Acute care/NICU Flashcards
What tests are done as part of the IPS (integrated prenatal screen)?
- Frist trimester screen (12 week nuchal translucency +PAPP-A+ BHCG)
- Maternal serum screen (AFP + E + HCG)
Can detect: trisomies, open NTD, Placental insufficiency
When can chorionic villius sampling be completed? What does it detect?
9-12 weeks
Chromosome abnormalities
1% pregnancy loss
When can aminocentesis be completed? What does it detect?
>16 weeks
Chromosome AbN, lung maturation, infection, renal
0.5% pregnancy loss
When is the anatomic ultrasound completed?
18-20 weeks
What is the diagnosis if a baby had: transient myeloproliferative disorder, AVSD, hypotonia, absence of rectal ganglion cells?
T21
What is the diagnosis if a baby had: cutis aplsia, cleft lip and clino/polydactyly?
T13
What is the diagnosis if a baby had rocker bottom feet, interupted aortic arch, overlapping fingers, microcephaly?
T18
What is the diagnosisif a baby had extra nuchal fold and lymphedema of the hands?
45 X0
Which of the following statements is FALSE?
- Antenatal steriods are indicated for women presenting with the risk of PTL
- Antenatal steroids are used for neuroprotection and reduce CP
- MGSO4 is indicated forwomen
- MgSO4 is used for neuroprotection and decreases CP
2
What are the prenatal interventions to prevent birth defects?
- Folic acid: decreased NTD
- Glucose control in diabetes
What are the antenatal interventions to improve outcomes in prematurity?
- Antenatal steroids,
- MgSO4
What is the most common cause of SN hearing loss?
CMV
What are the main findings in congenital CMV?
IUGR, Microcephaly, MR, deafness, HSM
What are the main findings in toxoplasmosis?
IUD, hydrocephalus, MR, chorioretinitis
What are the main findins in parvovirus B19?
Anemia, heart failure, hydrops, IUD
What are the main findings of prenatal varicella?
Hypertrophic scars, limb deformities, brain atrophy, cataracts
What are the main findings of prenatal syphilis?
Snuffles, skin findings, metaphyseal bone lesions
What is the diagnosis?
Transient neonatal pustular melanosis
What is the diagnosis?
Erytherma toxicum
Usually not hands/feet
What is the diagnosis?
Milia
How does HIV present at birth?
Usually asymptomatic at birth
PResents with CNS, DD, growth, diarrhea in the 1st year
Which of the following is NOT a risk factor for neonatal hypocalcemia?
- Maternal Graves disease
- Maternal DM
- Maternal Vitamin D defiency
- Maternal hyperparathyroidism
Maternal Graves
How can maternal diabetes effect the fetus?
HypoGlc, macrosomia, jaundice, polycythemia, small left colon syndrome, cardiomyopathy, RDS, jaundice
How does pregnancy induced hypertension effect the fetus?
IUGR, Low Plt, Low neutro, fetal demise
Prenatal NSAIDS/ASA?
Hemorrhage
PDAclosure
PPHN
Carbamazepine/VPA?
NTD
Midface hypoplasia
Phenytoin?
Midfacial hypoplasia
Hemorrhage
Fetal hydantoin syndrome (MR/IUGR/Hypoplasia of the distal phalanges)
What are risk factors for preterm delivery?
- SES status: 40Y, very low SES, low BMI
- Past Gyne/OB Hx: Pyelo, Cx abN, multiple abortion, preterm delivery
- Lifestyle: >10 cig/day, heavy work
- Pregnancy: multiples
What are risk factors for IUGR?
Maternal:HTN, renal diseas, diabetes, APL syndrome, nutritional deficiency, smoking, substance use, maternal hypoxia
Fetal: multiple gestation, placental abnormalities, infection, congenital anomaly
How can you prevent hemorrhagic disease of the newborn?
- Vitamin K IM at birth (0.5mg )
- Alternative: 2mg PO with 1st feed then 2-4 wk, 6-8 wks
What are the presentations of hemorrhagic disease of the newborn?
- Early: 1st 24 hours, due to maternal medication
- Classic: 1:400, bleeding in 1st week of life, vitamin K deficiency
- Late: 2-12th week of life (3-8 wk in CPS statement), exclusive BG
Rx: Vitamin K, FFP
When will most newborns void?
Within the first 24 hours
Can babies shiver?
Less likely to do so
Will use brown fat thermogenesis to generate heat
What % of babies pass stool in the first 24 horus?
96%
Think: Meconiumplug, Hirschprungs, meconium ileus, imperforate anus, small left colon (IDM)
What are the three questions you ask at the beginning of NRP?
- Term?
- Crying or breathing?
- Tone?
What does MRSOPA stand for in NRP?
M- Mask adjust
R- reposition head
S- suction
O- open mouth
P- Pressure increase
A-Alternative airway
Neonatal ETT sizes?
>35 weeks: 3.5-4
>1 kg: 3
At what GA do you use a plastic bag?
< 32 weeks
What are the early onset causes of respiratory disease in newborns?
TTN, RDS, Severe malformations, pulmonary hypoplasia
What are the evolving onset causes of respiratory disease in newborns?
PTX, RDS, MAS, PPHN, pneumonia, loabr emphysema
What is the diagnosis?
Hyperinflated
Fluid in the fissures
What is the diagnosis?
RDS
Hypoinflated
Ground glass
What are the clues on history for TEF?
Apnea, cyanosis, forthing, choking with feeds
LOOK FOR ASSOCIATED: VACTERL
NPO, NG to suction, surgical consult
How does surfactant therapy help preterm babies?
Decreased mrotality, PTX, PIE
Decreases duration of vent support, LOS
No effect on IVH, BPD, NEC, ROP
What are the indications for surfactant therapy?
Intubated preterm with RDS
MAS FIO@ >50%, sick with pneumonia + OI >15
Natural is better
May repeat, max 3doses
What are the risks of surfactant therapy?
PTX, bradycardia, blocked tube, hemorrhage
What is the definition of BPD?
Oxygen dependence beyond 28 days or 36 weeks CGA
How late can apnea be considered apnea of prematurity?
44 wk CGA
When does a PDA normally close? What are the clinical features?
- Closes at 5-7 days
- Clinical features: bounding pulses, hyperdynamic precordium, loud second HS, systolic murmure
What are the risk factors for PVL?
CAN OCCUR INDEPENDENT OF IVH
PVL=CP
- Twin-twin transfusion
- Chorioamnionitis
- Asphyxia
- Severe lung disease
- Hypocarbia
- NEC
- Post natal dex
When is the screening for ROP?
Who?
When? At 4weeks of age (>26+6) OR after 31 CGA (
What are the risk factors for ROP?
- Hypotension
- Prolonged ventilation
- Oxygen therapy
What are the risk factors for NEC?
- Prematurity
- Ischemia: asphxia, CHD, PDA, severe UGR, exchange transfusions
What are the organisms and treatment for early onset sepsis (1st week of life)?
- GBS, Ecoli, Listeria
- FSWU
- Amp/Gent
What are the organisms and treatment for late onset sepsis (1 month)?
CONS, staph aures, enterococci
What are the indications for therapeutic hypothermia in HIE?
>36 weeks GA
Both 1&2:
1- Any 2 of APGAR 16 (Cord or one hour)
- Signs of moderate to severe encephalopathy
How do you cool?
Aim for temp 34+/- 0.5 degrees
Passive cooling in the community
Active cooling when in teritary centre
Method: Total body or selective cranial cooling
When? Within first 6 hours of life
Complications: hypotension, bradycardia, coagulopathy, fat necrosis
What is the outcome of HIE? What are the benefits of cooling?
Prognosis: Severe 80% morbidity, Moderate 30-50%, mild usually no deficits
Benefits of cooling: risk reduction 25% combined mortality and major NDD (NNT 11 for 1 mortality)
How do you calculate GIR?
GIR = (IV Rate (mL/hr) * Dextrose Conc (g/dL) * 1000 (mg/g))/
Weight (kg) * 60 (min/hr) * 100 (mL/dL)
What are red flags for neonatal jaundice?
Onset before 24 hours
Hemolysis
Pallor, unwell
HSM
Pale stools, dark urine
Conjugated hyperbili
What are the symptoms of acute bilirubin encephalopathy?
- Lethargy, decreased tone and suck
- Increased tone, opisthoclonus, retrocollis,
High pitched cry, seizure, coma
Any of these signs: EXCHANGE
What are the complications of exchange transfusion?
NEC, thrombocytopenia, anemia, hemolysis, portal vein thrombosis
When do you treat polycythemia?
Hct >70 or symptomatic: partial exchange transfusion
How do you calculate the volume of blood to be exchanged in partial exchange for polycythemia?
Volume= ((actual-desired hct) x wt x 90)/actual hct
What is the mechanism of TTN?
Pulmonary edema from delayed resorption of fluid from alveoli
Excess water =decreased pulmonary compliance therefore tachypnea used as a compensatory mechanism
What are the risk factors for TTN?
C/s, preterm birth, IDM, maternal asthma
What stage of lung development occurs between 16-25 weeks?
Canalicular stage: the transition between previable and potential viable lung occurs, as respiratory bronchioles and alveolar ducts are formed
What stage of lung development occurs > 25 weeks GA?
Saccular stage: potential for viability because gas exchange possible due to large and primitive forms of future alveoli, alveoli at 32 weeks= ZERO, term 50-150 million
Does alveolar growth continue after birth?
Yes, for at least two years!
What is RDS caused by?
- Surfactant deficiency
- Increase in the amount of pressure needed to open alveoli and collapse leading to V/Q mismatch and hypoxemia
- Also leads to inflammation and epithetial injury
Where is surfactant produced?
Type II alveolar cells
Composed of 90% lipids and 10% proteins
Antenatal steroids help to stimulate surfactant synthesis
What are the CXR signs of RDS?
- Low lung volumes
- Reticulogranular ground-glass appearance with air bronchograms
What are the two main groups of diseases that lead to PPHN
- Underdevelopment: pulmonary hypoplasia (CDH, CCAM, renal agensis, IUGR)
- Maldevleopment: post-term delivery, meconium
- Maladaption: normal development of pulmonary vascular bed however acive vasoconstriction occurs
What are the general management guidelines for PPHN?
- Keep O2 >90%
- Correction of acidosis (low pH causes increased PVR)
- Sedation
- Circulatory support
- iNO, sildenafil, ECMO
What are the mechanisms that keep the PDA open?
Decrease sats, PGE2, increase NO
When does functional closure of the PDA occur?
50% within 24 hour, 90% within 48 hour, all within 72hour
What are the physiologic effects of a PDA?
- Increased PBF
- Decreased SBF
What are the clinical features of a PDA?
Murmur over the entire precordium, LUSB, initially systolic only however as pulmonary pressures decrease will become present in both systole and diastole
Bounding pulses
Widened pulse pressure
Tachypnea, apnea
What is the treatment of PDA?
Indomethacin or ibuprofen
SE: decreased renal, cerebral and GI blood flow
When does vascularization of the retinal occur?
No blood vessels are present before 16 weeks
Retinal vascularization begins a 15-18 weeks, starts from optic nerve and moves outward
Vascularization is complete by 34 weeks in the nasal retina and 40 weeks in the temporal retina
What are prevention strategies for NEC?
Human milk
Trophic feeds
Avoidance of H2 blockers
Probiotics
Avoidance of prolonged ABx
What are the ways in which meconium interferes with normal breathing?
- Airway obstruction (Ball valve effect)
- Chemical irritation/pneumonitis
- Infection (riskfactor as mec is sterile)
- Surfactant disruption
- Hypoxemia
What are the risk factors for BPD?
Prematurity, mechanical ventilation, oxygen toxicity, infection, inflammation, genetics, late surfactant deficiency
What are the basic toxicology investigations?
Point of care glucose, acetaminophen, salicylate levels, serial ECGs, pregnancy tst, AXR, core temperature
What toxiodromes cause tachycardia?
- Anticholinergics
- Sympathomimetics
- Ethanol
What toxidromes cause bradycardia?
Opiods
Beta blockers
What toxidromes cause QRS widening?
TCAs
What toxidromes cause prolonged QTc
Neuroleptics
Celexa
What are the four main types of toxidromes?
- Cholinergic
- Anticholinergic
- Sympathomimetics
- Opiods
What drugs give you a cholinergic toxidrome?
- Organophosphates
- Carbamates: neostigmine!
- Alzheimers drugs
What is the acronym for a cholinergic toxidrome?
DUMBELS
Diaphoresis
Urination
Miosis
Bronchorrhea/Bradycardia
Emesis
Lacrimation
Lethargy
Salivation
What is the management of cholinergic exposure?
