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FNP II Final Exam Study Guide:
Behavioral:
objectives : how affect individuals, S/S behavioral disorders across the lifespan, screening tools,
management, acute distress or suicide, recognising need for referral
Autism Spectrum Disorder: BURNS chapter 20 zola.
Delay and deviance in development of social skills, communication and cognitive skills
● Diagnostic Criteria:
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Deficits in social communication and interaction across multiple contexts
Restrictive, repetitive patterns of behaviors, interests, and activities.
A total of more than 6 items from the following criteria with at least 2 of
them from criterion 1 and one each from criteria 2 and 3:
1. Qualitative impairment in social interaction as manifested by at least 2
of the following:
● Marked impairment in the use of multiple nonverbal behaviors,
such as eye-to-eye gaze, facial expression, body posture, and
gestures to regulate social interaction.
● Failure to develop peer relationships appropriate to developmental
level.
● Lack of spontaneous seeking to share enjoyment, interests, or
achievements with other people (lack of showing, bringing, or
pointing out objects of interest).
2. Qualitative impairment in communication as manifested by at least 1 of
the following:
● Delay in or total lack of development of spoken language (not
accompanied by an attempt to compensate through alternative
modes of communication, such as gesture or mime).
● In individuals with adequate speech, marked impairment in the
ability to initiate or sustain a conversation.
● Stereotyped and repetitive use of language or idiosyncratic
language.
● Lack of varied, spontaneous make-believe play or social imitative
play appropriate to developmental level.
3. Restricted, repetitive, and stereotyped patterns of behavior, interests,
and activities as manifested by at least 1 of the following:
● Encompassing preoccupation with one or more stereotyped and
restricted patterns of interest that is abnormal either in intensity or
focus.
● Apparently inflexible adherence to specific, nonfunctional routines
or rituals.
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Stereotyped and repetitive motor mannerisms (hand, or finger
flapping or twisting, or complex whole-body movements).
● Persistent preoccupation with parts of objects.
Delayed/abnormal functioning in at least 1 of the following areas with onset
before 3 y.o.
● Social interaction
● Language as used in social communication
● Symbolic or imaginative play
Disturbance not better accounted for by Rett d/o or childhood disintegrative d/o.
● Behaviors Indicative of ASD:
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Problems with social interactions, communication, and language skills show by
their unusual ways of relating to people, objects, and events. Abnormal
responses to sensory stimuli, usually sound; and restricted, repetitive, or
stereotyped behaviors and echolalic speech.
Language delays, lack of social relatedness, severe behavior problems.
Expressive language is delayed, repetition of words/phrases, decreased eye
contact, detached, repetitive movements. Insistent on routines.
● When to Refer:
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Screening is recommended by the AAP at 18 & 24 months.
If there is a concern that a child has Autism, referral for a comprehensive
diagnostic assessment should be done by a multidisciplinary team.
Be sure that you understand what the core domains of ASD are and be able to identify the
diagnostic criteria for ASD
ADHD: BURNS chapt 20
Affect cognitive, educational, behavioral, emotional, social functioning
s/s: inattention, hyperactivity, impulsivity in at least 2 settings: home, school or work
Impairment in social, academic or occupational functioning
● THREE TYPES OF ADHD;
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314.01 (F90.2) Combined presentation:
○ If both Criterion A1 (inattention) and Criterion A2 (hyperactivity-impulsivity) are
met for the past 6 months.
314.00 (F90.0) Predominantly inattentive presentation:
○ If Criterion A1 (inattention) is met but Criterion A2 (hyperactivity-impulsivity) is not
met for the past 6 months.
314.01 (F90.1) Predominantly hyperactive/impulsive presentation:
○ If Criterion A2 (hyperactivity-impulsivity) is met and Criterion A1 (inattention) is
not met for the past 6 months”.
CLASSIFY CURRENT SEVERITY:
● “Specify Mild”: Few, if any, symptoms in excess of those required to make the
diagnosis are present, and symptoms result in no more than minor impairments in
social or occupational functioning.
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Moderate: Symptoms or functional impairment between “mild” and “severe” are present
● Severe: Many symptoms in excess of those required to make the diagnosis, or
several symptoms that are particularly severe, are present, or the symptoms
result in marked impairment in social or occupational functioning”.
● Prevalence of each:
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ADHD, combined type: accounts for majority of ADHD cases
ADHD, predominantly inattentive: accounts for one-third of ADHD cases
ADHD, predominantly hyperactive/ impulsive: accounts for the fewest ADHD
cases
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
DSM V Diagnostic Criteria:
- “A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with
functioning or development”.
Prevalence: Occurs in 5% of children (all cultures) and 2.5% of adults
IMPORTANT TO NOTE- The symptoms are not clearly due to something else! Are they bored?
Do they not understand directions and that’s why they aren’t doing it?
- Ages 4 and 18 years old. (really can’t distinguish before 4).
- Might notice when the child is older because their grades are showing for it
- Information must be from 2 different environments (parent, teacher, other).
- Comorbidities should be addressed; regarding emotional and behavioral,
developmental and physical.
- Conduct comprehensive medical, developmental, family and educational history.
SIGNS MAY BE MINIMAL OR ABSENT
- Frequent positive reinforcement
- Well supervised: are they helicoptering and catching the bad behavior before it
starts? This is sometimes why the behavior is totally different at home
- NEW setting (of course they are behaving and aren’t showing their problem
behaviors yet)
- Interested : again, bored?
- Electronics: makes diagnosis hard
- Office visit: may not see it here because of the 1:1 attention
RISK AND PROGNOSTIC FACTORS
- Possible traits: adventure seeking and negative emotions
- Environmental: LBF, child abuse, toxins like lead
- Genetic : White children > more freq diagnosed, strong genetic links in families
- Culture
- Gender: boys> girls for ADHD
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DIFFERENTIAL DIAGNOSIS
- Oppositional defiant disorder
- Intermittent explosive disorder: extreme behaviors, no issues with attention.
- > pts with the above 2 need psych help
- Other neurodevelopmental disorders
- Specific learning disorder
- Intellectual disability (intellectual developmental disorder)
- Autism spectrum disorder (ADHD and Autism) – may be inattentive and have social
dysfunction masking making discerning social issues hard
- Reactive attachment disorder
- Anxiety disorders
- Depressive disorders
- Bipolar disorder
- Disruptive mood dysregulation disorder
- Substance use disorders
- Personality disorders – emotional dysreg, emotional intrusiveness
- Psychotic disorders
- Medication-induced symptoms of ADHD – think thyroid
- Neurocognitive disorders
>> not characterized by fear of abandonment or ambivalence which are characteristic of these
personality disorders.
AGE RELATED CRITERIA
- Ramtekkar (2013), suggested using age related criteria for diagnosing ADHD, he
reported that older girls were underdiagnosed.
- The new DSM V uses specific criteria for diagnosing adolescents 17 and older. In
addition, the age of symptoms can now be present up to age 12 (DSM V) as compared to
age 7(DSM IV).
DIAGNOSTIC CRITERIA
DSM IV (2000) DSM V
(2013)
DIAGNOSTIC CRITERIA
DSM IV (2000) DSM V
(2013)
DIAGNOSTIC CRITERIA
DSM IV (2000) DSM V
(2013)
AGE OF SYMPTOM
ONSET
BEFORE AGE 7
BEFORE AGE 12
MULTIPLE SETTINGS (1+)
CLINICALLY
SIGNIFICANT
IMPAIRMENT
SYMPTOMS
INTERFERE
EXAMPLES
CLIMBS/RUNS
FEELING RESTLESS (for older
patient)
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EXCLUDING DIAGNOSIS
PDD
Schizophrenia
Psychotic
disorders
CLASSIFICATION
Schizophrenia Psychotic
disorders or other mental
disorder
Classify mild severe
Placed in
Neurodevelopment
Chapter
DSM IV
“There must be clear evidence of clinically significant impairment in social, academic, or occupational
functioning”.
DSM V
“There is clear evidence that the symptoms interfere with, or reduce the quality of, social,
academic, or occupational functioning”.
