extrapyramidal effects
 Heavy metals: lead, mercury  Atypical options: olanzapine
 Liver chemistries, altered in liver failure or toxicity o Second-line: lorazepam for patients with
 Urinalysis, UTI (pyuria, bacteriuria) or renal failure alcohol or benzodiazepine withdrawal only
(casts)  **avoid antipsychotics in patients with underlying
SYMPTOM-BASED ADIDTIONAL alcohol or benzodiazepine withdrawal (risk of
 Neurological: focal neurological symptoms, seizures) and in patients at high risk for QTc
seizure, fever with headache prolongation (risk of torsades de pointes)
o Neuroimaging, CT or MRI PREVENTION
o EEG: diffuse slowing of background  Reduce exposure to risk factors
activity in patients with delirium o Avoid drugs that can worsen (benzo,
o LP and CSF analysis: infections anticholinergics, opioids)
 Pulmonary: cough or SOB o Avoid restraints
o CXR o Comfortable environment similar to home
 Cardiac: abnormal hemodynamics, chest pain,  Reorient patient regularly
worsening peripheral edema o Clock and/or calendar
o ECG o Visual and hearing aids
o Echocardiogram  At night, reduce noise and procedures
 Nutritional: malabsorption or malnutrition o Uninterrupted sleep
o Vitamin B12, folate, thiamine levels  Follow episodes and adjust medications
 Toxic: alcohol or recreational drug use, suspicion of o One of biggest problems in geriatric
CO poisoning medicine is polypharmacy
o Urine toxicology
o Serum drug levels MAJOR DEPRESSIVE DISORDER
 Infectious: fever, qSOFA criteria
o Bacterial cultures (e.g. urine or blood RISK FACTORS
culture) +/- serum lactate if sepsis  Third decade of life
suspected  Neuroticism (negative affectivity) increases risk of
o HIV, syphilis serology MDE in response to stressful life events
 Endocrine: thyroid storm, myxedema coma,  Sleep hygiene/disturbance - OSA
adrenal crisis  ADEs, especially when multiple of diverse types
o Thyroid function  First-degree family members increases risk 2-4x
o Random cortisol  All major nonmood disorders, and when this
 Psychiatric: major depressive disorder happens more likely refractory course
o Substance use, anxiety, and borderline  D. MDE not better explained by mental disorder
personality disorders more common such as schizophrenia spectrum
o Neurodegenerative diseases (Alz) and  E. There has never been a manic or hypomanic
chronic inflammatory diseases (SLE) episode
o Chronic or disabling medical conditions GRADING
PATHOPHYSIOLOGY  Self-rated: PHQ-9
 Monoamine hypothesis: associated with decreased  Clinician-rated: Hamilton depression rating scale
serotonin, NE, dopamine  Mild, moderate, severe
o Most antidepressants increase levels  With or without psychotic features
o Block re-uptake or inhibit breakdown   In partial remission or full remission
higher level in synapses  Unspecified
 Diathesis-stress: different levels of sensitivity  Recurrent = at least 2 consecutive months between
(diatheses) based on biological and psychological episodes in which criteria are not met
factors  reach critical level of stress (less needed TREATMENT
if more sensitive)  dysfunction of HPA axis  First-line: psychotherapy
o Excess cortisol released  If no remission, add pharmacotherapy
o Impaired negative feedback  CBT: recognize cognitive distortions  respond 
o Desensitization of cortisol receptors adapt
 Immune: increased activity of o Easier to administer than other types,
macrophages and release of pro- efficacy similar to antidepressants
inflammatory cytokines  Behavioral activation: behavioral target (e.g.
 CNS: disturbances in noradrenaline avoidance, inertia)
and serotonin transmission o less time-intensive than CBT
 Psychological: traumatic and stressful experiences  Interpersonal therapy: focus on at least one area:
CLINICAL PRESENTATION role transitions, interpersonal disputes, grief,
 Many bipolar illnesses begin with one or more interpersonal deficits
depressive episodes o CBT level I evidence for efficacy in
 More likely in individuals with onset of illness in maintenance phase
adolescence, with psychotic features, family history o IPT and BA have level 1 evidence for
DIAGNOSIS efficacy in acute but level 2 for maintenace
RULING OUT PHARMACOTHERAPY
 Hypothyroidism (TSH), anemia (ferritin, B12,  Start SSRI low dose  if no improvement within
folate), substance/medication (coping mechanisms), two weeks continue to increase until optimize
bipolar I or II disorder, adjustment disorder with o If no improvement, switch to agent with
depressed mood, schizophrenia superiority (escitalopram, mirtazapine,
 CBC, electrolytes, TSH, urine toxicology sertraline, venlafaxine, citalopram)
(withdrawal or crash) o If some improvement but not optimal, add
MAJOR DEPRESSIVE EPISODE another agent
 Five or more of following present during 2-week  When no prior history of depression, period of 6-9
period most of day, nearly every day, change from months followed by taper and discontinue
previous functioning TRICYCLICS
o Depressed mood, or irritable in children  Rarely used in modern times
and adolescents, by subjective account or  Block re-uptake of 5-HT and NE
observation  Problem is “broad spectrum”
o Markedly diminished interest or pleasure in o Anti-histamine: sedation, weight gain
all, or almost all, activities
o Anti-muscarinic: blurry vision,
o Significant weight loss when not dieting or constipation, dry mouth, urinary retention