Early intubation, 100%
Decontamination
Atrophine until secretions and wheezing stops (muscarnic symptoms)
Inhaled atrovent/ventolin
Pralidoxime (Nicotininc symptoms)
What drugs give you anticholinergic toxidromes?
TCA
Antihistamines
Benztropine
Atropine
Lomotil
Neuroleptics
Jimson weed
What are the symptoms of an anticholinergic toxidrome?
Blind as a bat (mydriasis-dilated)
Mad as a hatter
Red as a beet
Hot as a desert
Dry as a bone
Tachycardia, absent bowel sounds
What is the management of anticholinergic exposures?
Sodium HCO3 for wide QRS
Lorazepam for agitation
Water spray and cooling fans for hyperthermia
Physostigimine is ++ toxicity
What drugs give you a sympathomimetic toxidrome?
Cocaine
Amphetamine/Meth
MDMA
Ephedrine
What are the symptoms of a sympathomimetic toxidrome?
Mydriasis
Diaphoresis
Hypertension
Tachycardia
Seizure
Hyperthermia
Psychosis
Agitation
What are the serious side effects of MDMA?
HTN
Hyperthermia: rhabdo, DIC
Hyponatremia
Serotonin syndrome
Cardiac ischemia
Hepatotoxcity
What is lysergic acid?
- LSD
- Rapid oral adsorption, symptoms within 30-60 min
Most of the potent hallucinogens
Mydriasis, HTN, Increased RR HR, diaphoresis
Massive OD: fever, autonomic dysregulation, vomiting, respiratory arrest, ICH
What is phencyclidine?
PCP or Angel Dust, similar to ketamine
Fluctuating behavior with delirium, paranoia, agitation
NYSTAGAMUS WHILE AWAKE
When do you suggest giving milk?
Only if toxin produces simple irritation
What metabolic diagnosis is represented by respiratory alkalosis?
Hyper NH4 until proven otherwise
In a baby presenting with a possible metabolic d/o with gram negative sepsis, what is the likely diagnosis?
Galactosemia
How do you calculate an anion gap?
AG= [Na+K]-[Cl+HCO3]
Normal
What are the first tests you order when suspecting a metabolic condition?
- VBG
- Electrolytes
- Glc
- Lactate
What are the three metabolic specific tests you should order?
- Urine organic acids
- Serum amino acids
- Acylcartinine profile
What is the difference between breastmilk and formula that effects the presentation of metabolic conditions?
Breastmilk 1g protein/100cc
Formula 2.5g/100cc
Therefore breastfeeding delays the presentation
What is the specific differential diagnoses for AG metabolic acidosis?
- Ketones
- Lactate
- Organic acids
What is the differential diagnosis for nonketotic hypoglycemia?
- Hyperinsulinism
- FAOD
How do you calculate BSA?
BSA=SqRt of Ht x Wt/3600
How do you calculate insensible losses?
300-400 ml/m2/day
(30 ml/kg/day)
What must you not forget with high urine outputs in water/Na dysregulation?
Osmotic diuresis from glucose
When can you give charcoal?
Within one hour of ingestion
Must have protected airway if low LOC
What can activated charcoal NOT remove?
PHAILS:
P:Potassium
H: Hydrocarbons
A: Alcohols
I: Iron
L: Lithium
S:Solvents
Is gastric lavage recommended?
NO- not been shown to improve outcomes
What is the antidote to iron?
DFO/Deferoxamine
What is the antidote to carbon monoxide?
Oxygen
What is the antidote to pesticides?
Atropine
What is the antidote to nifedipine (CCB)?
Glucagon, Insulin
What is the antidote to amitriptyline (TCA)?
Na HCO3
What is the antidote to methanol?
Fomepizole
How to hydrocarbon ingestions kill?
Aspiration and pulmonary toxicity
Present in: gasoline, nail polish remover, lighter fluid
Approach with STAT CXR and repeat 4-6 hours later
Rx with oxygen and bronchodilators
What do you see on the CXR of a hydrocarbon ingestion?
Perihilar infiltrates
Pneumatoceles
Which diabetic medication will present without hypoglycemia with Kussmaul respirations and an acidosis?
Metformin
Lactic acidosis
What drugs cause hypoglycemia?
- Glyburide (difficult to control)
- Beta blockers
- Ethanol
- Salicylates
What is the toxic metabolite of acetaminophen? What dose is toxic?
NAPQI
Dose 150 mg/kg
Hepatoxicity reported >90mg/kg/day
How will an acetaminophen overdose present?
AG metabolic acidosis
Acute tubular necrosis
Fulminant liver failure
What is the treatment of acetaminophen overdose?
Activated charcoal within 1 hour
Avoid AC if sedated
NAC dosing based on Rumack-Matthew nomogram
Best outcomes if NAC started within 8 hours
Follow LFTS/live function
What are the symptoms of a salicylate overdose?
Hyperpnea/tachypnea
AG metabolic acidosis
Nausea, vomiting, GI bleed
TINNITUS (progresses to hearing loss)
Hyperglycemia
Diaphoersis
What is the management of a salicylate overdose?
Charcoal up to 6 hours (to avoid bezoar formation)
Glucose to all patients
Treat hypokalemia
Alkalinize serum
Hemodialysis for CNS sypmtoms
What are the radio-opaque drugs?
COINS
Chloral Hydrate
Opiod packets
Iron and other heavy metals
Neuroleptics
Sustained release tablets
What is the presentation of iron?
10% of intentional overdoses are fatal
Stage 1 (30min-6hr): Nausea, vomiting, diarrhea
Stage 2 (6-12 hours): “Quiesent phase”
Stage 3 (12-24 hours): Metabolic acidosis, shock, GI bleed, coagulopathy, resp failure
Stage 4 (2-3 days): ARDS, liver failure
Stage 5 (3-4 weeks): GI stricture at gastric outlet
What are the clues to iron exposure?
GI symptoms
Acidosis
Multiorgan failure
What is the treatment of iron exposure?
No role for either charcoal or gastric lavage
Fluid resus
WBI if tablets seen or ,6 hours
IV deferoxamine 15mg/kg/hr until urine clears
What is unique about the presentation of isoproyl alcohol ingestion?
Ketosis without acidosis (cannot be metabolized past ketones)
Why is methanol so toxic?
- Less inebriating than ethanol
- Toxicity in little as one teaspoon
- Formate causes retinal injury
Profound AG acidosis presents late
What substance is in antifreeze, paints, brake fluid?
Ethylene glycol
Colorless, ordorless, sweet taste
Inebriation without smell of ethnaol
Metabolic acidosis
Hypocalcemia (prolonged QTc)
Oxalate crystals
What are the clues to toxic alcohol exposures?
Inebriation
Odor
Osmolar gap or acidosis
How do you calculate osmolality?
Two salts and a sticky bun
OG= 2x NA + Glucose + BUN
How do you calculate an osmolar gap?
OG= Measured-Calculated Osmolarlity
What is the general management of toxic alcohol exposure?
- Wash skin if exposed
- Fomepizole or ethanol
- Hemodialysis if high AG acidosis or end-organ damage
- Cofactor therapy with folic acid
- Thiamine and pyridoxine
What are the common TCAs to be ingested?
Amitriptyline, despiramine, imipramine
What are the clinical effects of TCA overdoses?
Inhibit NE and serotonin reuptake
Block cardiac fast Na channels- wide QRS
block muscarinic receptors-weakly anticholinergic
Block histamine receptors- sedation
Block alpha receptors- hypotension
block GABA- seizures
What is the treatment for a TCA overdose?
Activated charcoal
Intubation
NAHCO3 for QRS >100mS
NE if hypotension
How does carbon monoxide poisoining present?
Headache, dizziness, nausea, confusion, seizure, syncope, coma
Most commonly from smoke inhalation
Tasteless, odourless, non-irritating gas
240x higher affinity to Hb than O2
Dysrhythmia, cardiac arrest in up to 30%
Cherry red skin colour after excessive exposure
What is the treatment of a carbon monoxide exposure?
Remove from source and r/o smoke inhalation
Check cyanide level
Follow ECG and cardiac enzymes
Provide 100% FiO2
Hyperbaric O2 if COHb> 25%
What are the clues to a carbon monoxide exposure?
Flu-like symptoms
Fire exposure
Normal Sats
What is the most common cause of pediatric death in children 1-4 years?
Trauma
What preventative strategies are used to prevent submersion injury?
- Four sided self closing fence with a self locking gate (MOST EFFECTIVE)
- At least 4 feet high
- Toddlers should always be wtihin arms length of an adult, even in a tub
- 1 adult per baby, 1 adult per 2 young children
- Swimming
What are the risk factors for submersion injury?
- Leaving children unattended
- Alcohol or drug abuse
- Limited swimming ability
- Underlying medical condition: seizure disorder, toxin, prolonged QTc, syncope
A 14 year old male is pulled from an icy lake after being found face down. What is the most important strategy influencing survival?
- Imediate c-spine
- immediate CPR by rescuers
- Passive external rewarming, EMS activation and transport to a health care facility
- Early placement of definitive airway
2
What are GOOD prognostic indicators in submersion injuries?
IMMEDIATE BYSTANDER CPR is the most important factor influencing survival
ROSC in
Submersion
Pupils equal and reactive at the scene
NSR at scene
What are BAD prognostic indicators in submersion injuries?
Delayed CPR
ROSC > 25 min
Submersion >10 min
What do you see at different degrees of hypothermia?
31-32: Normal ECG, Increased HR, Increased BP, loss of shivering
28-31: Decreased HR, Decreased BP, Flipped T, afib, sluggish dilated pupils
What are the ECG changes you will see in hypothermia?
- Marked bradycardia
- First degree AV block
- Osborn or J waves
- Associated prolonged QTc and bradycardia
What are the principles of rewarming without a pulse?
>30: CPR, IV meds as needed, defibrillation as needed
Gentle intubation
Warm O2, Warm IVF
What is heat stroke?
Core temp >40 and CNS dysfuntion
Headache, disorientation, dizziness, weakness, gait disturbance
What are the clues to a superficial partial thickness burn?
Pain, moist, blisters
What is the initial management of burns?
- Cover sterile bandages
- Early cooling (
- TETANUS
- Analgesia
- Remove shoulder clothing
What are indications for early intubation in burns?
Carbonaceous sputum
Singed nasal hairs
Soot in airway
Hoarseness
How do you calculate fluid management in burns?
Age > 9: Rule of 9s
Age
Age > 5: Parkland formula: 4cc/kg/BSA over 24 hours, 1st half in 8 hours, 2nd half in 16 hours
What are the physical findings of a post term infant?
Cracked, dry, peeling skin
Creases covering the entire sole of the foot
Mature, long fingernails
Basence of lanugo over the back
Palpable breast buds
What is the way to remember gastroschisis vs omphalocele?
Gastroschisis: Good baby, bad bowel
Omphalocele: Baby baby, good bowel
What is the appearance of gastroschosis?
Centrally located, full thickness, abdo wall defect
- Extruded intestine NEVER has protective sac
- Umbilical cord intact to the left of the defect
25% associated with bowel atresias
What are the risk factors for gastroschsis?
Young mom, EtOH abuse, ASA, ibuprofen, pseudoephedrine
What is the immediate management of a baby with gastrochisis?
Temp regulatin
Protective covering
Right lateral position and ensure bowel not kinked
NG decompression
IV fluids 2-3 maintenance
Surgical correction ASAP
What is the clinical appearnace of omphalocele?
- Protective membrane covered gut
- Cord is always attached to membrane
What is the likely mortality of a baby with omphalocele?
30%
What are the syndromes associated with omphalocele?
Beckwith-Wiedemann, conjoined twins, T18, meningomyelocele, imperforate anus
What are the breastfeeding benefits for baby?
Immunologic: IgA, lower rate of OM, LRTI, gastro,
Less allergenic
Less constipating
Better jaw/mandible development
What are the breastfeeding benefits for Mom?
ABCDEFGH
Allergic conidtions reduced
Best food for infant
Close relationship with mother
Development of IQ, jaws, mouth
Economical
Fitness
Guards against cancers for mother (breast, ovary, uterus)
Hemorrhage reduced postpartum
How does breastmilk compared to cow milks?
67kcal/100cc
Lower portein content
Greater whey
Both lactose based
More fat!
Richer in A
Lower FE
What are the metabolic complications of TPN?
Electrolyte Ab
Glucose AB
Ca/PO4 abN
Cholestasis
Line infection
Bone D/o
What is the differential diagnosis for ambiguous gentalia?