● Comorbidities:
COMMON COMORBID DISORDERS
ODD: oppositional defiant disorder, will get worse if the patient is not properly medicated for
ADHD. Kids with this often won’t wear seatbelts, get lots of tickets, may get their license
suspended (signs to look out for when considering why the meds aren’t working)
LD: learning disorder, if you’re treating them with the right ADHD meds and they aren’t getting
better, need to consider this a possibility.
Conduct Disorder: less common but more severe, behaviors lead to jail time
Injuries- head injuries, incidental injury
Peer Challenges – relationship problems? Look for anxiety, delinquency, mood disorder
COMORBID DISORDERS IN THE MINORITY
Anxiety/Depression
MOOD Conduct
Intermittent explosive disorder
COMORBIDITY MAY OCCUR WITH ADHD
- Adults: antisocial and other personality disorders
- Obsessive-compulsive disorder
- Tic disorders
- Autism spectrum disorder
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● Treatments and side effects:
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Stimulants are considered the most effective medication, but three nonstimulants (one selective norepinephrine- reuptake inhibit and two alpha2adrenergic agonists) are also efficacious.
First line: stimulants, methylphenidate and amphetamine compounds. They
work by increasing the availability of neurotransmitters at the neuron synapses
by blocking the transporters that remove dopamine and norepinephrine in the
pathways in key areas of the brain where ample bioavailability of these
compounds is essential by decreased.
■ Stimulant side-effects: decreased appetite, weight loss, insomnia,
stomach-ache, and headache. Typically, symptoms resolve after a while.
Concerns about growth exist but studies do not confirm this. 20% of
children may develop tics after starting medication—often mild and
typically resolve within a year.
First line for preschoolers is behavioral therapy or group parent training
Atomoxetine (straterra) is a non controlled, non-stimulant medication approved
as a first-line medication for ADHD for children older than age 6 years old.
■ Common side effects: decreased appetite, GI complaints (anorexia,
nausea), somnolence/ dizziness, mild increase in BP or HR. Most sx
resolve, headache usually persist but can be managed with dose
reduction or change of med
■ Few reports: liver toxicity, SI/ SA; not to be used in pts with HTN or
tachyarrhythmias
Second line or adjunct medications:
■ ER guanfacine (Intuniv) and ER clonidine (Kapvay) used in children 6
years old and older. Intuniv helps improve oppositional symptoms
especially impulsivity
■ Kapvay (CLONIDINE) especially helpful in children with sleep issues.
■ These meds are less likely to be abused, do not worsen tics, take 2
weeks to work
■ AE: these alpha agonists may cause sedation, bradycardia, abdominal
pain
You should review the Burn’s chapter and take note of the section on the statistics related to
ADHD.
Estimates in US - from 5% (APA) to 8% (AAP) to 11% (CDC).
Males 13.2% and females 5.6% per CDC
% of children diagnosed with ADHD ages 4 to 17 increased 42% b/w 2003 to 2011 in one study
but in another, no evidence to suggest increase - just better awareness, access to treatment,
and changes in clinical practice (possibly).
7 years old is the average age of diagnosis. Severe is diagnosed earlier than age 7.
Prevalence varies by state: low in Nevada of 5.6% to high in Kentucky of 18.7%
Boys have higher prevalence 2:1 in childhood; 1.6 to 1 across all ages and girls are more likely
to have the inattentive features.
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Racial and ethnic disparities - African American or Hispanic children are 69% less likely to be
diagnosed.
Becoming more aware internationally - very few people receive diagnosis due to lack of
awareness and social stigma and lack of community frameworks
Be sure you review the meds used to treat ADHD and know the side effects of the meds. What
are the most common side effects of stimulant ADHD drugs?
Side Effects, Contraindications, Cardiac Warning, and Tics.
Decreased appetite, weight loss, insomnia, stomach-ache and headache.
Contraindications: psychosis.
Cardiac warning - no association b/w stimulants and atomoxetine (see below about
atomoxetine) and CV effects - stroke, MI, or sudden death - however, do not give to those with
“serious heart problems” ...
Screen for 1) cardiac history - SOB with exercise, exercise intolerance, fainting or seizures with
exercise, palpitations, elevated BP, previously detected cardiac abnormalities, rheumatic fever,
cardiomyopathy, &/or dysrhythmia.
2) Family cardiac history sudden unexplained or cardiac death before age 35, any rate, rhythm,
or structural cardiac problems in the family, and
3) complete physical examination with special attention to the cardiovascular system.
A screening tool for sudden death risk factors among children starting stimulant medication is
available online ( https://www.icsi.org/_asset/60nzr5/ADHD-Interactive0312.pdf )
Tics - about 20% develop tics
Stimulants may worsen anxiety disorders
Liver toxicity with Atomoxetine have been reported
Few reports of suicidal thinking or attempts with atomoxetine
Atomoxetine - possible increased BP or HR so FDA recommends not to use in hypertension or
tachyarrythmias
Second line med - guanfacine-> sedating, bradycardia, abd. pain
From Burns….
Saltine crackers with the morning dose of stimulant medication can decrease complaints
of stomach aches. Instant breakfast drinks and other high-calorie foods supplement
calories when the child has low caloric intake because of difficulty sitting through meals
or side effects of medications. Cyproheptadine (Periactin) is sometimes used as an
appetite stimulant.
For sleep: Melatonin (2 to 6 mg/day), low dose clonidine, or an antihistamine may be
helpful; however, long-term use of these agents is not supported by clinical evidence.
Medication selection depends on the age of the child, the desired timing and length of
coverage, other coexisting conditions, and insurance coverage.
Amphetamines and methylphenidates - first line med’s - need to assess substance
abuse
Adderall XR) (mixed amphetamine salts) for ages 6+
Amphetamine and dextroamphetamine (Adderall) (mixed amphetamine salts) - not
extended release - for ages 3 and up, FDA approved for ages 3-5.
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Dextroamphetamine (Dexedrine) for ages 3-5
Lisdexamfetamine (Vyvanse) ages 6-12
Methylphenidates
Methylphenidate (Concerta) - non-crushable - ages 6+
Dexmethylphenidate (Focalin) ages 6 - 17
Methylphenidate (Ritalin) ages 6+
Non-stimulant and alpha agonists
Strattera - Atomoxetine - may take 2-4 weeks to peak effect, give with food to minimize
adverse effects.
Guanfacine - Intuniv - may take 2 weeks, do not give with high fat meal, do not stop
abruptly
Clonidine - may take 1-2 weeks, do no stop abruptly
Depression: BURNS chapt. 19
Specific etiology unknown. Some biology and genetics + environmental factors responsible.
● Screening: USPSTF recommends screening only when there are supports in
place for you to assure a dx, treatment, and follow-up. If all these are met,
screening adults is appropriate.
> looks a lot like bipolar! Be sure to ask if they can stay up for days on end, impulsive or
reckless behaviors? Interspersed in depressive episodes.
> depression can also be mistaken for dementia: impaired or inconsistent mood,
disorientation, neuro deficits (aphasia, apraxia). Ppl with this were previously able to
function, Use the mini mental tool to rule this out.
> notes: weight changes, sleep dist, fatigue, decreased interest in pleasurable things may be
indicators that something is going on if this person doesn’t identify as depressed and/or anxiety.
s/s - ruminating, memory impairment, difficulty making day to day decisions, poor concentration,
sleep, psychomotor, appetite
PE - flat affect, slow speech, anxiety, hyper, evidence of self neglect (unbathed, dirty clothes),
decline in work and school performance
Diagnosis: test only to rule out other conditions like CBC if you’re worried about fatigue or
metabolic syndrome, TSH?. Diagnosis is made off the HPI and hx.
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Hard to read chart, but stick to DSM V and make sure the symptoms are disruptive and they
have at least 5 s/s.
● SIGECAPS
○ Sleep
○ Interest
○ Guilt
○ Energy
○ Concentration
○ Appetite
○ Psychomotor
○ Suicidal
SIGECAPS FOR DEPRESSION
Dysthymic = s/s 2 yrs, milder, need 2 or more s/s rather than 5.
Treatment:
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First line treatment of MDD is psychotherapy and/or antidepressant medication.
■ GOLD STANDARD is to combine psychotherapy and medication
○ Can be mutually decided by you and the patient depending on disease severity.