weight gain, or decrease in appetite
o A-1: orthostatic hypotension
o Insomnia or hypersomnia
 Tertiary amines (3 N attachments)
o Psychomotor agitation or retardation
o Amitriptyline, clomipramine, doxepin,
o Fatigue or loss of energy imipramine, trimipramine
o Feelings or worthlessness or excessive or o More sedating (anti-histamine)
inappropriate guilt
 Secondary amines (2 N attachments)
o Diminished ability to think or concentrate,
or indecisiveness o Desipramine, nortriptyline, protriptyline
o Recurrent thoughts of death or suicide – o More activating (NE)
does not have to be every day  Overdose
o At least one must be (1) or (2) o Seizures and coma (antagonize GABA
 Clinically significant distress or impairment in receptors)
areas of functioning o Anticholinergic toxicity (hyperthermia due
 Not attributable to substance, medical condition to loss of sweating, skin flushing, dilated
pupils, ileus, urinary retention)
 A-C is criterion for MDE
o Hypotension (alpha blockade)  major o Lots of tyramine in cheese, red wine, some
cause of death meats
o Prolongation of QT interval (block cardiac SSRIs (SELECTIVE SEROTONIN)
Na channels)  torsade de points  Inhibits 5-HT reuptake by neurons
 Monitor ECG for increased QRS interval  Takes 4-8 weeks to have effects
 Treat with sodium bicarbonate  Fluoxetine, fluvoxamine, paroxetine, sertraline,
o Na overcomes Na channel blockade escitalopram, citalopram
o Raises pH, favors inactive form of tricyclic  Other disorders:
 Non-depression uses o Depression, GAD, panic disorder, OCD,
o Clomipramine for obsessive-compulsive bulimia, social anxiety disorder, PTSD
o Amitriptyline, desipramine for diabetic  Adverse effects
peripheral neuropathy o Sexual dysfunction due to increased
o Amitriptyline, doxepin, imipramine, serotonin effects in spinal cord
nortriptyline, desipramine for chronic pain  Decreased libido, anorgasmia,
o Amitriptyline for migraine headaches erectile dysfunction in males
o Imipramine, amitriptyline, desipramine for o GI upset due to increased serotonin
bed wetting (enuresis)  Nausea, abdominal pain,
 First-line is desmopressin constipation
o Doxepin is insomnia o Drowsiness, weight gain, SIADH and
MAO INHIBITORS hyponatremia (rare), QT prolongation (rare)
 Rarely used in modern times SNRIs (SEROTONIN-NOREPINEPHRINE)
o Refractory depression, anxiety, selegiline in  Inhibits 5-HT and NE reuptake by neurons
Parkinson’s  Takes 4-8 weeks to have effects
 Monoamines = benzene ring with amine group  Venlafaxine, desvenlafaxine, duloxetine,
 Inhibits monoamine oxidase  decreased levomilnacipran, milnacipran
breakdown of monoamines  Other disorders:
o MAO-A: dopamine, NE, serotonin (5-HT) o Depression, GAD, social anxiety disorder,
o MAO-B: dopamine panic disorder, PTSD, OCD
 Non-selective MAO inhibitors  Adverse effects
o Tranylcypromine, phenelzine, o Sexual dysfunction, highest rate
isocarboxazid venlafaxine
 MAO-b selective o May increase BP due to NE effects
o Selegiline o Nausea (diminishes with time)
 Serotonin syndrome: MAO inhibitor plus another OTHERS
serotonin drug  thus two-week washout  Bupropion
o SSRIs, SNRIs, TCAs o Blocks reuptake of NE and dopamine
o MDMA o Increases presynaptic release of
o Ondansetron (nausea; 5-HT3 antagonist) catecholamines
o Tramadol (weak opioid; inhibits 5-HT o Used in depression and smoking cessation
reuptake) o May improve sexual dysfunction of SSRIs
o Meperidine (opioid; inhibits 5-HT o Toxicity related to stimulant effects:
reuptake) anxiety, insomnia, seizures (rare). Don’t
o Triptans (migraines; 5-HT agonists) take at night
o Linezolid (antibiotic; weak MAO inhibitor)  Mirtazapine
o Dextromethorphan (cough suppressant; o Blocks presynaptic a-2 receptors (negative
weak SSRI) feedback with NE)  more NE and
o St. John’s wort (herbal supplement; serotonin release
increase 5-HT activity) o Blocks postsynaptic serotonin 5-HT2 and
 Classic triad 5-HT3  more 5-HT1 activity
o Mental status changes: agitation, o Also anti-histamine: sedation, dry mouth,
restlessness, disorientation increased appetite, weight gain
o Autonomic hyperactivity: diaphoresis,  Serotonin modulators
tachycardia, hyperthermia o Inhibit reuptake of serotonin but also
o Neuromuscular hyperactivity: tremor, antagonists/agonists of serotonin receptors
clonus, hyperreflexia, bilateral Babinski o Trazadone: affects 5-HT2A and 5-HT2C
 Treatment with cyproheptadine, 5-HT antagonist receptors, low dose antagonist, high dose
 Cheese effect agonist
 No longer used as antidepressant,
o Tyramine is naturally occurring monoamine main clinic use is insomnia
o Metabolized by MAO in GI tract o Vilazodone: partial agonist of postsynaptic
o Patients on MAOi  tyramine in blood  5-HT1A receptors
sympathetic activation, hypertensive crisis  Diarrhea, sexual dysfunction
o Vortioxetine: blocks reuptake of serotonin
 Nausea
PROGNOSIS
 Highly variable course, with some never
experiencing remission and others years with few
symptoms
 Recovery typically begins within 3 months of onset
for 2/5 individuals with within 1 year for 4/5
individuals
 Risk of recurrence high if severe episode, younger,
multiple episodes, persistence of symptoms during
remission
 Risk of recurrence lower as duration of remission
increases
OTHER DEPRESSIVE DISORDERS
PERSISTENT DEPRESSIVE DISORDER