- Undervirilization of males
- Virilization of females
- True hermphroditism
- Incomplete gonadal dysgenesis
What does VACTERL stand for?
Verterbal
Anal
Cardiac (VSD)
TEF
Eo Atresia
Renal
Limb
NORMAL DEVELOP AND INTELLIGENCE
What does CHARGE stand for?
Coloboma
Heart d/s
Atresia (chonal)
Retarded growth and developemtn
Gential AbN
Ear abN
How does galactosemia present?
Within first few days after bith
Jaundice, vomiting, HSM, FTT, poor feeding, lethargy
E coli sepsis!
What are the causes of early onset hemorhhagic disease of the newborn?
0-24 hours
Maternal drugs
Inherited coagulopathy
What are the causes of classic hemorhhagic disease of the newborn?
Vitamin K deficiency
BF
(
What are the causes of late onset hemorhagic disease of the newborn?
Cholestatis
Warfarin
ABLP deficiency
Lack of Vitamin K
What are the components of the APGAR scores?
Appearance
Pulse
Grimace
Activity
Respiratory effort
When should rH negative moms receive rHoGAM?
28 weeks
Invasive procedures
What is the most common cause of severe thrombocytopenias in the first day of life?
Neonatal alloimmune thrombocytopenia (NAIT)
Maternal alloimmune antibodies against HPA on fetal platelets results in NAIT
Can occur in first pregnancy
What is the treatment of NAIT?
Need to administer a specific HPA type to avoid continued destruction of transfused platelets.
Subsequent pregnancies: weekly IVIG to minimize the incidence of thrombocytopneia and ICH.
Which infants have a set-up for ABO incompatilibility?
Mom O, Infants A or B
Individuals with type A or B have naturally occuring Anti-A and anti B isoantibodies that are frequently igM and do not cross the placenta
Individuals with type O have isoantibodies that are IgG and can cross the placenta.
What are the contraindications to a lumbar puncture?
- Low platelets
- Infections of the skin at the puncture site
- Lumbosacral anomalies
- Cardioresp instability
- Increased ICP
What are the contraindications to breastfeeding?
HIV
HTLV
Galactosemia
Active TB
What does cryo contain?
Plasma thats been spun: fibringoen, factors V,VIII, XIII, VWF
1 unit/5 kg (1 unit=15mL)
What is the dose of FFP?
10 ml/kg
Should you never glue a hand?
NO
Which is more likely to cause infection: dog or cat bites?
CAT >50% will get infected
When is antimicrobial therapy indicated for bite wounds?
- Moderate or severe bite wounds
- Puncture wounds
- Facial bites
- Hand and foot bites
- Wounds in IC and asplenic people
- Wounds with signs of infection
What would be your first choice of antibiotic for human and animal bites?
Amoc/Clav
What are the exclusions for organ donation?
- Severe untreated systemic sepsis
- AIDS
- Active HBV, HCV, CMV
- Active extracranial malignancy
- CJD
- Active disseminated TB
- HIV
What are the confounders of NDD?
- Unresusciated shock
- Hypotension
- Severe metabolic disorders
- Neuromuscular blockade
- Significant drug intoxication
What type of current in present in high voltage burns?
AC pulls victim towards source, tetany prevents release
Deep muscle injury is common
What type of current is lightning burns?
DC, short duration that throws victim from source
What are the different types of arrests for high voltage vs. lightning burns?
high voltage:VF
Lightning: asystole
When should you expect inhalational injury?
Carbonaceous sputum
Singed nasal hairs, eyebrows
Hoarseness/stridor
COHB> 10-50%
SOB, CP
Burn in closed space/fireworks
What is the most common form of abuse?
NEGLECT
What fractures are concerning for non-accidential trauma?
Metaphyseal clip #, bucket handle
Spiral # of femur/humerus
Posterior rib #
Skull #
Scapula, sternum
Spinal processes
What is the PCP triad?
Halluications
Nystagmus
Rigidity
What is the triad for an ASA overdose?
- Tinnitus
- Hyperventilation
- Resp Alkalosis
What 3 medications can kill with one pill?
- Oral hypoglycemics
- TCAs
- Calcium channel blockers
What are the clinical features of TCA overdose? (think triad)
Overall blocks Na channels and inhibition of GABA reuptake
- CNS:
- seizures - CVS
- prolonged PR/QRS/QT
- arrhythmias
- hypotension
- LOOK at AVR = positive R’ wave in AVR - Anticholinergic
- hot as hell (hyperthermia has very bad prognostic effect)
- blind as bat
- mad as hatter
- red as beet
- dry as bone
- bowel and bladder lose their tone
In a TCA overdose, what is a predictor of toxicity?
Widened QRS –> get ECG asap: if widened, this is predictive of seizures and ventricular dysrhythmias
-nothing else is predictive besides QRS (not drug level, not symptoms)
What is the management for TCA overdose?
-how long should you monitor them for if asymptomatic?
Charcoal: give even if > 1 hr since gastric emptying may be delayed (due to anticholinergic effect)
If decreased LOC: intubate asap
Bicarb: for QRS > 100 msec, arrhythmias, hypotension, acidosis
-NaHCO3 1-2 mEq/kg bolus, then start infusion
Pressors: norepinephrine for hypotension always!
Active cooling if hyperthermic
Monitor x 6 hours
How to treat seizures secondary to toxic ingestion?
Use benzos ONLY! Do not use phenytoin since this may worsen Na channel blockade (most drugs cause Na blockade)
What are the toxic doses for:
- acetaminophen
- ibuprofen
- ASA
Acetaminophen: 150 mg/kg
Ibuprofen: 100 mg/kg
ASA - 150 mg/kg
What is the progression of acetaminophen overdose?
0-24 hrs: GI irritation or asymptomatic
24-48 hrs: liver involvement, increased PTT is the earliest marker, than rise in AST
72-96 hrs: fulminant hepatic failure, renal failure
4-14 days: recovery or death
What are signs of salicylate overdose? Treatment?
Tinnitus is often 1st symptom
GI upset (vomiting), confusion/cerebral edema, impaired plt function, pulmonary edema, central hyperventilation (tachypnea)
(Causes uncoupling of oxidative phosphorylation)
-give bicarb for urine alkalination
-call nephro (may need dialysis)
-need to order salicylate levels q2h until they peak and then document at least 2 decreasing ones
What are the steps to clearing C-spine on xray film?
- Ensure adequacy of film
- need to see C1-C7 and space between C7 and T1 on lateral film to qualify as adequate film
- if cannot see space between C7 and T1, need swimmers view - Assess vertebral alignment
- anterior vertebral line, posterior vertebral line, spinolaminar line, posterior spinal line - Assess bony integrity
- Assess disc spaces
- Odontoid view
- look for disruptions in odontoid and atlas - Soft tissues
- prevertebral soft tissue should be
What is the most common arrthythmia associated with halogenated hydrocarbon abuse?
VT and VF
What are the steps of RSI?
AMPLE
Preparation: SOAP-ME (suction, oxygen, airway assessment & equipment, position, medications, environment)
Preoxygenation
Premedication
Sedation
Sellick Maneuver
Paralysis
Intubation & confirmation
What are the main differences between adult and pediatric airway? (5)
For pediatric airway:
- Large head and occiput
- Large, floppy epiglottis
- Larynx is more anterior
- Cricoid is narrowest portion of airway
- Small oropharynx with large tongue
What are the 4 contraindications to rapid sequence intubation?
- Anticipated difficult airway and unsuccessful attempt
- Significant facial or laryngeal trauma
- Upper airway obstruction
- Cardiopulmonary arrest
What are the indications for use of atropine as premedication in rapid sequence intubation?
Neonate
What are the actions of atropine in rapid sequence intubation? (2)
- Minimizes vagal stimulation (prevents bradycardia)
- Decreases oral secretions
What is evidence for use of lidocaine as premedication in rapid sequence intubation?
Used in head injury
and thought to reduce rise in ICP associated with laryngoscopy
No evidence to support use in 2001 literature review (no improvement in neurological outcome)
What are the effects of the following when used in rapid sequence intubation:
- Fentanyl
- Midazolam
- thiopental
- etomidate
- ketamine
- propofol
- Fentanyl: sedation, analgesia
- little hemodynamic effect - Midazolam: sedation, amnesia, NO ANALGESIA EFFECT
- respiratory and hemodynamic depression - Thiopental: sedation with NO ANALGESIA
- respiratory and hemodynamic depression
- laryngospasm and bronchospasm
- reduces ICP - Etomidate: sedation with NO ANALGESIA
- minimal respiratory and hemodynamic depression
- decreases cerebral blood flow, metabolic rate and ICP
- suppresses cortisol production and may produce myoclonus
- do NOT use in sepsis! - Ketamine: dissociative sedation, amnesia AND analgesia!
- minimal hemodynamic effects
- bronchodilation
- may cause laryngospasm
- increases oral secretions
- no longer thought to increase ICP (multiple studies) - Propofol: sedation, rapid onset and offset
- hypotension
What are the biggest concerns with use of etomidate in rapid sequence intubation for critically ill patients? (2)
- Adrenal suppression
- Hypotension
***Most studies show there is little evidence to support this though
What are the adverse effects of succinylcholine and subsequent relative contraindications?
- Hyperkalemia –> do not use in renal failure
- Increased intraocular pressure –> do not use in patients with open globe injury
- Malignant hyperthermia
- Rhabdomyolysis and myoglobinuria –> do not use in trauma or burns > 48 hrs after injury
- Neuromuscular disease
What is the onset and half life of:
- succinylcholine
- rocuronium
Succinylcholine:
- onset 15-30 secs
- duration: 5-15 minutes
Rocuronium:
- onset 30-60 secs
- duration: 30-45 mins
How do you reverse rocuronium?
Neostigimine
What is an alternative to neuromuscular blockade in RSI if contraindicated?
Propofol + Fentanyl may be just as effective in some studies
What medication choices for RSI would be appropriate for an infant with tracheomalacia, croup, severe stridor, previous difficult intubation?
Do NOT paralyze!
Propofol 3 mg/kg (rapid onset and offset) and topical lidocaine sprayed on the vocal cords
-this will allow you to bag
-will wear off quickly if difficult intubation
What medication choices for RSI are appropriate for a patient in status epilepticus?
Propofol - anti-epileptic properties
Succinylcholine - short acting
(caution with rocuronium as you may not be able to tell if they’re still seizing or not)
NOT KETAMINE
What are the most important steps in sepsis guidelines that affects mortality? (3)
- Need 20 cc/kg NS bolus within first 10 minutes
- Need 60 cc/kg NS bolus within first 60 minutes
- Need antibiotics in within first 60 minutes
Why does ketamine have minimal effect on blood pressure in sepsis?
Causes catecholamine surge to maintain blood pressure
-however, in children who are catecholamine deplete (severe sepsis), may still get hypotensive with ketamine since there are no catecholamines left
What are the indications for abdo CT in trauma patients?
- Seat belt sign
- Hx or mechanism suggestive or distracting injuries
- AST > 200 or ALT > 125
- Gross or microhematuria > 50 RBCs
- Decreasing HCT or HGB
What are the 3 components of abdominal compartment syndrome?
- Hypotension (from IVC compression)
- Respiratory distress (from increased intraabdominal pressure)
- Decreased urine output (from bladder compression and from hypotension)
How do you estimate ETT size?
(Age/4) + 4 CUFFED
How do you estimate a patient’s weight based on age?
(Age x 2) + 9
What are anatomical considerations in pediatric patients that influence effect of abdominal trauma? (4)
- Less fat and muscle for protection
- Flexible ribs = less likely to fracture but underlying structures can still be injured
- Multiple injuries more common since organs are in close proximity
- Increased risk for gastric distention (aspiration risk, can be mistaken for abdo distension as result of trauma)
In abdominal trauma, in general terms, which structures are more likely to be injured in a crush injury?
Midline structures since they are compressed against the spine
What are the 3 most commonly injured organs in abdominal blunt trauma?
- Spleen
- Liver
- Bowel
What is Waddell’s triad?
Pattern of injury when a child is struck by a car while crossing the street
- Fractured femur (impact from car)
- Head injury (thrown a distance and hit their head on ground)
- Intra-abdominal or intra-thoracic injury (thrown a distance)
What 4 organs are commonly injured in bike handlebar injury?
- Liver
- Spleen
- Pancreas
- Duodenal injury
What are contraindications to a foley catheter in a trauma? (4)
- Blood at the urethral meatus
- Pelvis injury (high risk for associated GU injury)
- Rectal injury
- High riding prostate
What are contraindications to CT scan in a trauma patient?