○ Medication preferred if:
■ Hx of good response to medication
■ Sx are severe
■ Significant disturbance of sleep and appetite
■ Severe agitation
■ Lack of available alternative tx
○ SSRIs= 1st line treatment
○ SNRIs= 2nd line treatment or 1st line treatment in patients who complain of
fatigue, chronic pain disorders, chronic back pain, or migraines.
■ May cause HTN! BE AWARE!
○ TCAs and MOAIs= 2nd line treatment due to more side effects.
Length of treatment? 6-9months then reassess
● Side Effects
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SSRI and SNRI Side Effects: Sexual dysfunction, GI disturbances such as
nausea, slowed GI motility
■ Others: agitation, anxiety, sleep disturbance, tremors, headaches
Serotonin Syndrome: ABD pain, diarrhea, flushing, sweating, hyperthermia,
lethargy, mental status changes, tremor, rhabdomyolysis, renal failure, CV shock
and potentially death. (Usually occurs when coadministered with MAOIs, triptans,
lithium, amphetamines, and some analgesics such as tramadol or meperidine).
● esp. special populations such as youth or the elderly: higher rates and risk in
elderly.
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Physical disorders that are chronic and painful are assoc with depression in
elderly
Stressful life events
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Normal grief responses need to be differentiated from Major Depressive
Disorder(MDD).
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Associated disorders: anxiety, OCD, substance abuse, stroke, HTN, diabetes, Cancer
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Special Populations:
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Pregnant women: TCAs and SSRIs can be used in pregnancy for moderate to
severe depression
■ SSRIs are 1st line- Fluoxetine most safety data.
○ Breastfeeding women: 1st line is Sertraline, Paroxetine, and Nortriptyline
(safe in breastfeeding mothers).
○ Pediatrics: Fluoxetine and Escitalopram are the only antidepressants
approved for children 12 year old and older.
■ Paroxetine has shown to increase adolescent suicide!
■ Black box warning for SSRIs and suicide amongst adolescents, especially
in the beginning, monitor closely! FOLLOW UP IN 1 WEEK.
■ Combination therapy of CBT and pharmacotherapy gold standard
○ Geriatrics: High risk group. Dementia can be mistaken for MDD.
■ Look for signs of dementia: insidious onset, long duration of symptoms,
impaired or inconsistent mood orientation or behavior, cognitive
impairment, neuro deficits, memory loss, no psych hx, confusion,
disorientation.
■ TCAs can cause anticholinergic side effects in this population
■ When dosing, start low and go slow!
Somatic symptoms
Bipolar Disorder: Must be certain patient does not have bipolar because treatment is different!
-> Cause them to be manic more often.
■ Cardinal feature is mania/hypomania mixed with MDD
■ Other Sx: Inflated self esteem, little need for sleep, racing thoughts,
distractibility, irritability, reckless behavior, clear pattern of mood
fluctuations, alternating depression and mania, family hx.
Schizophrenia: BEWARE of red flag symptoms: Severe personality change, thought disorder,
delusions, hallucinations, bizarre behavior.
● Onset usually in middle or late teens
● More common in males
When to Refer or Consult:
● Suicide or homicide risk
● Severe mental confusion
● Delusions or hallucinations
● ETOH or drug abuse
● Bipolar disorder
● Depression not responding to typical measures
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Depression with psych features
SSRIs are generally considered to be safe drugs. They are the preferred class of
antidepressants for treating children and adolescents, as well as elderly patients. They have a
better side effect profile than other classes of antidepressants.
● GI disturbances, like altered GI motility and nausea & sexual dysfunction are the most
common side effects.
● Agitation, anxiety, sleep disturbance, tremors, and headaches can also be side effects of
SSRIs.
Review the SSRIs and know which of the specific drugs should be avoided in certain
populations of patients, as well as which specific SSRIs are considered to be safe in special
populations (like peds (Fluoxetine & Escitalopram), geriatrics (Citalopram, Escitalopram, &
Sertraline), pregnant (Fluoxetine), and breast feeding women(Sertraline and Paroxetine).
SNRIs can be used as a second line treatment for depression or as a first line treatment for
patients with significant fatigue or chronic pain syndromes like neuropathy chronic back pain, or
migraines. The safety, tolerability, and side-effects include those found with SSRIs, but SNRIs
can also cause hypertension so just be aware of this when prescribing them. Bupropion,
mirtazapine, moclobemide, and venlafaxine
*Bupropion is better for sexual side effects but it can make ppl more active. So be careful if the
patient also has anxiety.
Risk for suicide:
● Prior attempt
● Adolescent and young adults (impulsivity)
● Females more attempts than males
● Males more successful attempts
● Elderly white males (highest rate of suicide, especially with access to a gun)
Review lecture from Athey
St. John’s Wort (https://nccih.nih.gov/health/stjohnswort/sjw-and-depression.htm)
In a 26-week clinical trial with 124 participants, St. John’s wort, a standard antidepressant
(sertraline, an SSRI), and a placebo were similarly effective in treating major depression of
moderate severity. NCCIH and NIMH funded this 2012 analysis of data collected in 2002.
Combining St. John’s wort with certain antidepressants can lead to a potentially lifethreatening increase of serotonin, a brain chemical targeted by antidepressants. Symptoms
occur within minutes to hours, and may include agitation, diarrhea, fast heartbeat, high blood
pressure, hallucinations, increased body temperature, and more.
●
Taking St. John’s wort can weaken many prescription medicines, such as:
○ Antidepressants
○ Birth control pills
○ Cyclosporine, used to prevent the body from rejecting transplanted organs
○ Digoxin, a heart medication
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○ Oxycodone, a pain medicine
○ Some HIV drugs, including indinavir
○ Some cancer medications, including irinotecan
○ Warfarin, an anticoagulant (blood thinner).
Other side effects of St. John’s wort are usually minor and uncommon. They may include
upset stomach, dry mouth, headache, fatigue, dizziness, confusion, sexual dysfunction,
or sensitivity to sunlight. Also, St. John’s wort is a stimulant and may worsen feelings of
anxiety in some people.
Anxiety
● Screening:
● Treatment:
● Side Effects
● esp. special populations such as youth or the elderly
Often patients present with other comorbidities (90% of the time) including:
● Mood
● Substance abuse psychosis
GAD is often mistaken for other diagnoses and can easily be missed:
● Physical/psyc distress
● Somatic disturbance
● Sleep disturbance
Four Common Anxiety Disorders:
1. Panic Disorder (PD): Reaches peak within minutes (10 minutes) and with palpitations,
sweating, shaking, SOB, choking, CP, N/adb distress/dizzy Intense fear, unexpected —>
progresses to —> full on panic attack
2. Social Anxiety Disorder (SAD): a person fears they will do something weird or wrong during
a social situation. This causes them to compensate or act strangely in social situations,
validating fear and eventually avoid these situations.
Must last longer than 6 months, must cause clinical distress, and not attributed to other causes
3. Generalized Anxiety Disorder (GAD): Persistent, excessive, worry and tension Common
worries 3/6, only one for children Restless, easily fatigued, impaired concentration, irritability,
muscle tension, sleep disturbance 6 months, present for more days than not
4. No longer lists Obsessive Compulsive Disorder (OCD) and Posttraumatic Stress Disorder
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(PTSD)
● Screening: PC-PTSD, PCL-PC, M-3 —> Have you experienced a trauma that still haunts
you?
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Treatment: Daily SSRI/SNRI, Use prazosin for nightmares, anxiolytics may be needed
as a bridge for severe symptoms until antidepressants provide relief, Benzos are
generally not recommended, prolonged exposure - cognitive processing therapy
Side Effects: SSRIs - HAs, nervousness, insomnia, sedation, fatigue, nausea, diarrhea,
dyspepsia, appetite loss
Bipolar:
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Looks a lot like depression!
Screening
○ Characterized by: presence of mania (bipolar I disorder) or hypomania and
depression (bipolar II disorder)
○ Mania: euphoria, expansive/irritable, co-occurring with persistently increased
goal-directed activity or energy, inflated self-esteem, confidence, decreased need
for sleep, pressured speech, racing thoughts, distractibility, increased
involvement in goal-directed activities
○ The MDQ is a tool that combines DSM-IV criteria and clinical experience to
screen for bipolar disorder in primary care settings. It uses a brief, one-page selfreport questionnaire with 13 yes-or-no items and two additional questions
regarding functioning and timing of mood symptoms and typically can be
completed in 5 minutes or less.