(DYSTHYMIA)
 Symptoms present for >=2 years
 Depressed mood, in addition to >=2 of following
o Poor appetite or overeating
o Insomnia or hypersomnia
o Low energy, fatigue
o Low self-esteem
o Poor concentration or indecisiveness
o Feelings of hopelessness
DEPRESSION WITH SEASONAL PATTERN PRACTICAL GUIDE TO CARING FOR CAREGIVERS
 Typically occurs in fall or winter (PATIENTS WITH DEMENTIA)
 Symptoms same as MDD
MINOR DEPRESSIVE DISORDER  https://www.aafp.org/afp/2000/1215/p2613.html
 Symptoms are present during 2-week period for <2 CAREGIVER BURDEN
years  Physical, emotional, financial toll of providing care
 2-4 diagnostic criteria for MDD, must include  Zarit Burden Interview most widely referenced
depressed mood or anhedonia scale – frequency from 0 to 4 of 22 questions
GRIEF
 Loss of death or loved one
 No functional impairment nor suicidal ideation
 Typically occur in waves
 Level of burden no correlation with duration of time

spent as caregiver, progression of memory loss,
degree of functional impairment
 Degree of behavioral problems and dementia
associated with higher levels
 Active coping skills (being firm in directing  Fill out Medical Condition Report and send to
relative’s behavior, constructing larger sense of Ministry of Transportation by fax or email
illness), management strategies, family support,
strong social network, associated with lower levels
CONSEQUENCES
 Increased risk to place patient in long-term care
facility and formal in-home services
 May increase morbidity: depression, anxiety,
alcohol use, psychotropic drugs, decreased
immunity
 Also higher mortality risk
OFFICE-BASED APPROACH
 Increased risk of depression and anxiety – assess
 Skill in managing behavioral problems – assess
 Practical counseling about common caregiving
stresses, ways to handle behavioral management
issues, resources that benefit caregivers
 Screening questions:
 Normal visual field is an island of vision measuring