UNSTABLE or indication for emergent OR
-CT should NOT be used for screening; should be used for characterizing and staging of suspected injuries
What are the general management principles for a hemodynamically stable patient with:
- Lower penetrating chest wounds
- Anterior penetrating abdominal wounds
- Lower penetrating chest wound: serial chest exams, thoracoscopy, laparoscopy, CT scan to look for diaphragm injury
- Anterior penetrating abdo wound: FAST, wound exploration, DPL, serial exams, laparoscopy
****remember not to miss diaphragmatic injuries = commonly missed and never heal on their own leading to diaphragmatic herniation
What are indications for laparotomy in abdominal trauma? (4)
- Hemodynamically unstable patient with positive FAST or DPL
- Free air on AXR
- Peritonitis
- Positive CT scan
Which structures are commonly injured with pelvic fractures? (3)
- Urethra
- Bladder
- Rectum
***ALWAYS do a GU/rectal/vaginal exam in these patients
What are the reversal agents for the following:
- benzos
- non-depolarizing muscle blocking agents (ie. rocuronium)
- depolarizing muscle blocking agents (ie. succinylcholine)
- Benzos: flumazenil (gaba receptor antagonist)
- rocuronium: neostigmine (acetylcholinesterase inhibitor)
- succinylcholine: no reversal agent, just TIME
What are the management steps in TBI?
Maintain normal:
- O2 sats
- PCO2 (35-40)
- BP (>5th percentile)
- Temp (no hyperthermia, do not cool)
Avoid:
- Hypoglycemia
- Seizures
**Treat elevated ICP + impending herniation with hyperosmolar therapy
What are 3 things that increase risk of mortality in TBI?
- Hypoxia
- Hypo or hypercarbia
- Hypotension
What is TBI management stps in PICU?
-what are indications for hyperventilation?
- ICP probe if 20 x 5 mins, then:
- give sedation
- muscle relax
- hyperosmolar therapy
- drain EVD if present
- elevate HOB
**Only hyperventilate (PCO2 25-30) if impending herniation (Cushing’s triad, blown pupil) = this is the fastest way to decrease ICP in a herniating patient
What is a normal ICP?
Criteria for pediatric brain death?
- Established etiology capable of causing neurological injury in absence of reversible conditions
- No confounders including: unresuscitated shock, hypothermia ( 60 mmHg AND rise > 20 mm Hg
- Ancillary tests: ONLY do this if cannot perform an element of clinical NDD (angiography [CT-angio] or nuclear med, NO MORE EEG IS ALLOWED)
What personnel can perform neurological determination of death?
Any licensed physician with the requisite knowledge and skill
-should be done by 2 physicians
What are side effects of ketamine? (6)
- Hypertension
- Tachycardia
- Amnesia
- Analgesia
- Bronchorrhea
- Bronchodilation
***causes endogenous release of catecholamines
-great for kids who are hemodynamically unstable
What is systemic vascular resistance in cold shock?
Increased!
Why do we need O2? (on a biochemical level)
Glycolysis = 2 ATP + pyruvate
-then pyruvate can either combine with O2 in Kreb’s cycle to make 32 ATP
OR
-pyruvate can under anaerobic metabolism and create lactate and only 2 ATP
-lactate = acidotic, cells don’t like acidosis and thus they stop working and they die
What are the characteristics of warm shock vs. cold shock?
Warm shock:
- vasodilators > vasoconstrictors
- warm, flash cap refill, wide pulse pressure, bounding pulses
- shock because of low preload and loss of autoregulation
Cold shock:
- vasoconstrictors > vasodilators
- cold, poor pulses, prolonged cap refill, narrow pulse pressure
- shock because of myocardial depression + increased afterload (possible effect of endotoxin on myocardium)
What are the definitions of:
- SIRS
- Sepsis
- Severe sepsis
- Septic shock
SIRS: 2+ hyper/hypothermia, increased heart rate and/or RR, low or high WBC
- sepsis = SIRS + presumed infection
- severe sepsis = sepsis + organ dysfunction
- septic shock = sepsis + refractory hypotension
What are the effects of epinephrine in shock?
- low dose
- high dose
Epinephrine:
- low dose: decreases alpha 1, increases beta 1, beta 2, decreases SVR (reduces vasoconstriction)
- high dose: alpha 1, beta 1, beta 2, increases SVR
Causes of cardiogenic shock? (5)
- signs/symptoms?
- investigations?
- treatment?
- Cardiomyopathy
- Viral myocarditis
- Post bypass
- Coronary artery anomalies
- Arrhythmias
- signs and symptoms: cold shock, poor perfusion, heart failure
- investigations: CXR, EKG, 4 limb BPs, ABG, lytes, lactate, echo
- treatment: - Increase oxygen delivery (fluid and or lasix, afterload reduction, inotropic support with milrinone for ex)
- Decrease oxygen demand (positive pressure ventilation, sedation, etc)
What are signs of neurogenic shock?
Spinal cord injury at level of sympathetic chain (T1 to L2)
- loss of sympathetic output to heart, vessels, etc.
- signs: inappropriately normal HR in hypotension
What is the management for shockable rhythm (ie. VT/VF)?
Shock as SOON as you can with 2J/kg –> then CPR x 2 mins, then shock again at 4 J/kg if able + epi –> CPR x 2 mins, recheck rhythm and pulse q2mins, epi q3-5mins
- coordinate 15:2 if no advanced airway, no need to coordinate once intubated
- epi dose = 0.01 mg/kg 1:10000 IV
***Remember that CPR is your first priority, THEN defibrillation, then epi is your last resort (don’t have great evidence about whether it helps or not)
What are 3 things you can tell the team to ensure good quality CPR?
- Compress 1/3 of AP diameter of chest
- Aim for 100 compressions/min
- Allow complete recoil
- Minimize interruptions
- No leaning (stool if needed)
- Change CPR providers q2min
What is the treatment for ventricular tachycardia?
- stable?
- unstable?
- Stable: call cardio and may start amio, lidocaine, etc.
- Unstable = refer to pulseless arrest (shock + CPR)
When would you consider an epinephrine infusion in anaphylaxis?
After 3 doses of epi IM needed
What are the 2 divisions of the lung?
Conducting zone = rigid passageways from oropharynx to terminal bronchioles = physiologic dead space
-respiratory zone = from respiratory bronchioles and alveoli = sites of gas exchange
What are the equations for oxygenation and ventilation?
Oxygenation: PaO2 = [(Atm - humidity) x FiO2] - (CO2/0.8)
ie. [(760-47) x 0.21] - (CO2/0.8)
-ventilation: RR x TV
(this is minute ventilation)
What are the 3 causes of hypercapnea?
- Hypoventilation (eg. CCHS, drugs)
- Obstructive lung disease (eg. asthma, OSA)
- Neuromuscular disease (low tidal volumes)
Cs of confirmation of intubation
- Clinical by auscultation
- Clinical by direct laryngoscopy
- CO2 detected
- CXR
- Condensation in the ETT
Burns
1, Remove clothes and other exposures
2. ABCDEs (100% FiO2) + rapid trauma assessment ALWAYS (increased risk of having secondary trauma)
3. Wash burns with tepid water, flush chemical burns, cool minor burns with cool saline
4. Estimate %BSA involved with partial/full thickness
5. If > 10%, then at risk for SIRS response and fluid resuscitate with:
Parkland formula = 4 cc/kg/% BSA + maintenance crystalloid (1/2 in first 8 h, 1/2 in 16 h)
-monitor urine output with foley
What are risk factors for airway involvement in burns?
- Closed space
- Any respiratory distress
- Singed hairs
- Soot around face
- Burns involving steam/combustibles, etc
- Carbanaceous sputum
What are the clinical features of organophosphate toxicity?
- pathophysiology?
- treatment and 2 antidotes?
Think DUMBBELS (tells you effects at muscarinic receptors)
Diarrhea
Urination
Miosis
Bradycardia
Bronchospasm/bronchorrhea
Emesis
Lacrimation
Salivation
-at nicotinic receptors: muscle weakness, fasciculations and eventually paralysis, delirium
=these are all cholinergic symptoms (ie. the opposite of anticholinergic signs)
Pathophysiology:
-organophosphates bind to and inhibit the action of acetylcholinesterase THUS nothing to break down acetylcholine at the NMJ (muscarinic receptors) so you can a lot of parasympathetic activation
Treatment:
- Basic decontamination = washing all exposed skin with soap and water and immediately removing all exposed clothing
- Supportive care with intubation if decreased LOC/risk of aspiration
Antidotes for treatment:
- Atropine boluses or continuous infusion = competitive antagonist for muscarinic receptors so less acetylcholine can bind to the receptors; target to resolve respiratory secretions
- controversial whether you should give activated charcoal if ingested insecticides - Pralidoxime: breaks the bond between the organophosphate and the enzyme reactivating acetylchoinesterase (only effective if used before bond ages and becomes permanent)
What is the action of neostigmine?
Acetylcholinesterase inhibitor = thus increases acetylcholine action at the muscarinic receptors
How can pupillary findings assist in the diagnosis of toxic ingestions?
- miosis? (5)
- mydriasis? (2)
- nystagmus? (3)
Miosis:
- opioids
- organophosphates
- clonidine
- barbiturates
- ethanol
Mydriasis:
- anticholinergics (atropine, antihistamines, TCAs)
- sympathomimetics (amphetamines, caffeine, cocaine, LSD, nicotine)
Nystagmus:
- Ketamine
- Phenytoin
- Barbiturates
- PCP (think darting eyes)
What are 2 commonly used insecticides?
- how do they differ in action and clinical features?
- antidotes?
- Organophosphates
- bind irreversibly to acetylcholinesterase if left untreated and permanently inactivates the enzyme (known as AGING)
- takes weeks to months to regenerate inactivated enzymes - Carbamates
- form temporary bond only, allows reactivation of acetylcholinesterase within 24 hrs
Antidotes:
- Atropine (competitive antagonist of muscarinic receptors)
- Pralidoxime (reverses binding of organophosphate to acetylcholinesterase)
- not needed in carbamate poisoning since the bond degrades spontaneously
What is the dose for chloral hydrate?
-possible side effects?
20-75 mg/kg/dose 60 minutes prior to procedure
-side effects: possible resp depression, unreliable absorption, unreliable in children > 3 yo
What are advantages of ketamine over other sedatives?
-side effects?
- Maintains upper airway muscle tone and does not cause resp depression (maintains spontaneous breathing)
- Does NOT cause hypotension = causes endogenous catecholamine release so maintain blood pressure and heart rate
- Provides sedation, analgesia, amnesia all at once
- Rapid onset and short duration of action
Side effects:
- Increased secretions
- Post-sedative vomiting
- Hypertension
- Unpleasant hallucinations
- Laryngospasm (rare)
What are the underlying cause of Reye syndrome?
- clinical features? (3)
- what is ONE distinguishing feature that helps you differentiate between Reye syndrome vs. liver failure?
- treatment?
Precipitated in a genetically susceptible person by the interaction of a viral infection (influenza and varicella) and ASA use = secondary mitochondrial hepatopathy
Clinical features: overall, acute onset of vomiting and encephalopathy
- Neurologic symptoms: can progress to seizures, coma and death
- Liver dysfunction (coagulopathy, transaminitis, hyperammonemia) BUT NORMAL SERUM BILIRUBIN LEVELS (unlike in liver failure)
- Increased intracranial pressure and resultant herniation = very important contributor to morbidity and mortality
Treatment: no effective therapy except supportive care
-may need liver transplant
What are 3 types of electrical burns?
- Minor electrical burns (ie. result of biting an extension cord)
- High-tension electrical wire burn
- Lightning burn
Clinical features seen in minor electrical burns?
-treatment?
Usually from biting an electrical cord
- Localized burns to mouth
- Hospital admission is not necessary since these are nonconductive injuries (do not extend beyond site of injury)
- Treat with topical antibiotic cream until the patient can be seen by plastics
What are clinical features of high-tension electrical wire burns?
-treatment?
Clinical features:
- Deep muscle injury that cannot be readily assessed initially from high voltage = look for points of entry of current through the skin and exit site (usually current enters through upper extremity with exit through lower extremity onto the ground and injuries any organ or tissue in its path)
- Cardiac abnormalities: arrythmias, asystole
- Resp: resp arrest, aspiration
- Renal: acute renal failure from rhabdomyolysis and myoglobinuria
- Neurologic: motor paralysis, loss of consciousness
- Abdominal: viscus perforation and solid organ damage
- MSK: compartment syndrome from deep burns
Treatment goals: supportive basically with focus on AGGRESSIVE hydration in order to wash out the kidneys, ALWAYS admit for observation given you don’t know the extent of the injury, early debridement of wounds, tetanus prophylaxis
What are possible internal complications from lightning burns? (3)
- Cardiac arrest (asystole, PVCs, VF, MI)
- CNS: cerebral edema, hemorrhage, seizures
- Renal: rhabdomyolysis and renal failure
What is the most important complication of hydrocarbon toxicity?