Treatment/ Side effects:
○
one mood-stabilizing drug and/or atypical antipsychotic, plus
psychotherapy. The most widely used drugs for the treatment of bipolar
disorder include lithium carbonate and valproic acid (also known as
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Depakote or generically as divalproex)
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○
Suicide Risk Factors:
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●
●
Historical and biological risk factors (history of suicide attempts, family history of suicide,
male gender, history of childhood trauma)
Mood, anxiety, and psychotic symptoms; substance abuse; encourage patient to mobilize
psychosocial resources-contact family members for support.
Access to firearms
Eating Disorders:
● Eating disorders cause abnormal eating behaviors that are secondary to altered body image
(dysmorphism). Anorexia nervosa (commonly called anorexia) and bulimia nervosa
(commonly called bulimia ) are the primary eating disorders of concern; however, there are
other conditions in this diagnostic cluster, including eating disorder not otherwise specified,
rumination disorders, pica, and feeding disorders of infancy.
● Diagnostic criteria for anorexia:
○ Refusal to maintain body weight at least 85% expected for age and height or failure
to gain weight during growth periods so that weight drops below 85% expected
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○ Intense fear of weight gain and “being fat”
○ Body dysmorphism
○ Binge eating/ purging subtype, which is associated with frequent purging although
bingeing episodes are rare
■ Diagnostic criteria for bulimia:
■ Consuming large quantities of food in a short period of time (within 2 hours)
■ Loss of control during binge episodes (e.g., can't control the amount of food
they eat or are shocked at the amount consumed)
■ Engaging in repeated behaviors to lose weight, including purging, excessive
exercise, or fasting
■ Binging or purging behaviors that occur at least once a week for at least 3
months
● Screening tool: SCOFF questionnaire:
○ Do you make yourself Sick because you feel uncomfortably full?
○ Do you worry that you have lost Control over what you eat?
○ Have you lost Over 10 pounds in the last 3 months?
○ Do you believe you are Fat when others say you are thin?
○ Would you say Food dominates your life?
● Treatment: CBT, antidepressants, atypical antipsychotics, fluids/ electrolytes (inpatient
management
GI/Adult
General recommendations to narrow diagnoses
• History is essential:
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●
●
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Timeline Of Symptoms
Associated Symptoms,especially bowel changes
Relationship To Meals,specific foods,or dietary changes/travel
Other Associated Risk Factors,particularly smoking and drinking history (social hisotry)
Location of pain and has that changed?
• This will help you to narrow your focus, based on anatomy that corresponds to the location of
pain
● Consider special populations
○ Who will decline more rapidly?
○ How might children and elderly patients present differently
■ Infant with abd pain- what should be done when compared to an adult
○ When must you do additional work up or what red flags require more urgent
evaluation?
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Appendicitis
Acute infection of the appendix caused by obstruction of the appendiceal lumen followed by
bacterial overgrowth and invasion of the wall of the appendix
Risk factors:
Median age for children is 10-11 year age for adults is 28 year, most common in summer
months, foreign body, obstructive neoplasms (10-30 y.o.).
● Symptoms:
○ Fever, R sided abdominal pain that might start closer to umbilicus
(periumbilical), localizing to RLQ over time, +/- nausea and vomiting. Rebound
and guarding.
○ Positive Peritoneal signs: guarding & rigidity
○
○ Obturator sign - passive R hip flexion and tightening of internal obturator muscle
causing abd discomfort,
○
○ Mc Burney’s point - most pain with pressure found here in RLQ,
○ Psoas - lie on L side, passive extension of R hip while supine causes pain IN
RLQ
● Diagnostic Labs:
○ CBC w/ Diff, CT Scan, Ultrasound in children and pregnant women, UA
○ Imaging only recommended when diagnosis is equivocal
● Differential diagnoses:
○ Mesenteric Adenitis, gastroenteritis, UTI, ureteral calculus, diverticulitis, IBS,
Ectopic pregnancy, ovarian cyst, PID
● Treatment:
○ Removal of appendix
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Pancreatitis:
Rapid onset of LUQ and epigastric pain that radiates to the mid back (boring).
Severe pain, particularly LUQ or epigastric often radiating to the back
Associated with heavy alcohol use, episodic binge drinking
● Risk factors:
○ Associated with
■ heavy alcohol use
■ Hypertriglyceridemia
■ episodic binge drinking
■ Gallstones
■ biliary sludge
■ microlithiasis.
● Symptoms:
○ Severe pain, particularly LUQ or epigastric area, often radiating to
the back. Acute onset of fever, nausea and vomiting. Abdominal exam reveals
guarding and tenderness over the epigastric or upper abdomen.
● Presentation:
○ may see a Cullen’s sign - ecchymotic discoloration to periumbilical region,
edema of the SQ tissue ⇒pancreatic necrosis. Grey Turner sign - blue/bruising
discoloration to flanks → retroperitoneal hemorrhage.
○
○ Hypoactive bowel sounds can signal ileus, jaundice, guarding, and board-like
upper abdomen if peritonitis.
● Evaluation:
○ Diagnosis of acute pancreatitis is typically defined by at least two of the following
criteria:
■ (1) abdominal pain consistent with the disease,
■ (2) serum amylase or lipase greater than three times the upper limit of
normal, or
■ (3) characteristic findings from abdominal imaging
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● Diagnostic labs:
○
○
○
○
AST, ALT, Amylase, CBC
Elevated amylase, lipase, and trypsin
Elevated AST, ALT, GGT, Bilirubin, Leukocytosis, and other values
Abdominal US and CT- usually provides a visual of the inflamed pancreas..
● Differential diagnoses:
○ PUD, Abdominal aorta aneurysm, hepatitis, cholecystitis
●
● Medical therapy of acute pancreatitis is primarily supportive, with the major objective
being hemodynamic stabilization. Antibiotics should not be started routinely but should
be given for extrapancreatic infection. In mild acute pancreatitis, oral feedings can be
started immediately if there is no nausea and vomiting and abdominal pain has resolved.
In mild pancreatitis, initiation of a low-fat solid diet appears as safe as a clear liquid diet
● Hydration (with LR or NS), analgesia, nutritional support, O2, antiemetic, Ca and Mg
replacement therapy, Blood Glucose monitoring and control
PUD:
Most common cause of upper GI Bleed. Epigastric pain, improves/not worsening with meals.
Can experience changes in their stool or bloody emesis.
● Risk factors:
○ H.Pylori, daily use of NSAID/Aspirin
● Symptoms:
○ Epigastric pain, improvement with meals or no change with meals
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○ Associated symptoms, such as stool changes or bloody emesis
■ Dark stools, melena, coffee-ground emesis
○ Dyspepsia
○ LUQ, RUQ, or back pain
○ GI bleeding
○ Or asymptomatic
○ Duodenal ulcers: pain occurs 2-5 hours after eating and at night → improves with
eating
Gastric ulcers: epigastric pain worse after eating. May experience postprandial belching
and fullness, early satiety, intolerance to fatty foods, nausea, vomiting, bloating, gas,
weight loss, and loss of appetite
○ OLDER PEOPLE AND THOSE ON NSAIDs are unlikely to show symptoms
until bleeding!!
● How does this compare to GERD? It is similar, but PUD is more abdomen associated
symptoms with GERD being more esophagus and upper respiratory tract discomfort.
● Evaluation:
○ Endoscopy (if showing signs of bleeding or suspicious for other conditions) and
Barium Esophagography
○ CBC, lipase, CMP
● Diagnostic labs:
○ testing for H. Pylori
■ Stool antigen or mucosal biopsy
■ Can use urea breath test
○ Test of cure for H. Pylori
■ Urea breath test or stool antigen after tx complete
● Differential diagnoses:
○ esophageal ca, GERD, gastroparesis, IBS, Celiac, pancreatitis
● Treatment:
○ Treat the cause, and stop the cause. PPI, H2 agonist, or sucralfate.