90 degrees temporally to central Fixation, 50
degrees superiorly and nasally, and 60 degrees
inferiorly. Visual acuity increases from movement
discrimination in the extreme peripheral vision to
better than 20/20 in the center of vision
 Central vision = inner 30 degrees
PHYISOLOGICAL EFFECTS OF AGING
TREATMENT MSK
 Respite care, e.g. adult day services  Increased bone resorption and osteoporosis 
 Behavioral issues: firm and directive, encourage to increased risk of fracture esp. in females
engage family member in activities o Postmenopausal osteoporosis: decreased
 Stress relief: emotion-focused strategies have estrogen levels  increased bone
higher burnout than problem-focused strategies resorption
o E.g. worrying and self-accusation o Senile osteoporosis: decreased osteoblast
o Vs. confronting issues and seeking activity  decreased osteoid production
information  Decreased lean body mass due to atrophy and loss
of muscle cells (sarcopenia)
 Degenerative changes in joints
o Stiffer and less flexible joints
o Decreased synovial fluid and cartilage
o Calcification
o Height loss
SKIN
 Noncancerous skin growths
o Seborrheic keratosis (benign growth of
immature keratinocytes. Most frequently
located on the trunk, the back of the hands,
the face and neck, and the forearms)
o Keratocanthomas (rapidly-growing tumor
of the skin derived from the glands
surrounding a hair follicle (pilosebaceous
glands). Typically presents on hair-bearing
areas of skin that are exposed to sun (e.g.,
face, neck) as a round, erythematous nodule
ONTARIO REGULATION 340/94 with a central hyperkeratotic crater)
 Cancerous growths such as basal cell cancer and
squamous cell carcinoma
 Xerosis cutis and pruritus due to decreased lipid and IMMUNE SYSTEM
sebum synthesis and increased moisture loss  Impaired immune response and regulation of
 Wrinkles: inflammation  recurrent infection, impaired
o Decreased elastin synthesis  increased wound healing, malignancy, autoimmune disease
skin laxity and rigidity  Decreased antibody and cell-mediated immune
o Decreased collagen synthesis  atrophy of responses to new antigen
dermis  wrinkle formation and decreased o Decline in counts of most subsets B and T
strength  increased risk of damage (e.g. o Decreased affinity of antibodies for new
decubitus and bruises) antigens (decreased variety of BCRs,
o Increased crosslinking of elastin and increased proportion of monoclonal cell
collagen lines, impaired affinity maturation and VDJ
o Decreased glycosaminoglycan synthesis  recombination)
decreased dermal moisture retention   Total Ig level remains the same
decreased volume  Macrophage and neutrophil counts do not decrease
o Decreased subdermal fat but less effective in functions
CARDIOVASCULAR SYSTEM  Increased NK cells, PGE2, and autoantibody
 Vascular sclerosis and stiffness  increased production
systolic BP ENDOCRINE SYSTEM
 Left ventricular hypertrophy and progressive  Decreased calcitonin, growth hormone, renin,
stiffening with 10% increase in wall size aldosterone, melatonin (loss of normal circadian)
 Mitral and aortic valve thickening and calcification  Estrogen and prolactin in women  breast atrophy
 Marked decline in stress-induced and exercise- NERVOUS SYSTEM
induced maximal HR due to decreased response to  Presbycusis and presbyopia
action of catecholamines  Reduced ability to detect vibration, touch,
RESPIRATORY SYSTEM temperature, pressure changes
 Weaker chest mall muscles + calcification of o Increased risk of pressure ulcers,
costochondral junctions + osteoporosis-induced hypothermia, burns
kyphosis  chest wall stiffness and decreased chest  Decreased/absent deep tendon reflexes
wall compliance  Lower-extremity weakness
 Decreased elastin in pulmonary parenchyma   Fluid intelligence declines but crystallized
decreased elastic recoil and increased lung intelligence increases
compliance  Altered sleep: early morning awakening, later sleep
 Decreased wall compliance + increased lung onset, decreased REM, decreased slow-wave sleep
compliance   Increased suicide risk in case of physical and
o Increased alveolar-arterial gradient, V/Q mental illness (particularly depression), functional
mismatch, functional residual capacity, impairment, and stressful life events
residual volume AGING AND THE EYE
o Decreased PaO2, FVC, FEV1
o Unchanged total lung capacity except in  ILM, NFL, GCL, IPL, INL, OPL, ONL, ELM, IS
cases of severe kyphosis and OS, RPE, Bruch’s membrane, choroid
 Weakened baroreceptor/chemoreceptor response 
poor ventilatory response to decreased O2 and
increased CO2  hypoxia and hypercapnia
 Weakened respiratory muscles  decreased cough
reflex  increased susceptibility to aspiration and
infection
GENITOURINARY SYSTEM
 Decreased GFR, diffuse sclerosis of glomeruli,
decreased acid load excretion
 Increased urinary frequency and urgency
 Increased risk of UTI
 Decreased libido typically more in women
 Women
o Postmenopausal estrogen deficiency 
vaginal atrophy, dryness, irritation,  AMD, leading cause of blindness in adults over 50
increased risk of yeast infections and UTIs, years of age
possibly dyspareunia o Deterioration of the macula and loss of