-baseline investigations (2)?
Aspiration pneumonitis due to inactivation of type II pneumocytes and resulting surfactant deficiency (aspiration occurs during coughing and gagging at time of ingestion or vomiting after ingestion)
-baseline investigation: blood gas and CXR, monitor for 6 hours
How does the viscosity of a hydrocarbon determine risk of aspiration pneumonitis?
The LESS viscous, the MORE chance of aspiration pneumonia (think that if it’s thin, it can spread out more in the lungs to cover larger surface area)
-ie. gasoline, lamp oil, kerosene
What is “sudden sniffing death?”
-treatment?
Volatile hydrocarbons that are commonly abused by inhalation (ie. halogenated ones) can sensitize the myocardium to the effects of endogenous catecholamines = increased risk of Vtach and Vfib (usually refractory to conventional management)
Treatment: still follow PALS algorithm but consider treatment with beta blocker to block effects of endogenous catecholamines on sensitized myocardium
What is the treatment of hydrocarbon ingestion?
- main complication of hydrocarbon ingestion?
- main complication of hydrocarbon inhalation?
Observation and supportive care for respiratory symptoms!!!
- emesis and lavage are CONTRAINDICATED given the risk of aspiration
- activated charcoal is NOT useful because it does not bind the common hydrocarbons and can also induce vomiting
- main complication of ingestion:
1. ARDS (some require intubation and ECMO) from aspiration pneumonitis - main complication of inhalation:
1. Arrhythmias and cardiac arrest
What are the antidotes for the following:
- acetaminophen
- anticholinergics
- benzos
- beta-blockers
- calcium channel blockers
- ethylene glycol/methanol
- iron
- methemoglobinemia
- organophosphates
- salicylates
- sulfonylureas
- TCAs
A.
- acetaminophen: N-acetylcysteine
- anticholinergics: neostigmine or physostigmine
- benzos: flumazenil
- beta blockers: glucagon
- calcium channel blockers: insulin and calcium salts
- ethylene glycol/methanol
- iron: deferoxamine
- methemoglobinemia: methylene blue
- organophosphates: atropine & pralidoxime
- salicylates: sodium bicarb
- sulfonylureas: octreotide
- TCAs: sodium bicarb
- acetaminophen: N-acetylcysteine
- anticholinergics: neostigmine or physostigmine
- benzos: flumazenil
- beta blockers: glucagon
- calcium channel blockers: insulin and calcium salts
- ethylene glycol/methanol
- iron: deferoxamine
- methemoglobinemia: methylene blue
- organophosphates: atropine & pralidoxime
- salicylates: sodium bicarb
- sulfonylureas: octreotide
- TCAs: sodium bicarb
What are methods of GI decontamination after ingestions? (4)
-Which two are the only ones likely to have significant clinical benefit in management of poisoned patient?
- Activated charcoal
- Whole bowel irrigation
(THESE ARE THE ONLY TWO THAT ARE RECOMMENDED FOR USE) - Gastric lavage
- Syrup of ipecac to induce vomiting
Is activated charcoal recommended for use in poisonings?
- how does it work?
- when should it be given?
- contraindications? (10)
YES!!! Thought to be potentially the most useful
- activated by heat and creates network of pores that have large absorptive area, thus adsorbing toxins onto its surface and preventing absorption from GI tract
- should be given within 1 hr of ingestion!!!!!
- can cause vomiting
Contraindications: CHEMICAL CamP
Cyanide
Hydrocarbons
Ethanol
Metals
Iron
Caustics
Airway unprotected
Lithium
Camphor
Potassium
What is the dose of activated charcoal?
-common side effects? (2)
1 g/kg in children and 50-100 g in adolescents and adults
- common side effects:
1. vomiting (20%)
2. constipation
What is whole bowel irrigation?
-what are the usual indications? (3)
Whole bowel irrigation: instill large volumes through NG tube (35 ml/kg/hr in children or 1-2 L/hr in adolescents) of GoLYTELY to cleanse the entire GI tract until rectal effluent runs clear
- indications:
1. For slowly absorbed substances (sustained release preparations)
2. Substances not well absorbed by charcoal
3. Drug packets (ie. heroin or cocaine)
What fractures should raise suspicion of child abuse? (5)
- Spiral fractures
- Posterior rib fractures
- Spinal fractures
- Metaphyseal fractures
- Femoral fractures in non mobile child
- Scapular fractures
Up to what age should a skeletal survey be ordered?
Up to age of 2 years (yield is lower after that)
What are clinical features of osteogenesis imperfecta? (5)
- Blue sclera
- Wormian bones (extra bones in between sutures)
- Dentinogenesis imperfecta (poorly developed, discolored teeth)
- Hearing loss
- And of course, frequent fractures with little force
After initial ED visit for sexual assault, what follow-up care should be offered to the patient? (4)
- Supportive counselling
- HIV follow up and counselling with ID/HIV team in 3-5 days
- Follow up gyne exam in 1-2 wks
- Repeat serologic tests for syphilis and HIV in 6 wks, 3 mo and 6 mo
What 4 infections are diagnostic for sexual abuse in a non-sexually active child?
- HIV
- Syphilis
- Gonorrhea
- Chlamydia
(other infections such as trichomonas, condyloma acuminata, herpes, BV is less clear)
What is the most common physical finding in sexual abuse?
Normal examination
What organ systems are affected in patients suffering from heat stroke?
- CNS: confusion, seizures, LOC
- Cardiac: hypotension due to hypovolemia and peripheral vasodilation, myocardial dysfunction
- Renal: ATN and renal failure from hypoperfusion
- Hepatocellular injury
- Heme: abnormal hemostasis (DIC usually)
- Muscle: rhabdomyolysis from high temp
What bloodwork should be ordered for a patient in a housefire?
- CBC: look for signs of bleeding
- Lytes: look for hyperkalemia
- Renal function to rule out renal failure
- BLOOD CARBOXYHEMOGLOBIN (HbCO = rule out carbon monoxide poisoning)
- Gas
- Urinalysis for myoglobin
What is the criteria for transfer to burn centre? (8)
- Partial thickness and full thickness burns of greater than 10% BSA
- Partial thickness and full thickness burns involving face, eyes, ears, hands, feet, genitalia, joints
- Full thickness burns of any size in any age group
- Significant electrical burns
- Burns suspicious for abuse
- Significant chemical burns
- Inhalation injury
- Burn injury in patients with preexisting illness that could complicate treatment
Why are alkali burns worse than acid burns in the eye?
Alkali = causes liquefactive necrosis (eats through tissue leaving more extensive injury) whereas acid = coagulation necrosis (buffered by tissue and limited penetration)
What lacerations should not be sutured? (4)
- Puncture wounds
- Mucosal surface lacerations (mouth, vagina)
- Contaminated wounds that cannot be reliably cleaned
- Human bites
****Some authorities recommend that wounds > 12 hrs on arms and legs and > 24 hrs on face should not be sutured and left to heal by secondary intention
What are key questions to ask on history for a patient coming in with an animal bite?
- Circumstances surrounding the bite
- type of animal (domestic or wild)
- provoked or unprovoked
- immunization status of child (tetanus) and animal (rabies)
When should you consider ordering an xray in a patient presenting with an animal bite? (2)
- Penetrating injury over bone or joint for suspected fracture
- Foreign body inoculation
Which animal bites are most likely to become infected? (2)
-which should be cultured? (cat? human? dog?)
- Human bites (regardless of mechanism of injury, ie. bite vs. closed fist against tooth) = high risk of infection, especially anaerobes
- Cat bites = at least 50% even if early medical attention is received
Thus need to culture ALL cat and human bites!
-culture dog bite IF deep and extensive, > 8 hrs old, early signs of infection, or immunosuppresed patient
What are risk factors for infection after an animal bite? (7)
- Immunocompromised patient
- Crush or deep puncture wounds
- Delay in treatment > 24 hrs
- Human and cat bites
- Bites on hand, foot, genitals
- Perforation of bone or tendons
- Presence of foreign material
Which microorganisms are associated with bites:
- dog?
- cat
Dog: staph, strep, pasteurella, capnocytophaga, anaerobes
Cat: pasteurella (higher carriage in cats than dogs), staph, strep
What is the initial management of ALL animal bites?
-what about hand bites?
- If needed, obtain culture
- Apply local anesthetic
- Clean and vigorously irrigate with copious amounts of normal saline
-no evidence for antibiotic containing solutions over saline and can actually cause local irritation - Debride devitalized tissue
- MAY be able to do primary closure on facial bite wounds 24 hrs old
***Hand bites: all need to be immobilized until follow up assessment 3 days later
Which animal bites require operative debridement and exploration? (3)
- Cranial bites by large animal
- Closed fist injury (involvement of metacarpophalangeal joint aka knuckle)
- extensive wounds with a lot of devitalized tissue
What are the indications for antibiotic therapy in a patient presenting with a bite? (7)
- oral vs. IV?
- first choice for abx coverage?
- Moderate or severe bite wounds (especially if edema or crush injury present)
- Puncture wounds (especially if penetration of bone, tendon or joint)
- Facial bites
- Hand and foot bites
- Genital area bites
- Wounds in immunocompromised
- Wounds with signs of infection
- All human and cat bites (dog = controversial)
***Oral vs. IV depends on the wound, signs of infection, and immune status
1st line: PO amoxi-clav for empirical therapy or IV ampicillin/sulbactam
(do NOT use first gen cephalosporins since they don’t have good coverage for oral microbes)
-if pen allergic: azithromycin
Which patients require tetanus after an animal bite?
ALL patients who are incompletely immunized or if it’s been longer than 10 years since last immunization
-tetanus immunization schedule: 2, 4, 6, 18 mo, 4 yo and q10 years after that
What emergency drugs can be given through an ETT? (5)
LEAN-V
- Lidocaine
- Epinephrine
- Atropine
- Naloxone
- Vasopressin
**Epi = 10x IV dose
**other meds = 2x IV dose
-need to follow administration with a 5 ml NS flush and PPV to bag it in
What are 4 contraindications to the use of an IO?
- Placement in fractured bone
- Placement through dirty or infected skin
- Use in patients with bone disorders (osteopetrosis or osteogenesis imperfecta)
- Repeat attempt into the same bone
What are possible complications of IOs? (4)
- Extravasation of fluid
- Superficial skin infection
- Osteomyelitis (rare)
- Theoretical risk for bone growth arrest, fat embolism but these have not been reported
What are the 6 Hs and 4 Ts?
- Hydrogen ion
- Hypoglycemia
- Hypovolemia
- Hyper/hypokalemia
- Hypothermia
- Hypoxemia
- Toxins
- Tension pneumothorax
- Tamponade
- Thromboembolism
What are predictors for good outcome in pediatric cardiac arrest? (6)
- Initiation of prompt CPR
- Witnessed event
- Out of hospital arrest
- Short interval to EMS
- Short duration of CPR
- Initial rhythm of VT or VF
What two ingestions are treated with urinary alkalinization with sodium bicarb?
- TCA overdose
- Salicylate overdose
What ingestions are radioopaque on abdominal radiograph?
CHIPS
- Chloral hydrate
- Heavy metals (iron, lead, arsenic)
- Iodides
- Phenothiazines, psychotropics (TCAs)
- Slow release capsules (enteric coated tablets)
What are the key distinguishing clinical features of ingestion of the following:
- ethanol (triad)
- methanol
- isopropyl alcohol
- ethylene glycol
- Ethanol triad: hypoglycemia, hypothermia, coma
- methanol: severe metabolic acidosis and permanent retinal damage leading to blindness (due to formic acid formation = blocks mitochondria, thus metabolic acidosis)
- isopropyl alcohol: gastritis, hyperglycemia, hypotension
- ethylene glycol: severe metabolic acidosis, cranial nerve palsies and cause renal damage by precipitation of calcium oxalate crystals
What arterial blood gas pattern is classic for salicylate poisoning?
Metabolic acidosis with respiratory alkalosis!
- salicylates directly stimulate the medullary respiratory drive center causing tachypnea
- also cause lactic acidosis due to uncoupling of oxidative phosphorylation
What is water intoxication?
Swallowing lots of water and thus getting hyponatremia and secondary seizures
-can see in babies who go swimming and swallow a lot of water
What are the changes in your lungs during air transport? (2)
- Decreased pressure and thus increased gas expansion
- Decreased PaO2
What baseline investigations will you order for an ingestion?