○ The best evidence-based recommendation for H. pylori eradication is for 14day triple therapy: PPI + clarithromycin + either amoxicillin or
metronidazole
○ Quadruple therapy: PPI + Bismuth + Metronidazole + Tetracycline
○ Sequential Therapy: PPI + Amoxicillin x5 days, then Clarithromycin +Tinidazole
x4 days.
○ Test of cure? How often do you perform a test of cure?
■ Once is adequate, 4-6 wk after tx complete and off PPI x 1-2 weeks to
avoid false negative
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Cholecystitis and Cholelithiasis:
● Risk factors:
○ Women, cystic fibrosis with pancreatic insufficiency, diabetes mellitus, or family
history of biliary colic; pregnancy; rapid weight loss; Native American Pima
Indian or Scandinavian descent; patients taking estrogens, progestins, or
ceftriaxone; and those requiring total parenteral nutrition.
○ A mnemonic for remembering risk factors for cholesterol gallstones is the 5 F's:
■ Fat (overweight)
■ Forty (age near or above 40)
■ Female
■ Fertile (premenopausal- increased estrogen is thought to increase
cholesterol levels in bile and decrease gallbladder contractions), and
■ Fair (gallstones more common in Caucasians).
● Symptoms:
○ RUQ pain, may be worse after meals- 1 hour after fatty meals on occasion.
○ Accompanied by N/V
○ Positive Murphy’s sign: indicative of gallbladder inflammation. ask pt to exhale,
place hand below costal margin on R at mid clav line, ask to inhale and palpate
area near gallbladder fossa near liver edge: positive when pt winces or catches
their breath as you do the test.
● Differences between
○ Cholecystitis: Inflammation of the gallbladder
○ Cholelithiasis: presence of gallstones in the gallbladder
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○ Differences in treatment?
● Evaluation:
○ Abdominal ultrasound and ruling out other causes of abdominal pain, When
calculi, gallbladder wall thickening, and gallbladder sludge are found, the
diagnosis of acute cholecystitis is almost certain. HIDA scans can give false
negative with ETOH/opiate abuse and other liver disease. MRCP tells you if any
stones are lodged in gallbladder.
● Diagnostic labs:
○ CBC, C-reactive protein, LFTs: Nothing truly diagnostic of this dx
● Differential diagnoses:
○ Cholangitis, PUD, Pancreatitis, GERD, Appendicitis
● Treatment:
○ Cholecystitis without signs of perforation: PO antibiotics, NSAIDS, Early
laparoscopic cholecystectomy
○ Symptomatic Cholelithiasis: Cholecystectomy
○ Asymptomatic Cholelithiasis: Observation
Intestinal Obstruction:
A mechanical disruption in patency of the
GI tract
→ Small Bowel VS Large Bowel:
→ Ileus: A slowing of gastric motility that
is not associated with a mechanical
obstruction: lasts 2-4 days
●
Risk factors:
Previous surgery, inguinal hernia
incarceration, Crohn's disease,
Appendicitis
●
Symptoms:
○
Abdominal pain, nausea, vomiting,
constipation, abdominal distention.
Cramping or discomfort. Changes in stool
frequency and form.
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● Evaluation:
○ Abdominal X Ray, CT Scan, laparoscopy
● Diagnostic labs:
○ CBC, BUN, CMP
● Differential diagnoses:
○ Ileus, gastroenteritis, appendicitis, pancreatitis
● Treatment:
○ SBO: Nasogastric decompression, IV fluids, surgery is possible LBO: More likely
to have surgery
Mesenteric Ischemia:
Poor circulation in the vessels supplying blood flow to your mesenteric organs: your
stomach, liver, colon and intestine. With poor circulation, blockages can form and
compromise the function of these organs.
●
●
●
●
●
Risk factors: atherosclerosis, blood clot
Symptoms: abdominal pain, bloating, dark stool, n/v
Evaluation: abdominal XR, CT Scan
Diagnostic labs: CBC, CMP, Coagulation panel, ABG, ECG
Differential diagnoses: UC, Infectious colitis, large bowel obstruction, peptic ulcer
disease, Pancreatitis
● Treatment: Resuscitation, antibiotics, ex lap/laparotomy
Cirrhosis vs. NAFLD (Non-Alcoholic Fatty Liver Disease):
●
Cirrhosis and esophageal varices
○ Stool changes? Frank or occult blood?
○ Hepatomegaly
○ Skin changes and physical findings?
○ History of heavy drinking over time
● Risk factors:
○ Cirrhosis: ETOH, hepatitis B or C
○ NAFLD: Obesity, PCOS, Metabolic syndrome, diabetes, dyslipidemia
● Symptoms:
○ Cirrhosis: Jaundice, enlarged or tender liver. Stool changes, occult blood. Skin
changes and a history of drinking over time- liver disease
○ S/S of liver dysfunction: Temporal and proximal muscle wasting, Stigmata-spider
nevi, palmar erythema, gynecomastia, and caput medusae, Ascites, Hepatic
encephalopathy. Increase jugular venous pressure-seen with right sided heart
failure-suggest hepatic congestion. Right pleural effusion- May have enlarged
liver and spleen. Hard, nodular liver suggests malignancy.
○ NAFLD: No symptoms, normal exam, Elevated LFTs
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● Evaluation:
○ Cirrhosis: GGT (Gamma-glutamyl transferase), AST, ALT, Albumin, Sodium,
Prothrombin time, platelets, antibodies for hep B and Hep C
● Diagnostic labs:
○ Cirrhosis: An AST to ALT ratio of 2:1 is suggestive of alcoholic liver disease,
especially with an elevated GGT.
○ NAFLD: Liver ultrasound, AST and ALT >4X the UNL
● Differential diagnoses:
○ Splenic vein thrombosis, sarcoidosis, Budd-chiari syndrome, Hep B, Hep C
● Treatment:
○ Cirrhosis: Exercise, diet, avoidance of hepatotoxins, liver transplant
○ NAFLD: Weight loss, lipid lowering medications, antioxidant
medications(These agents include vitamins E and C, N-acetylcysteine
(NAC), mitoquinone (mitoq), and polyenylphosphatidylcholine (PPC)
Diverticulitis:
Diverticulosis refers to the presence of diverticula, or herniations of the intestinal mucosa and
submucosa, most often in the sigmoid colon. Diverticulitis is the most common complication of
Diverticulosis.
● Diverticula are small pouch-like herniations on the external surface of the colon
secondary to a chronic lack of dietary fiber; higher incidence in Western
societies
● Diverticulitis occurs when diverticula; high risk of rupture and bleeding; can be
life-threatening
● Hospitalize if: Patient is elderly, has a high fever, leukocytosis, comorbidities, or
is immunocompromised
● Acute diverticulitis: If acute abdomen, positive for rebound, positive Rovsing's
(sign of acute appendicitis) sign, and board-like abdomen, refer to ED
● Diverticulosis: Physical exam is normal; no palpable mass; no tenderness
● Risk factors: old age, obesity, smoking, diet low in fiber and high in animal fat, lack of
exercise, medications such as NSAIDs, steroids, or opioids.
● Symptoms:
○ Associated with constipation
○ Lower abdominal pain and tenderness, often in LLQ
○ Fever
○ Not associated with alcohol
○ Possibly associated with dietary changes -> ask about dietary changes
● Evaluation: Diagnosis can be made solely on assessment and history once ruling out
other causes of abdominal pain
● Diagnostic labs: CBC, urinalysis, and flat and upright abdominal radiographs (shows
free air). CT with contrast for suspected acute colonic diverticulitis
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● Differential diagnoses: IBS, IBD, colon cancer, ischemic colitis, bowel obstruction, and
gynecologic and urologic disorders
● Treatment: Conservative medical management of uncomplicated diverticulitis includes
bowel rest and IV fluoroquinolones or extended-spectrum penicillins. Cipro and
Metronidazole is the antimicrobial treatment along with rest and hydration.
● ** If the patient does not improve after several days, an abscess should be suspected and
diagnostic imaging considered.
Hepatitis:
Treatment for each, pharmacologic options for each, prognosis for each?
Acute inflammation of the hepatic parenchyma.