o Decreased tone of pelvic floor muscles  central vision
prolapse of vagina, uterus, bladder o Dry AMD: extracellular breakdown
 Men products (drusen) accumulate in Bruch’s
o Testicular atrophy, enlarged prostate gland, membrane  nutrients and waste can’t
o Slowed urination, erection, ejaculation percolate
o Increased refractory period
o Wet AMD: break in Bruch’s membrane  If gait, strength, or balance problem
choroidal neovascularization  can bleed o 0 falls, 1 fall no injury  moderate risk
and create edema, rapidly destroy vision  Modify meds, vitamin D, physical
 Anti-VEGF injection and therapist or community program
photodynamic therapy o 2 falls or 1 fall injury  multifactorial risk
 Lens assessment
o Lens fibers and zonules stiffen with age   Same as above + occupational
loss of accommodation and difficulty therapist (home), podiatrist (low
seeing nearby objects heel and high surface contact area),
 Lens assistive devices
o Proteins called crystallines lose MULTIFACTORIAL RISK ASSESSMENT
transparency over time, leading to cataracts  Falls history including circumstances and
o Most common type is nuclear sclerotic lens: frequency, associated symptoms, injuries, meds,
become larger and brunescent other relevant medical problems, ADLs, dizziness,
(yellow/brown) esp. in central nucleus  syncope
visual obstruction and glare  ROS: vision, urinary or fecal incontinence, MSK,
 Can become so big that pushes iris osteoporosis, foot pain, footwear, neurologic,
forward and leads to closed-angle cognitive impairment
glaucoma  Other: alcohol use
o Creates ‘second sight’: round lens offsets  Physical exam: postural hypotension, medication
coexisting presbyopia as if improving close review, cognitive screen, neurological, MSK, feet
sight and footware, use of assistive devices, VA
MANAGEMENT
FALLS IN ELDERLY INDIVIDUALS  Community-dwelling older persons at low-
moderate risk should participate in exercise
 Leading cause of fatal and nonfatal injuries in program or physical therapy and take vitamin D
persons older than 65 years supplements
RISK FACTORS  Community-dwelling older persons at high risk OR
NONMODIFIABLE older persons hospitalized for extended time OR
 >80 years, arthritis, cognitive impairment, female nursing home residents at risk  thorough risk
sex, history of CVA/TIA, history of falling or assessment and intervention tailored to needs
fractures, recently discharged from hospital  Potential components
MODIFIABLE o Exercise, particularly balance, strength, gait
 Cardiac: HTN, arrhtyhmias, CHF training
 Metabolic: DM, low BMI, vitamin D deficiency o Vitamin D3 supplementation at least 800IU
 MSK: balance impairment, foot problems, gait o Withdrawal or minimization of
impairment, impaired ADLs, limited activity, lower psychoactive and other medications
extremity muscle weakness, MSK, assistive device o Adaptation or modification of home
 Neurologic: delirium, dizziness or vertigo, environment
movement disorders, peripheral neuropathy o Management of foot problems and footwear
 Psychological: depression, fear of falling o Management of postural hypotension
 Sensory impairment: auditory impairment, o Consider dual chamber cardiac pacing in
multifocal lens, visual impairment patients with carotid sinus hypersensitivity
 Environmental hazards PRESCRIBING GUIDELINES
 Medications: anticonvulsants, antidepressants,  Do not lie in bed or only get up to a chair during
antihypertensives, antiparkinsonian, antipsychotics, hospital stay
benzodiazepines, digoxin, diuretics, laxatives,  No physical restraints
opioids, NSAIDs, sedatives and hypnotics  No benzodiazepines or other sedative-hypnotics as
 Other: acute illness, anemia, cancer, inappropriate first choice for insomnia, agitation, delirium
footwear, nocturia, OSA, postural hypotension,  Do not give medication without thorough review
urinary incontinence  Match frequency, intensity, and duration of exercise
DIAGNOSIS/RISK ASSESSMENT to individual’s abilities and goals
 Screening PREVENTION
o Falls in past year? How many? Feels  Minimize # of medications that may contribute
unsteady when standing or walking?  Physical therapy
Worries about falling?  Elimination of potential environmental hazards
o If no to all questions  low risk
 If yes to any questions then evaluate gait, strength,
and balance
o Recommended: Timed Up and Go
o Optional 30-second chair stand and 4-stage
balance tests
o If no concerns  low risk
o Balance between potential harms and
benefits of screening interventions
 Approaches to overcome insufficient average
visit length
o United Kingdom preventive program
involved free health check every 5 years
o Prevention facilitator or practitioner
embedded in primary care practices
o Web-based wellness portal linked to
EMR; users receive recommendations
CHOOSING WISELY CANADA
 Follow recommended immunizations and
screening times and times and frequencies
recommended by Canadian Task Force on
Periodic Health Examination
 High blood pressure
 Cervical cancer
 High cholesterol men >40 or women >50
 Diabetes
 Breast and colon cancer
 Osteoporosis
 Abdominal aortic aneurysm
PERIODIC HEALTH EXAMINATION
 Canadian Task Force on Preventive Health