- Glucose
- Lytes
- Renal Function
- LFTs
- EKG
- Serum osmolality
- Blood gas
- Urine tox screen
- Ethanol level
- Other alcohol levels
- Acetaminophen, salicylate level
What is the treatment for isopropyl alcohol ingestion?
Supportive care
What is oil of wintergreen?
A salicylate!!!
A patient presents with an ingestion but won’t tell you what they took and are asymptomatic. What is your management plan?
- Supportive management
- Observe 4-6 hours if asymptomatic
- if you do eventually find out what they took, need to figure out half life and observe for at least that long
A patient overdoses on cocaine is extremely agitated and a danger to himself and others. What immediate treatment would you start?
Benzos (used for agitation or hallucinations)
Which 4 organs are most commonly injured with blunt abdo trauma?
- Liver
- Spleen
- Kidneys
- Pancreas
OCCASIONALLY bowel (seatbelt injuries, handlebars)
Indications for laparotomy in abdo trauma?
- Persistent hemodynamic instability with evidence of abdo injury
- Penetrating injury to abdo
- Pneumoperitoneum
- Multisystem trauma and they need other OR procedures if evidence of abdo injury
What is the management of carbon monoxide poisoning?
Think about this in the winter time!!! May have CO leak in house while heat is on. Whole family may present with flu like symptoms, delayed neuropsychiatric syndrome (can happen up to weeks after poisoning)
1. Order carboxyhemoglobin level on blood gas
Treatment:
1. 100% oxygen until levels
What temperature should you rewarm to in resuscitation of a hypothermic patient?
34 degrees
What are the clinical features of lower abdominal lap belt injuries? (3)
- Bladder rupture
- Chance fracture: L1 & L2
- Bowel rupture
What are the indications for imaging prior to LP?
- Papilledema
- Focal neuro signs
- Decreased LOC or coma
What is the treatment for methanol overdose? (2)
- Fomepizole
- Folate
What are two coingestions you should ALWAYS check for in a patient with suspected ingestion?
Acetaminophen and salicylate
What is the treatment for cyanide toxicity?
- 100% oxygen
- You have two options:
a) Cyanide antidote kit:
- sodium nitrite (produces methemoglobin which then reacts with cyanide to form cyanmethemoglobin)
- sodium thiosulfate (increases metabolism of cyanmethemoglobin to hemoglobin and less toxic thiocyanate)
b) Hydroxocobalamin (vitamin B12) (reacts with cyanide to form nontoxic cyanocobalamin which is then excreted in urine) = superior to cyanide antidote kit so is now the preferred antidote
What are the clinical features of iron toxicity?
-toxic dose?
Think GI symptoms! Iron is directly corrosive to the GI mucosa:
- GI bleed from ulceration and perforation–> hematemesis, melena
- Hypotension: due to massive volume losses from increased permeability of capillaries
- Accumulation of iron in liver and heart = liver toxicity, cardiac dysfunction
- Anion gap metabolic acidosis due to hypotension and hypovolemia
- toxic dose: > 40 mg/kg
What are the 4 stages of iron toxicity?
- Initial stage: 30 min - 6 hr post ingestion
- profuse vomiting and bloody diarrhea
- volume losses - Second stage: 6-24 hrs post
- quiescent phase, GI symptoms resolve - 3rd stage: 12-24 hrs post
- multisystem organ failure, shock, hepatic and cardiac dysfunction, ARDS, metabolic acidosis
- death occurs most cmomonly during this stage - 4th stage: 4-6 wks post
- GI strictures and obstruction
What is the management of iron toxicity?
- Draw serum iron levels 4-6 hrs after ingestion along with gas, CBC, glucose, liver enzymes, LFTs
- AXR to look for iron tablets
- Monitor closely for hypotension with aggressive fluid support
- Whole bowel irrigation!!!! (remember that activated charcoal does NOT absorb iron)
- Deferoxamine for moderate to severe iron intoxication
- IV infusion at 15 mg/kg/hr until urine runs clear (deferoxamine iron complex colors urine red)
What is the antidote for lead toxicity?
2,3-dimercaptosuccinic acid
What are the clinical features of foxglove or lily of the valley poisoning?
CARDIAC effects! = nausea, vomiting, bradycardia, AV block, hyperkalemia
What is the definition of heat stroke vs. heat exhaustion?
Heat stroke: temp > 40 with neurologic symptoms
-heat exhaustion: T 38-40 without neurologic symptoms
What are ECG findings in a patient with hypothermia?
- J wave (pathognomonic) = after R wave, see a rounded bump (kind of like RSR’ but rounded contour)
- PR, QRS, QT elongation
Indications for dialysis? (5)
AEIOU
- Acidosis
- Electrolyte imbalance (hyperkalemia)
- Ingestion
- Overload (fluid)
- Uremia
What are side effects of lasix? (4)
- Hyponatremia
- Hypokalemia
- Nephrocalcinosis
- Metabolic alkalosis
What toxidrome does gravol cause?
Anticholinergic
What are the side effects of NSAID use in neonates? (ie. treatment of PDA)?
- Transient increase in GFR
- Platelet dysfunction
- Increased NEC (slight mesenteric vasoconstrictor = decreased blood flow to gut)
- Hypoglycemia
What are side effects of risperidone? (7)
- Acute dystonic reaction
- Neuroleptic malignant syndrome
- Diabetes
- Weight gain
- Seizures
- Hepatotoxicity
- Prolonged QT
What are the clinical features of increased ICP in an infant?
- Sunsetting sign
- Shrill cry
- Irritability
- Bulging AF
What is the management of a 13 yo who was just sexually assaulted?
- History and physical, document findings
- Report to CAS
- Pregnancy test and emergency contraception
- STI screen and prophylaxis
- Forensic kit if
What are 3 side effects of anthracyclines?
- Cardiomyopathy
- Red urine
- Myelosuppression
A patient has hypopigmented scar after minor trauma and vesicular rash in sun exposed areas. This is most likely due to which medication?
NSAIDs = pseudoporphyria
What cardiac medication taken during pregnancy increases risk of hypothyroidism in baby?
Amiodarone = has a lot of iodide in it!
-amiodide :)
What are the points in GCS?
EVM!!!!
Eyes:
1 - no eye opening
2 - eye opening to painful stimuli
3 - eye opening to verbal stimuli
4 - spontaneous eye opening
Verbal:
1 - none
2 -incomprehensible sounds
3 - incoherent words
4 - disoriented conversation
5 - normal conversation
Motor:
1 - None
2 - decerebrate posturing (extension)
3 - decorticate posturing (flexion)
4 - withdrawal to pain
5 - localizes pain
6 - follows commands/normal
What is the most common bacterial etiology of spontaneous bacterial peritonitis?
Strep pneumo!!!
What are the clinical features of serotonin syndrome?
SHIVERS
- Shivering
- Hyperreflexia
- Increased temperature (hyperthermia)
- Vitals: increased HR, RR, labile BP
- Encephalopathy (agitation, delirium, confusion)
- Restlessness
- Sweating
How much should TFI be increased by in order to ensure feed safety?
20-30 ml/kg/d –> if calculating this for oral feeds, divide by 8 for q3h feeds
What is the definition of polycythemia?
Hct > 65% or Hgb > 220
What are the differences between gastroschisis and omphalocele?
Omphalocele:
- midline
- protective cover (guts herniating through umblical cord)
- 25-40% have congenital anomalies (Beckwidth Wiedemann, Trisomy 13 & 18)
Gastroschisis:
- not midline (right sided most common)
- no protective cover (full thickness abdo wall defect)
- 10-15% have intestinal atresia
What is the Kleihauer-Betke test?
Tests mom for baby’s blood
- bleeding from the fetal into the maternal circulation (fetomaternal hemorrhage)
- put mom’s blood into some filter thing and it breaks down mom’s beta chains but not fetus’ gamma chains
What are the causes of apnea in:
- prems
- terms
- both
Prem:
- apnea of prematurity
- IVH
- eye exams
- PDA
- RDS
- anemia
Term:
- cerebral infarct
- polycythemia
Both:
- infection
- NEC
- cardiac
- asphyxia
- hypothermia
- aspiration
- seizure
Differential diagnosis for neonatal hematuria?
- Vascular: renal artery or venous thrombosis (common in infants of diabetic moms)
- both can be caused by umbilical catheterization - Coagulation disorder: vitamin K deficiency
- Renal:
- renal cortical necrosis
- neonatal glomerulonephritis (seen in maternal syphillis) - Trauma: birth, iatrogenic, perinatal asphyxia
- Infection
- Neoplasm
- Wilms
- Neuroblastoma
- Nephroblastoma
- Rhabdomyosarcoma
- Polycystic kidney disease
Complications seen in infants of diabetic mothers?
- Large for gestational age
- Hypoglycemia
- Congenital anomalies (neural tube, renal, cardiac malformations
- Polycythemia –> hyperbilirubinemia
- Shoulder dystocia/birth trauma
- Renal vein thrombosis
- Hypocalcemia
- Hypomagnesemia
- Congenital anomalies (neural tube, renal, cardiac malformations
What are prenatal signs of TEF (3)?
- Frequent fetal hiccups
- Polyhydramnios
- Microgastria
What is the most common type of TEF?
-second most common?
Think from most common to least common: CAE-BD (It’s CAE’S BIRTHDAY!)
C (85%) = Esophageal atresia with distal TEF
-on CXR after insertion of NG tube, will see coiling
-esophageal atresia
-distal tracheoesophageal fistula
-gastric distension
-respiratory distress/aspiration secondary to GERD
Second most common: type A (9%) = isolated esophageal Atresia (think A for ATRESIA!)
- esophageal atresia without tracheoesophageal fistula
- no gas in abdomen
- scaphoid abdomen
Third most common: type E (6%) = isolated TEF (no esophageal atresia)
- presents later in life
- recurrent pneumonias/persistent cough due to aspiration
Fourth most common: type B (1%) = Proximal TEF with esophageal atresia
Fifth most common: Type D (!) = Double TEF with esophageal atresia (tracheoesophageal fistula between proximal and distal esophageal ends)
(Esophageal atresia: presents in neonate because they can’t eat and the food comes back up!)
What are the risk factors for neonatal polycythemia? (10)
- IDM
- SGA
- Graves disease
- Neonatal hypothyroidism
- Maternal hypertension
- Postmature
- Recipient of twin-twin transfusion
- Delayed cord clamping
- Beckwith-Wiedemann syndrome
- Trisomy 13, 18, 21
What are the clinical manifestations of neonatal polycythemia? (8)
What are the complications of neonatal polycythemia? (6)
***Many affected infants are asymptomatic
***Symptoms and complications secondary to stasis and hyperviscosity in vasculature
Clinical manifestations:
- Irritability
- Lethargy
- Poor feeding
- Hypoglycemia
- Hyperbilirubinemia
- Thrombocytopenia
- Respiratory distress
- Cyanosis
Complications:
- Seizures
- Stroke
- Renal failure
- Renal vein thrombosis
- Pulmonary hypertension
- Necrotizing enterocolitis
What are the indications for partial exchange transfusion in neonatal polycythemia?
Should be considered if:
- Hct > 70-75%
- S/S of hyperviscosity
In partial exchange transfusion for neonatal polycythemia, what is the formula for volume to be exchanged?
Volume of exchange (ml) = blood volume x (Observed-desired hematocrit)/observed hematocrit
***withdraw the blood slowly and replace with crystalloid (NS)
Describe the hyperoxic test.
Arterial gas is obtainedi n the right radial artery prior to placing the patient on 100% O2 via oxygen hood or I&V. Leave 100% O2 on for 10 minutes. Then repeat the art gas.
- PaO2 > 150 post hyperoxic test: pulmonary disease
- PaO2
What are the side effects of PGE1 (6)?
- Apnea
- Hypotension
- Fever
- Bradycardia or tachycardia
- Seizures
- Cutaneous flushing
What is the cause of hemolytic disease of the newborn aka erythroblastosis fetalis?
Rh incompatibility: pre-natal transplacental passage of maternal IgG antibodies active against paternal RBC Rh antigens on the fetus’ RBC
ABO incompatability: post-natal destruction of fetal RBCs by maternal IgM antibodies
What is RhoGAM?
Rho (D) immunoglobulin: IgG anti-D antibodies
-given to Rh negative mothers at approxiamtely 28 weeks and the Rho (D) immunoglobulin will remove any anti-D positive fetal RBCs before the maternal immune system can respond to them (prevents maternal sensitization)
During what events can maternal sensitization occur in hemolytic disease of the newborn caused by Rh incompatibility?