● Risk factors: IV drug use, bacterial and fungal sources, autoimmune and metabolic
disorders, toxic poisoning, and various hepatotoxic medications (e.g., isoniazid,
acetaminophen)
● Hepatitis may result from various causes, both infectious (ie, viral, bacterial, fungal, and
parasitic organisms) and noninfectious (eg, alcohol, drugs, autoimmune diseases, and
metabolic diseases).
● Symptoms: low-grade fever, fatigue, lethargy, anorexia, RUQ pain, nausea, vomiting,
diarrhea, arthralgias and myalgias, and (in severe cases) dark urine and jaundice
● Evaluation: Tenderness over the liver occurs with percussion and deep palpation.
● Diagnostic labs: AST/ALT, Hepatitis Panel, Bilirubin, transaminases, ALP, GGT
● Differential diagnoses: EBV, HSV, Cytomegalovirus
● Treatment: Therapy with pegylated interferon and ribavirin has been shown to achieve
sustained viral eradication in almost 50% of patients with hepatitis C. Antiviral
treatments for Hepatitis B are indicated for patients with moderate to severe disease
diagnosed on liver biopsy; which includes interferon, lamivudine, and adefovir. Remove
the cause, avoid hepatotoxic agents such as alcohol, tylenol, and statins (Pravachol).
Treatment is supportive.
Drugs that may cause elevated liver enzymes:
Acetaminophen
Augmentin and other ATBs
Herbal supplements
Valproic acid and other anti-epileptics
Ketoconazole
Vitamin A
Methotrexate
Dantrolene
Glyburide
Amiodarone
Thiazolidinediones
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Sulfonamides
Chemotherapy drugs
Synthetic retinoids
NSAIDs
Statins
Anti-tuberculosis drugs
Azathioprine
> intrahepatic cholestasis can be caused by: anabolic steroids, BCP, penicillins, cimetidine,
estradiol
> Cholestasis: is defined as a decrease in bile flow due to impaired secretion by hepatocytes or
to obstruction of bile flow through intra-or extrahepatic bile ducts. Therefore, the clinical
definition of cholestasis is any condition in which substances normally excreted into bile are
retained.
What are the pharmacologic options for management?
Acute Hepatitis A
Treatment for acute hepatitis caused by hepatitis A virus (HAV) is necessarily supportive in
nature, because no antiviral therapy is available. Hospitalization is warranted for patients
whose nausea and vomiting places them at risk for dehydration. Patients with acute liver failure
require close monitoring to ensure they do not develop fulminant hepatic failure (FHF), which is
defined as acute liver failure that is complicated by hepatic encephalopathy.
HAV IgM: acute infection.
HAV IgG: resolved HAV
Acute Hepatitis B
As is the case for acute hepatitis A virus (HAV) infection, no well-established antiviral
therapy is available for acute hepatitis B virus (HBV) infection. Supportive treatment
recommendations are the same for acute hepatitis B as for acute hepatitis A. Lamivudine,
adefovir, dipivoxil, and other antiviral therapies appear to have a positive impact on the natural
history of severe cases of acute HBV infection. A study by Schmilovitz-Weiss described a rapid
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clinical and biochemical response in 13 of 15 patients with severe acute hepatitis B who received
lamivudine.
HBsAG: chronic infection
● Typically, PEG-IFN treatment is continued for 48 weeks for both HBeAg-positive and
HBeAg-negative chronic hepatitis. Oral agents may be used for as short as 1-2 years;
however, most HBeAg-positive chronic hepatitis patients and almost all HBeAg-negative
chronic hepatitis patients require indefinite therapy with these agents. Withdrawal of oral
nucleoside/nucleotide analogue therapy in these individuals usually results in virologic
relapse.
Acute Hepatitis C
Acute hepatitis C virus (HCV) infection is detected infrequently. When it is identified, early
interferon (IFN) therapy should be considered. In one study, 44 patients with acute hepatitis C
were treated with IFN alfa-2b at 5 million U/day subcutaneously (SC) for 4 weeks and then three
times per week for another 20 weeks. About 98% of patients developed a sustained virologic
response (SVR), defined as an undetectable level of serum HCV RNA 6 months after completion
of antiviral treatment. Most experts now equate achievement of an SVR with viral eradication or
cure of HCV infection.
Treatment of Hepatitis D and E
Treatment of patients coinfected with hepatitis B virus (HBV) and hepatitis delta virus (HDV)
has not been well studied. The only effective treatment for HBV/HDV coinfection is pegylated
interferon (PEG-IFN); antiviral nucleos(t)ide analogues have limited or no effect on HDV
replication. However, multiple small studies have demonstrated that patients with HBV-HDV
coinfection are less responsive to IFN therapy than patients with HBV infection alone.Treatment
with PEG-IFN alfa-2b produced HDV RNA negativity in only 17-19% of patients. Lamivudine
appears to be ineffective against HBV-HDV coinfection.
Treatment of patients infected with hepatitis E virus (HEV) infection is supportive in nature.
https://emedicine.medscape.com/article/775507-treatment
GERD:
DIFFERENTIATE FROM PUD
Poor esophageal motility resulting in reduced clearance of the gastric contents in the esophagus
•A dysfunction of the lower esophageal sphincter. The LES acts as a valve that helps to reduce
the amount of gastric contents that refluxes into the esophagus. Relaxation can be related to
things like alcohol, drugs (benzos), and caffeine. •Delayed gastric emptying that results in
increased pressure forcing gastric contents to reflux. Overeating, eating too fast, diabetic
gastroparesis. •Hiatal hernia and obesity contribute to symptoms
● Risk factors:
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Conditions that can increase your risk of GERD include: Obesity, Bulging of the top of the
stomach up into the diaphragm (hiatal hernia), Pregnancy, Connective tissue disorders, such as
scleroderma, Delayed stomach emptying
Factors that can aggravate acid reflux include: Smoking, Eating large meals or eating late at
night, Eating certain foods (triggers) such as fatty or fried foods, Drinking certain beverages,
such as alcohol or coffee, Taking certain medications, such as aspirin
● Symptoms: heartburn, regurgitation, dysphagia. Associated with meals, exacerbating
foods and behaviours. Changes in behavior make it better.
● Evaluation:
○ EGD and manometry can help to confirm the diagnosis and evaluate for
complications like esophagitis, strictures, Barrett esophagus, and motility
disorders.
○ 24-hr pH probe test can help if the diagnosis is not clear, atypical symptoms
● Diagnostic labs: None- most often provider does a medication/lifestyle modification trial
and if symptoms improve the diagnosis is made
● Differential diagnoses: CAD, nonulcer dyspepsia, PUD, esophagitis
● Treatment:
○ LifestyleModifications
■ Weight Loss
■ Avoid alcohol, chocolate, citrus, tomato-based products, peppermint,
coffee, and any other products that contribute to symptoms
■ Avoid overeating
■ Wait several hours before lying down after meals
■ Elevate the head of the bed
○ PPI (“-zole”): Omeprazole (Prilosec), Esomeprazole (Nexium), Lansoprazole
(Prevacid), Pantoprazole (Protonix)
■
■
■
MOA: Proton pump inhibitor (PlPI); binds to H+/K+-exchanging ATPase
(proton pump) in gastric parietal cells, blocking acid secretion, metabolized in
the liver
Differences: PPI increase the pH of the stomach
Standard-dose PPI treatment should be prescribed for 4 weeks in patients
with duodenal ulcers and for 8 weeks in patients with gastric ulcers
■ Efficacy: most effective for tx ulcers
● Long-term use associated with hip fx, PNE, C-diff infection,
hypocalcemia, hypomangnesemia. Do not d/c PPIs abruptly
because doing so can cause rebound symptoms. Taper the
dose!!!.
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○ H2 Blockers (“-idine”) : Ranitidine (Zantac), Nizatidine (Axid), Famotidine
(Pepcid)
■ MOA: H2-receptor antagonist; blocks H2 receptors of gastric parietal
cells, leading to inhibition of gastric secretions, Metabolized in liver
■ Differences: Works best on empty stomach without food. Almost all H2
blockers don’t work well after 2-6 weeks. The stomach adjusts and they
become much less effective.