Care
 Typically encompasses review of health
history, medications, allergies, and organ
systems + “complete” physical exam
sometimes followed by lab testing and
discussion of health risks, lifestyle behavior,
and social situation
o Provide preventive counseling,
immunization, and effective screening
 Visits consume substantial time and resources
and whether provide health benefits debated
 More recently in collaboration with College of
Family Physicians of Canada recommend not
annual physical exams but periodic preventive
health checks
 Visit intervals depend on age, sex, health
conditions of individual; risks
 PTSD, postpartum depression, DVT, complications
of pre-eclampsia
 Liver doesn’t do much in womb, but stores
glycogen, buffer when born
 T1DMs are vasculopaths will get IUGR but T2DMs
are not vasculopaths get macrosomia
THRIVING IN OLDER ADULTS
COPING STRATEGIES
 Coping strategies goal to compensate or alleviate
stressful situations by means of reformulation of
objectives or adjustment to new and positively
assessed situation
 Compensation by two means
 Emotion: managing emotional distress associated,
involves self-regulation aiming at minimizing
emotional consequences
o Good when problem inalterable
 Problem: modifying problem at hand, actions to
deal with stressful situations
o Good when problem can be altered
PRACTICAL
 Care for caregiver
 Friends and family to stave off solitude, connect
virtually
 Community programs/support groups
 Reminiscence therapy: encourages storytelling and
meaning-making
 Avoid overarousal from TV/social media
 Do what you love
 Eat and exercise well, good sleep hygiene
EXTRA
 Read around intrauterine growth restriction

 Read around live vs. inactivated vaccines

Maternal

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Maternal

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MATERNAL HEALTH

 CIWA-Ar protocol: grades severity

 3-5 days after birth

OTHER DEPRESSIVE DISORDERS

PERSISTENT DEPRESSIVE DISORDER

 Level of burden no correlation with duration of time

 Normal visual field is an island of vision measuring

PHYISOLOGICAL EFFECTS OF AGING

PERIODIC HEALTH EXAMINATION

 Canadian Task Force on Preventive Health

THRIVING IN OLDER ADULTS

 Read around intrauterine growth restriction

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