- Blood transfusion: if Rh-positive blood is infused into an Rh-negative woman through error
- During pregnancy: when fetal blood enters mom’s circulation through spontaneous or induced abortion
- At delivery: fetal blood enter’s mom’s circulation
Why is hemolytic disease of the newborn caused by Rh incompatibility worse in subsequent pregnancies?
In first pregnancy, usually the mother is exposed to fetal blood during delivery. Initially IgM antibodies are produced which are then later replaced by IgG antibodies over time (baby has already been delivered at this point). In subsequent pregnancies, smaller amounts of antigen can stimulate IgG production which can then cross the placenta and cause hemolytic disease in subsequent pregnancies
-this is why RhoGAM should be given to Rh negative moms at 28 weeks and also immediately post-partum
What are the complications of hemolytic disease of the newborn caused by Rh incompatibility? (4)
- Severe anemia –> heart failure –> hydrops fetalis
- Extramedullary hematopoiesis: hepatosplenomegaly
- Bone marrow hyperplasia with increased erythropoiesis and subsequently, thrombocytopenia
- Severe hyperbilirubinemia (within 1st day of life)
What lab test is the best predictor of severity of hemolytic disease of the newborn caused by Rh incompatibility of the newborn at delivery?
Cord blood bilirubin level: indicates severity of hemolysis in utero
- Cord blood Hgb is less reliable since it can be normal if baby has compensatory bone marrow and extramedullary hematopoiesis
- Mom’s anti-Rh titers correlate poorly to severity of disease
Describe the steps in antenatal diagnosis of hemolytic disease of the newborn caused by Rh incompatbility.
- Determine whether mom is Rh-negative or Rh-positive.
- If Rh-negative, take history of previous transfusions, abortion or pregnancies
- Test dad’s blood type to check for incompatibility
- Measure maternal titer of IgG antibodies to D antigen at 12-16, 28-32, 36 wks of gestation
- presence of elevated antibody titers at the beginning of pregnancy, rapidly rising titers or titer of 1:64 or greater suggests significant hemolytic disease
What antenatal monitoring should occur for Rh negative mothers found to have Rh positive fetus?
If IgG antibodies to D antigen is found at a titer of 1:16 or more, monitor by Doppler US of middle cerebral artery flow, real time US for signs of hydrops and then percutaneous umbilical blood sampling if needed.
What is the antenatal treatment for hemolytic disease of the newborn secondary to Rh incompatibility?
-indications?
In utero transfusion of PRBCs through the umbilical vein
- maternal/fetal sedation with diazepam and fetal paralysis with pancuronium
- may need to be repeated every 3-5 wks
- indications:
1. Hydrops
2. Fetal anemia (Hct
What is the postnatal treatment for hemolytic disease of the newborn secondary to Rh incompatibility?
- . Resuscitation if severe hemolytic anemia is present
- IVIG
- May require exchange transfusion if severe hyperbilirubinemia
What is the cause of the classic form of galactosemia?
Galactose-1-phosphate uridyl transferase deficiency (GALT)
- enzyme responsible for metabolizing galactose-1-phosphate
- autosomal recessive
- without this enzyme, galactose-1-phosphate accumulates and causes injury to kidney, liver and brain
What is the dietary source of galactose?
-when do infants with classic galactosemia typicaly present and why?
Milk and dairy products - lactose is converted to glucose & galactose in our bodies!
-infants with classic galactosemia present usually within the 1st week of life since they are receiving high amounts of lactose through breast milk or formula
What are the clinical features of galactosemia?
- acute (7)
- if untreated, chronic complications? (5)
Newborn or young infant with:
- Jaundice
- Hepatomegaly
- Vomiting
- Hypoglycemia
- Seizures
- Lethargy/poor feeding
- E coli sepsis (thought to be secondary to phagocytic and neutrophil dysfunction due to impaired glycolysis secondary to galactosemia)
Later in infancy or childhood if untreated:
- Mental disability
- Cataracts
- Renal failure
- Vitreous hemorrhage
- Hypergonadotrophic hypogonadism
***Galactose-1-phosphate accumulates in liver, brain and kidney!
What are the diagnostic tests for galactosemia (2)?
- Urine for reducing substances: galactosuria is present
- Direct enzyme assay for GALT in RBCs - will be deficient
What is the treatment for galactosemia?
Elimination of galactose from the diet
- galactosemia is a contraindication for breastfeeding
- will need lactose free formulas
What are the acute issues seen in babies born with maternal heroine use?
- Respiratory depression
- RDS
- Lower birth weight
- Jaundice
What are the 3 main categories of neonatal coagulopathy?
-what are the 3 forms of hemorrhagic disease of the newborn?
- Hemorrhagic disease of the newborn: secondary to vitamin K deficiency
- early form (within 1st 24 hrs): maternal meds affecting vitamin K levels
1. Phenytoin
2. Isoniazid
3. Rifampin
4. Barbituates
5. Warfarin - classic form (DOL 2-7): vitamin K injection not given at birth
- late form (weeks 2-6): decreased vitamin K intake secondary to breastfeeding or hepatobiliary disease
2. Congenital coagulopathy: bleeding in deep tissues - hemophilia A or B
3. DIC: bleeding everywhere - decreased fibrinogen
- increased PTT
- increased INR
- decreased platelets
What maternal meds may lead to early hemorrhagic disease of the newborn? (5)
- Phenytoin
- Isoniazid
- Rifampin
- Barbituates
- Warfarin
What are the causes of neonatal DIC?
- maternal (2)
- infant (4)
Maternal
- Eclampsia
- Placental abruption
Infant:
- Sepsis
- Asphyxia
- Severe acidosis
- NEC
How long does it take umbilical cord to slough off?
2 weeks
-worry if it takes longer than 1 month since it might indicate neutrophil chemostatic defects
What is 2 vessel umbilical cord associated with? (4)
- Renal abnormalities
- Congenital malformations
- IUGR
- Trisomy 18
What are the recommendations for safe sleep practices (7)?
- Sleep in a crib that meets government standards
- Crib in parent’s room for 6 months
- room sharing protects against SIDS - Back to sleep
- No heavy blankets, toys, etc. Can have thin blanket and baby can be in a sleeper
- Decreased second hand smoke
- Baby should not be in a non-crib surface (water bed, couch)
- In hospital, baby and mom should not share a bed
What are the risk factors for contracting RSV bronchiolitis? (8)
- Prematurity
- Less than 2 years old with cardiac issues
- Second hand smoke
- Underlying lung pathology
- IUGR/SGA
What are the etiologies of polyhydramnios? (5)
- GI obstruction: esophageal, duodenal, intestinal obstruction
- Hypotonia (difficulty with swallowing): anencephaly, neural tube defects
- GDM
- Non-immune fetal hydrops
- Idiopathic (most common)
- Bartter syndrome
What is Bartter syndrome?
-clinical features
Chloride channel abnormality
- polyuria, hypokalemia, hyponatremia, hypercalcemia
- often presents with seizures secondary to hyponatremia
What are the indications for exchange transfusion? (4)
- Severe hyperbilirubinemia
- Hemolytic disease of the newborn
- Polycythemia
- Hyperkalemia
What are the side effects of exchange transfusion? (6)
- NEC
- Death
- Hyperkalemia
- Infection
- Thrombosis/air embolism
- Volume overload
Distinguish between G6PD, alpha, and beta thalassemia in terms of clinical presentation
G6PD: presents at 1 week
Alpha thalassema: presents at birth with hydrops and death in neonate
Beta thalassemia: presents at 2-3 months
How is G6PD inherited?
X-linked recessive
What is Erb palsy?
-associated complication?
C5-C6 nerve palsy: waiter’s tip
- assymetric moro
- palmar grasp present
- shoulder won’t move but hand can move
- associated complication: 5% can ipsilateral diaphragmatic paralysis (C5 keeps you alive)
What is Klumpke’s palsy?
-associated complication?
C8-T1 nerve palsy: Klumpke’s Klaw
-associated complication: 33% have Horner’s syndrome
How do you treat brachial plexus palsy?
Immobilize x 7-10 days, then physiotherapy for mobilization
What are favorable prognostic signs for brachial plexus palsy?
- Recovery within 2 wks
- Only involvement of proximal upper extremity
What percentage of babies with brachial plexus will have residual deficits?
20-30%
What is the most common cause of neonatal conjugated hyperbilirubinemia?
Neonatal hepatitis
What are the causes of conjugated hyperbilirubinemia? (8)
**Top 3 most common:
- Biliary atresia
- Cholestasis
- Alagille
- congenital - Idiopathic neonatal hepatitis
- Choledochal cyst
- Infections
- TPN
- Galactosemia
- Alpha-1-antitrypsin
What is the pathophysiology of congenital lobar emphysema?
-what are the CXR findings?
unilateral enlargement due to accumulation of air and/or fluid
- valve effect, hyperexpansion and air trapping
- left upper lobe most commonly affected
- on CXR: hyperlucency, hyperinflation of one lobe with mediastinal shift and compression of remaining lung
What are the 4 categories of lung bud abnormalities?
- Congenital lobal emphysema
- Congenital pulmonary adenomatoid malformation (CPAM) (used to be known as CCAM)
- Pulmonary sequestration
- Bronchogenic cyst
What is the pathophysiology of CPAM?
-CXR findings?
Congenital pulmonary adenomatoid malformation
- Proliferation of bronchiole structures but no alveoli
- a bunch of cysts of lung tissue that communicates with tracheobronchial tree
- CXR findings: cysts (white)
What is the pathophysiology of pulmonary sequestration?
- CXR findings?
- most common location?
Lung tissue not connected to bronchi and trachea
- blood supply is from systemic circulation and not pulmonary circulation
- most common location: left costophrenic sulcus
What is the major complication of subcutaneous fat necrosis?
Hypercalcemia
Differentiate between jiterriness and seizures.
Eye movements:
- normal in jitteriness
- horizontal deviation, nystagmus and staring and blinking in seizures
Movement:
- fine movements in jitteriness
- coarse movements in seizures
Able to stop movements:
- yes in jitteriness
- no in seizures
How long does erythema toxicum last for? What do the papules contain?
-what about pustular melanosis? What do the pustules contain?
Erythema toxicum = develops 1-3 d after birth, lasts up to 1 week, contains eosinophils
Pustular melanosis = present at birth, lasts 2-3 d, contains neutrophils
What are some conditions associated with a large anterior fontanelle?
- Hypothyroidism
- Apert syndrome
- Trisomy 13, 18, 21
- Hydrocephaly
- Osteogenesis imperfecta
Where is the position of a cephalohematoma vs. subgaleal hematoma vs. caput?
- Cephalohematoma: subperiosteal hemorrhage (doesn’t cross suture lines)
- Subgaleal: collection of blood BELOW the aponeurosis that covers the scalp and the entire length of the occipito-frontalis muscle = can lead to extensive bleeding, develop a consumptive coagulopathy leading to hypotension
- Caput: soft tissue swelling of the scalp (crosses suture lines)
What is Mobius syndrome?
Absence of hypoplasia of the facial nerve leading to symmetrical facial palsy
if retinal hemorrhages occur during delivery from instrumentation or C-section, when should they resolve by?
5% resolve by 2 weeks, they should ALL resolve by 4 weeks
What is the management of gastroschisis?
- Temperature monitoring since can lose heat from exposed bowel
- NG decompression
- Surgical intervention ASAP
- IV fluids
- Protective covering and keep bowels in right lateral position to protect kinking of bowel until surgical repair
- NPO = TPN
- Broad spectrum antibiotic coverage
What are the main differences between breast milk and cow’s milk? (5)
Breast milk:
- Lower protein content
- Greater whey:casein ratio (70:30 as opposed to 60:40)
- Higher fat content (30-50% compared to 3-4%)
- Richer in Vitamins A, C, E; lower in Vitamins D and K
- Lower iron but better absorption
What is the calculation for determining umbilical catheter length?
- UVC
- UAC
UVC: (3 x wt in kg) + 9
UAC: (0.5 x UVC insertion depth) + 1
What are the increased risks of twin pregnancies? (8)
- Prematurity
- Growth restriction
- Spontaneous abortion
- Placental abnormalities (abruption, previa)
- Increased perinatal mortality
- Birth asphyxia
- Fetal malposition
- Polyhydramnios
If maternal drug abuse is suspected, which specimen from the infant is most accurate for detecting exposure?
Meconium = greater sensitivity than urine with positive findings persisting longer
-contains metabolites gathered over as much as 20 weeks (as opposed to urine with more recent exposure)
What is the best way to assess gestational age in the fetus?