■ Efficacy:
○ Antacids: Calcium Carbonate (Tums, Caltrate), Aluminum-Mg-Simethicone
(Mylanta, Maalox), Aluminum Mg (Gaviscon)
■ MOA: Neutralizes gastric acidity, be mindful of renal clearance
Differences:
■ Efficacy: Antacids don’t do anything to prevent GERD, but they can be
used on demand for symptom relief. Only last a short period of time
○ In patients with mild, intermittent therapy: Step up therapy■ Incrementally increasing the potency of therapy until symptoms are
controlled. Adjust treatment every 2-4 weeks. Lifestyle and dietary
modifications and H2 receptor antagonist (i.e. Ranitidine), along with
antacids prn (i.e. Tums) If continued symptoms, increase the dose of the
H2RA to twice daily for a minimum of 2 weeks. If still persists, stop the
H2RA and initiate a PPI at a low dose, then increase to standard dose if
needed.Once controlled, continue treatment for 8 weeks.
● In patient with erosive esophagitis, frequent or severe symptoms, consider step
down therapy.
○ Start with potent anti-secretory, and then incrementally decrease the
potency of therapy until breakthrough treatment is controlled. Standard
PPI x 8 weeks, then low dose PPI, then H2RA. Only continue long term
therapy in patients with severe erosive esophagitis or Barrett’s esophagus.
○ Any patient with at least a decade or more hx of chronic heartburn should
be referred to a gastroenterologist for endoscopy to rule out Barrett’s
esophagus.
Irritable Bowel Syndrome (IBS)
● Functional GI disorder that presents with abdominal pain, bloating, altered bowel habits
in the absence of specific pathology
● Sx: constipation, diarrhea, postprandial urgency, alternating diarrhea and constipation;
may ℅ dyspepsia, n/v, GERD
○ Pain may be diffuse or specifically in lower abdomen / LLQ
○ Dull ache with episodic sharp pains
○ Pain may be precipitated by meals, may be relieved by BM
○ Splenic flexure gas may cause LUQ pain or anterior chest pain
● Stools may have mucoid appearance
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● ROME IV criteria for diagnosis of IBS
○ Abdominal pain averages at least 1 day / week during previous 3 months
associated with at least two of the following:
■ Pain with defecation
■ Associated with change in stool frequency
■ Associated with change in stool appearance or form
● Diagnosis for patients under 50 without alarm features based on history and physical
● Alarm features: weight loss, iron deficiency, family hx of IBD, celiac disease, colorectal
cancer
● Management
○ Fiber supplements
○ Increase water intake
○ Limit caffeine
○ Avoid gas producing foods like legumes
○ Possibly probiotics
○ If stress related, psychological interventions / therapy may help
● Pharmacologic therapy
○ Anticholinergics like dicyclomine (Bentyl)
○ Antidiarrheals (Lomotil, Imodium)
○ Bulk forming laxatives
○ Antispasmodics (peppermint oil, bentyl)
Inflammatory Bowel Disease (IBD) → (Ulcerative Colitis and Crohns):
Chronic functional d/o of the colon marked by exacerbations and remissions. Commonly it is exacerbated
by stress.
● Ulcerative colitis involves the mucosal layer of the sigmoid colon and rectum in the
vast majority of cases, causing proctitis and proctosigmoiditis. Mucosa is inflamed
● Crohn disease differs from UC in that it may involve any part of the GI tract from the
mouth to the anus, including the gallbladder and biliary tree, and involves the entire
thickness of the bowel wall. It is most often found in the immunologically rich terminal
ileum, and Crohns disease involves the rectum in less than 50% of cases. In contrast to
UC, the mucosal abnormalities are discontinuous (“skip lesions”), asymmetric, and
patchy, which account for obstruction, abscesses, and perianal fistulas to other organs and
skin. In Crohns likely to have small bowel strictures, upstream dilation of intestine and
increased fistula formation, and eventual bowel obstruction and the imminent need for
surgical intervention. Intestinal obstruction with scarring and strictures
First line therapy for Crohn’s Disease or UC is Oral aminosalicylates
● Risk factors: Genetic factors,
● Symptoms:
○ UC: mild to moderate diarrhea and intermittent with flare ups, patients can go into
remission without therapy, bloody stool
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○ Crohns: Vague abdominal pain, mild diarrhea, bloody as there is colonic
involvement, bone loss, growth failure in peds,
○ Mucous in the stool is not specific and is found in IBS and IBD
● Evaluation:
○ UC: Confluent erythematous rectal inflammation, pseudopolyp formations
indicate chronic inflammatory colitis
○ Crohns: solitary aphthous ulcers (canker sores), “rakelike” lesions, strictures, and
rectal sparing, Anal or perianal lesions, including sinus tracts, rectovaginal
fistulas, and abscesses, is consistent with Crohn disease. Mucosa may appear
cobblestoned or nodular
○ Colonoscopic evaluation should include ileal intubation and biopsies of both
normal and abnormal mucosa.
○ Colonoscopy and biopsy (Gastroenterologist): • Abnormal mucosa with or
without ulceration extending from the rectum to all or part of the colon. • Uniform
inflammation without intervening areas of normal mucosa • Contact bleeding and
mucus in the bowel lumen
Ulcerative Colitis grading:
● Mild - bleeding per rectum, <4 BMs/day, mild LLQ tenderness, PE might be normal
● Moderate - bleeding per rectum, >4 BMs/day
● Severe - bleeding per rectum, >4 Bms /day, fever or other systemic symptoms, abd pain,
weight loss.
● Diagnostic labs: CBC, CMP, LFTs, inflammatory markers (sed rate, CRP), stool studies,
serologic tests (ANCA, ASCA), xray (shows free air or obstruction), CT, MRI, EGD,
Colonoscopy
● Differential diagnoses of UC: Lower GI bleeding, acute diarrhea, Crohn’s dz.
● Differential diagnoses of Crohns: Abd pain, acute diarrhea, chronic diarrhea, UC, small
intestinal tumor.
● Treatment: Steroids are effective for inducing but not maintaining remission in IBD.
▪ The 5-aminosalicylic acid (5-ASA) medications, sulfasalazine, are effective in
ulcerative colitis (UC) for therapy induction and maintenance therapy but largely are
ineffective for Crohns disease
● Budesonide, a non systemic steroid used in an enema formulation, has been effective for
induction of remission in Crohn disease and distal UC flares.
● Azathioprine and its metabolite, 6-mercaptopurine, are slow-acting compounds proved
effective for inducing remission in Crohn disease.
● Methotrexate is also effective for remission induction in Crohn disease. Close monitoring
of CBC and serum transaminases is recommended, with monthly testing on initiation and
with dosage changes. Pregnancy and exposure to live-virus vaccines should be avoided.
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● Infliximab (remicade), an anti–tumor necrosis factor α antibody, is remarkably effective
in treating approximately 60% of steroid-resistant patients with Crohn disease. Infliximab
has significant side effect risks, including infusion reactions, and, rarely, worsening of
heart failure, activation of latent tuberculosis, serum sickness, and invasive fungal
infections
● Can supplement dietary fiber using psyllium (Metamucil/Konsyl) methylcellulose
(Citrucel) wheat dextrin (Benefiber). Start low and increase because it can cause gas.
● Avoid gas-producing foods-> beans, onions, cabbage, high-fructose corn syrup.
● For abd pain can give antispasmodics Dicyclomine (Bentyl) or Hyoscyamine PRN
● Most pts with Chron’s will need surgery at some point in their lives.
● Increase fiber intake!! For IBS
Alarm features: ** Alarm features would include weight loss, iron deficiency, family
history of IBD, celiac disease, colorectal cancer
GI Bleed, Melena:
● Risk factors: ETOH, Blood thinners, clotting factor disorder, liver failure, PUD
● Evaluation: EGD or Colonoscopy depending on where the blood is suspected to be
● Diagnostic labs: CBC, comprehensive panel, coagulation profile, iron studies (including
transferrin saturation), reticulocyte count (before transfusion), and blood type and
crossmatch
Aortic Aneurysms:
● Risk factors:
-MAIN RISK FACTORS: Male sex, >65 years old, smoking history
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-OTHER RISK FACTORS: family hx of AAA, CAD, HTN, PAD, previous MI,
cerebrovascular disease, atherosclerosis, other vascular aneurysms, hypercholesterolemia,
obesity.