***Historically Nagele’s rule is the best way: 1st day of last menstrual period
If this is not available:
- before 12 weeks gestation: crown-rump length on US
- beyond 12 weeks: biparietal diameter on US
What are the 5 components of the biophysical profile?
- Fetal breathing movements
- Gross movements
- Amniotic fluid level
- Fetal HR
- Fetal tone
***2 points each for possible total of 10 points
At what gestational age does pupillary reaction to light develop?
As early as 29 weeks but not consistently present until 32 weeks
When do premature infants “catch up” on growth charts?
Most catch up growth occurs during the 1st 2 years of life with most catching up by 3 years of age
What are risk factors for NEC in preterm infants? (5)
-one protective risk factor against NEC?
- Prematurity
- Low birth weight
- Use of steroids or NSAIDs
- Requiring ventilator support
- Symptomatic PDA requiring surgery
Protective risk factor: breast milk
How long should infants with NEC receive nothing by mouth?
Infants with true confirmed NEC (radiographic or surgical evidence): NPO + TPN x 2-3 wks
-infants with suspected NEC can be fed after 3-7 days of bowel rest
What are the 3 stages of NEC?
Stage 1: suspected NEC
- clinical signs: abdo distention, bloody stools, emesis, gastric residuals, apnea, lethargy
- radiological signs: ileus, distension
Stage 2: Proven NEC
- clinical signs + abdo tenderness +/- metabolic acidosis, thrombocytopenia
- radiological signs: pneumatosis intestinalis, portal venous gas
Stage 3: Advanced NEC
- clinical features in stage 2 + hypotension, significant acidosis, DIC, neutropenia
- radiological features: stage 2 findings with pneumoperitoneum
When should iron supplementation be initiated for preterm babies?
4-8 weeks of age and maintained x 12-15 months
A newborn presents with thrombocytopenia. What is the most likely etiology in each of the following if present?
- blueberry muffin rash
- absence of radii
- palpable flank mass and hematuria
- large hemangioma
- abnormal thumbs
- blueberry muffin rash: think TORCH or viral infection
- absence of radii: think TAR (thrombocytopenia with absent radii)
- palpable flank mass and hematuria: renal vein thrombosis
- large hemangioma: Kasabach-Merritt syndrome
- Abnormal thumbs: Fanconi syndrome
What are the lab findings of DIC?
- Decreased fibrinogen
- Increased PT/PTT
- RBC fragmentation on peripheral smear from microangiopathic hemolytic anemia
What is the differential diagnosis of hypocalcemia in the neonate?
- early (first 3 days of life) (3)
- late (after 1st week of life) (8)
Early:
- Premature infants
- Infants with birth asphyxia
- Infants of diabetic moms
Late:
- High phosphate cow milk formula
- Intestinal malabsorption
- Postdiarrheal acidosis
- Hypomagnesemia
- Neonatal hypoparathyroidism
- Rickets
- Citrate (from exchange transfusion)
- Alkalosis
What is the treatment for hypocalcemia in an infant presenting with seizures?
10% calcium gluconate, 2 ml/kg over 10 minutes
What is the most common pathogen causing late-onset sepsis in the prem infant in NICU?
-treatment?
Coag negative staph (nosocomial infection)
-treatment: vancomycin
What is the classification of IVH?
Grade 1: germinal matrix hemorrhage
Grade 2: IVH without ventricular dilatation
Grade 3: IVH with ventricular dilatation
Grade 4: IVH with parenchymal involvement
# Fill in the blank: in more than 90% of cases, IVH in prem infants occurs during the first \_\_\_\_ days of life. -what is a common complication of severe IVH?
3!
-complication: posthemorrhagic hydrocephalus
What are the benefits of breastfeeding? (9)
- Fewer episodes of otitis media, resp, GI illness
- Human milk facilitates growth of beneficial, nonpathogenic flora
- Increased immune protection
- Improved neurodevelopment
- Reduction in diabetes mellitus
- Economic
- Mom returns to pre pregnancy weight faster
- Protective for mom against certain cancers (ovarian, breast)
- Improved maternal-child bonding
What are contraindications to breastfeeding? (4 major categories)
- Metabolic d/o: galactosemia, PKU, urea cycle defects
- Infections: HIV, TB before treatment, Human t-cell lymphotropic viruses, HSV if present on breast
- Substance use by mom
- Medications: chemotherapy, radiation, lithium,
What are 3 clinical features of vitamin E deficiency?
- Hemolytic anemia (vitamin E is important for stabilizing the RBC membrane)
- Peripheral edema
- Thrombocytosis (increased platelets!!!)
In utero exposure to cocaine results in increased risk of which complications?
- Preterm labor
- Placental abruption
- Neonatal irritability
- SGA
- Microcephaly
***Usually requires no treatment
What is the timing of amniocentesis during pregnancy?
-what about CVS?
- Amniocentesis: between 15-17 wks typically
- CVS: after 10 wks
What causes the following?
- early decels
- variable decels
- late decels
- Early decels: head compression during contractions = not concerning
- Variable decels: most common, due to cord compression, may be concerning
- late decels: MOST concerning, due to uteroplacental insufficiency
When is the onset of neonatal acne?
At around 3 weeks of life = from sebaceous gland stimulation by maternal androgens
-usually resolves by 4 mo of age
What are the manifestations of neonatal lupus erythematous? (4)
- Cardiac: congenital heart block (usually 3rd degree), occurs during 18-30th week gestation, can lead to fetal hydrops
- Skin: annular erythematous scaling plaques on sun exposed areas during first 2 weeks of life and spontaneously disappears by 6 months when maternal abs are decreasing
- Thrombocytopenia
- Hepatitis
What is commonly seen in infants born to moms who were on the following medications during pregnancy?
- lithium
- phenytoin
- tetracycline
- phenytoin: digit and nail hypoplasia
- lithium: ebstein anomaly
- tetracycline: yellow-brown discoloration of teeth
Why do babies grunt in resp distress?
They are closing their glottis to maintain lung volume and gas exchange during exhalation
What is the most common neonatal cystic lung malformation?
Congenital lobar emphysema
What is the most common form of spina bifida?
Myelomeningocele: failure of the posterior neural tube to close
What is VACTERL syndrome?
Vertebral abnormalities
Anorectal malformations
Cardiac anomalies
TEF
Renal or radial anomalies
Limb malformations
What is the double bubble sign?
Represents duodenal atresia
-the 1st bubble on the left is the gas in the stomach and the 2nd bubble on the right is gas in the duodenum since it cannot pass through the atresia (no gas in the small or large bowel distal to the level of the obstruction)
What is the management of meconium ileus?
Diagnostic gastrografin enema (hypertonic, water soluble) = washes out meconium
-OR surgical management if this doesn’t work
What is the underlying pathophysiology of Hirschsprung disease?
-associated with what conditions? (3)
Failed migration of neural crest cells = affected bowel fails to relax causing a functional obstruction (dilated proximal colon, distal small caliber lumen)
- associated with:
1. Trisomy 21
2. Smith-Lemli-Opitz syndrome
3. Congenital central hypoventilation syndrome
What is the most severe complication of neonatal immune-mediated thrombocytopenia?
IVH (can occur in utero)
What are clinical features of congenital toxoplasmosis infection?
-treatment?
Hallmark is CNS involvement!!
- Chorioretinitis
- Diffuse intraparenchymal calcifications
- Hydrocephalus
- treatment: - Pyramethamine
- Sulfadiazine
- Leucovorin
The mother of a newborn baby develops varicella shortly after birth. What is the timing for which you should give VZIG to the infant?
Give VZIG if mother develops varicella 5 days before or 2 days after delivery
What is the most common cardiac defect seen in infants of diabetic moms?
Hypertrophic cardiomyopathy
What is the classic triad of congenital rubella syndrome?
- Sensorineural hearing loss
- Cataracts
- Congenital heart disease
Which infection is prevented by newborn eye prophylaxis with 0.5% erythromycin, 1% silver nitrate or 1% tetracycline?
N. gonorrhea!
-these reduce the incidence of C. trachomatis but does not PREVENT infection
What is the difference between neonatal alloimmune thrombocytopenic purpura vs. neonatal autoimmune thrombocytopenic purpura?
-treatment of each?
Neonatal alloimmune thrombocytopenic purpura: maternal antibodies directed against paternal antigen on baby’s platelets = see low plts in baby, normal plts in mom.
- tx:
1. planned C section to decrease risk of intracranial hemorrhage
2. Maternal IVIG prenatally
3. Washed maternal plts given to baby postnatally
Neonatal autoimmune thrombocytopenic purpura: maternal ITP with autoantibodies crossing placenta and destroying baby’s plts = see low plts in baby, low plts in mom.
- tx:
1. Maternal steroids prenatally
2. IVIG/steroids for baby postnatally
In electrical injury, is alternating or direct current more hazardous?
At low voltages (e.g., those found in household electrical devices), alternating current is more dangerous than direct current. Exposure to alternating current can provoke tetanic muscle contractions so that the victim who has grasped an electrical source is unable to let go, thereby prolonging the exposure and producing greater tissue injury. Direct current or high-voltage alternating current typically causes a single forceful muscular contraction that will push or throw the victim away from the source.
ETT depth?
Age/2 +12
Hs and Ts?
H’s: Hypoxemia, hypovolemia, hypothermia, hyper/hypokalemia, hypoglycemia, and hydrogen ion (acidosis)
T’s: Tamponade, tension pneumothorax, toxins, and thromboembolism
Blood loss= volume
25% of blood volume equals 20 mL/kg,
Newborn shock
The misfits
Trauma (nonaccidental and accidental)
Heart disease and hypovolemia
Endocrine (e.g., congenital adrenal hyperplasia)
Metabolic (electrolyte)
Inborn errors of metabolism
Sepsis (e.g., meningitis, pneumonia, urinary tract infection)
Formula mishaps (e.g., underdilution or overdilution)
Intestinal catastrophes (e.g., volvulus, intussusception, necrotizing enterocolitis)
Toxins and poisons
Seizures
Antidotes
Ingestion odours
What additional recommendations have been made regarding the most ideal sleep environment for infants?
In addition to supine positioning, recommendations to decrease the risk for SIDS or suffocation include”
use of a firm sleep surface
breastfeeding
room-sharing without bed-sharing
routine immunization
consideration of a pacifier
avoidance of soft bedding,
overheating, and exposure to tobacco smoke, alcohol, and illicit drugs.
MRSOPA
M = Mask adjustment
R = Repositioning
S = Suctioning
O = Open the mouth
P = Increase the pressure
A = Alternate airway
ETT Size Neonate
APGAR
- Appearance (pink, mottled, or blue)
- Pulse (> 100, < 100, or 0 beats/minute)
- Grimace (response to suctioning of the nose and mouth)
- Activity (flexed arms and legs, extended limbs, or limp)
- Respiratory effort (crying, gasping, or no respiratory activity)
Jaundice
Head bleeds
Breastmilk to cows milk comparison
67 kcal/100cc
ower portien content
Greater whey:casein ratio
CHO: both lactose
Fat 30-50% vs. 3-4%
Vitaimins: more ACE, lower DK
Minerals: lower Fe, better absorption
When does the suck-swallow reflex become coordinated?
32 weeks
TPN complications
Electrolyte ABN
Glucose AbN
Cholestasis
Line infections
Bone d/o
When do infants acquire most of their passive transplacental immunity?
After 32 weeks
NEC RF?
Prematurity
Asphyxia
Enteral feedins
Polycythemia and hypervisocity
Exchange transfusions
16 yo female on surgical ward in traction for femoral fracture and splenic rupture. She develops sudden onset CP, cough and O2 sats 84%. Give 3 of the most likely causes of the sudden distress. Give 3 investigations to do to confirm diagnosis.
Fat embolus, PE, pneumothorax. CT angiogram, CXR, Ultrasound of lower limb, EKG,D-dimer
4 “medical reasons” why brain dead patient may not be able to be an organ donor.
- Sepsis untreated
- HIV positive
- CMV active infection
- Malignancy
Polycythemic newborn. Hb 240, Hct 0.75. Wt 2000g. Child requires a partial exchange transfusion. What fluid do you use as the diluent? How much blood to you replace to decreae the Hct to 0.5?
- Exchange transfusion if Hct > 70 – 75% on venous sample
- Use normal saline, albumin or plasma
- Blood volume to be exchanged = [(Observed Hct – Desired Hct)/Observed Hct)]x blood volume (80cc/ kg)
= [(.75-0.5)/0.75] x 80mL/kg x 2 kg = 0.33 x 160
= 52.8 mL