●
●
●
●
●
●
●
●
Screen: The USPSTF recommends one-time screening for abdominal aortic aneurysm
(AAA) with ultrasonography in men ages 65 to 75 years who have ever smoked.
Symptoms: “tearing” epigastric pain and a pulsing sensation, no relation to activity or
meals, no n/v/d, pain may radiate to back
Evaluation: Abdominal US, Non-contrast CT although CT angiography (CTA) is the
best diagnostic and pre intervention planning study, accurately delineating the location,
size, and extent of the aneurysm and the involvement of branch vessels.
Diagnostic labs: U/S is initial imaging of choice. CTA best for pre intervention
Differential diagnoses: PUD, SBO, Diverticulitis
Treatment: Treatment of lipids and HTN, antiplatelet therapy, referral to vascular
surgery, surgery needed if >5.5cm or grows more than ½ cm in 6 months
Who is most at risk? Males, over the age of 65 who have a history of smoking
What populations should be screened in primary care? Men aged 65-75 y.o. Who have
ever smoked.
How might children or elderly patients present differently?
When must you do additional work up or what are red flag signs in these populations that require more
urgent evaluation?
● Infants & young children at risk because:
○ Greater % body water _GREATER FLD DEMANDS
○ More rapid metabolic rate and H2O turnover
● Elders at risk because:
○ Reduced kidney function
○ Less resilient body systems
○ Decreased fluid intake _GREATER FLD DEFICITS
○ More likely to take meds that affect fluids and electrolytes
GI/Peds
Urgent Evaluation:
●
●
●
●
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Risk factors:
Symptoms:
Evaluation:
Diagnostic labs:
Differential diagnoses:
Treatment:
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Hydration/Dehydration:
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Risk factors: Diarrhea, vomiting, inadequate fluid intake, excessive urine loss, draining wounds,
gastric suction, ostomies, burns, and excessive sweating
Symptoms:
○ Mild - can they still cry? Will be able to make tears, 3-5% weight loss, normal VSS,
maybe slight decrease in UO, USG >1.020 (concentrated). Normal skin turgor.
○ Moderate: decrease tears, poor skin turgor, 5-10% weight loss, thirsty, dry mucous
membranes, no urine for >8 hours, appears or ℅ thirst. Might see depressed anterior
fontanelle.
○ Severe: weight loss 10-15%, tachycardic, orthostatic hypotension, dry MM, thirsty, no
tears, anterior fontanelle is down, oliguria, skin is tented, cool, and mottled.
Evaluation: for recent travel, relationship to food, presence of blood, ill contacts, meds, I&Os,
associated pain?
Diagnostic labs: Electrolytes, Pregnancy test, drug levels for toxicity, CBC, ESR, UA, BUN/Cr,
Stool analysis
Differential diagnoses: Gastroenteritis, amebiasis, lactose or food intolerances, Meds (Abx), IBS,
Colitis, Diverticulitis
Treatment: Mild and moderate can be replaced orally with electrolyte fluids. Gatorade is ok but
not preferred d/t CHOs which can be hard to tolerate. If Breastfeeding- continue BF. use small
amounts of frequent ingestion so you don’t induce vomiting. If severe → IV therapy. Increase
diet slowly starting with bland solids.
Appendicitis:
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Risk factors: M>F
Symptoms: fever, anorexia, nausea, vomiting, tenesmus (feeling the urge to defecate, distressing
and painful), migratory RLQ abdominal pain, abdominal tenderness and guarding, and signs of
peritoneal irritation
Evaluation: Classically, hours after onset, the pain migrates to the McBurney point , defined as
the point two thirds the distance from the umbilicus along a straight line toward the anterior
superior iliac spine of the pelvis. The Rovsing sign (referred tenderness from LLQ → RLQ during
palpation), psoas sign (pain elicited by extending hip posteriorly with patient lying prone), and
obturator sign (pain elicited by abducting right hip with patient lying supine, flexion of the hip)
are often conducted but are of little diagnostic value.
Diagnostic labs:
Differential diagnoses:
Treatment:
Gastroenteritis:
Viral is most common, bacterial can be from food poisoning, c diff, salmonella... and don't forget about
Giardia (protozoa)
● Risk factors:eating contaminated food sources (giardia in wild game), salmonella
● Symptoms: n/v/d
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Evaluation:
Diagnostic labs: none needed unless you suspect severe dehydration.
Differential diagnoses:
Treatment: restore hydration, absorbent meds, reduce inflammation with pepto, anti spasmodics,
antiemetics. Stick with light diet, may use advil for fever and pain. Need to closely monitor and
watch
> Medications: If you do the above and the patient is not getting better in 48 hours or has blood
present in the stool…
> stool testing, o&p, cbc, cmp.
C Diff- Metronidazole first line, Vanc works too
E. Coli, Shigella, Campylobacter- If >18, Cipro
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PUD:
Duodenal ulcers are more common than gastric ulcers, but gastric are more likely to be malignant.
Helicobacter pylori is a common cause of both.
● Risk factors: chronic NSAID use that disrupts the prostaglandin production reducing GI blood
flow and reduces the protective mucus layer. Tobacco and/or alcohol use, stress after acute
illness, ventilator support, extensive burns, or a head injury.
● Symptoms:
○ Worrisome symptoms: early satiety, anorexia, anemia, recurrent vomiting, hematemesis,
wt. Loss.
○ Episodic epigastric pain, burning/gnawing pain, or ache. Pain is relieved by
eating/antacids with recurrence 2-4 hours after a meal. Pain recurs when the stomach is
empty or they are hungry.
○ Stools can be black/tarry, red/maroon, coffee-ground emesis, or iron-deficiency anemia
indication GI bleeding.
● Evaluation: Abd exam normal/mildly tender epigastric area during flare-ups. Hemoccult can be
+ if actively bleeding.
● Diagnostic labs:
○ CBC: iron-deficiency anemia-> bleeding, fecal occult blood test
○ All patients with PUD should be tested for H. Pylori infection
■ Positive-> refer to gastroenterologist.
■ Serology Titers: H. Pylori immunoglobulin IgG levels elevated. Don’t use to
evaluate eradication of H. Pylori after treatment.
■ Urea breath test: indicative of active H. Pylori infection and is commonly used to
document eradication of Hy. Pylori after treatment.
■ Stool Antigen: Can be used for screening and posttreatment to document
eradication.
● Stool antigen and Urea blood test are more sensitive for active infection
than serology/titers.
Gold Standard: Upper endoscopy and biopsy of gastric and/or duodenal tissue are gold standard tests.
● Differential diagnoses:
● Treatment: PPI to inhibit gastric acid secretion and promote ulcer healing
○ Stop the use of NSAIDs, can decrease the risk with use of PPI or Misoprostol.
○ Smoking cessation
○ Lifestyle changes + PPI or H2 Blocker. Duration of therapy is 4-8 weeks. If there is no
response, poor response, or recurrent ulcers after 4-8 weeks of therapy suspect a bleeding
ulcer and refer to GI.
○ PPI:
■ Omeprazole (Prilosec) 20mg Daily
■ Esomeprazole (Nexium) 40mg Daily
■ Lansoprazole (Prevacid) 15-30mg Daily
○ H2 Blockers:
■ Ranitidine (Zantac) 150mg BID of 300mg at bedtime
■ Nizatidine (Axid) 150mg BID or 300mg at bedtime
■ Famotidine (Pepcid) 40mg at bedtime.
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○
Treatment of H. Pylori- Positive Ulcers:
■ Triple Therapy:
● Clarithromycin (Biaxin) 500mg BID + Amoxicillin 1gm BID or
Metronidazole (Flagyl) 500mg BID (if allergic to Amoxicillin) for 14
days.
■ Quadruple Therapy:
● Bismuth subsalicylate tab 600mg QID plus
● Metronidazole tab 250mg QID plus
● Tetracycline capsule 500mg QID x2 weeks plus
● PPI for 4-8 weeks to allow the ulcer to heal.
Intussusception:
Intussusception involves a section of intestine being pulled antegrade into adjacent
intestine with the proximal bowel trapped in the distal segment. The invagination of
bowel begins proximal to the ileocecal valve and is usually ileocolic, but it can be
ileoileal or colocolic. Intussusception is thought to be the most frequent reason for
intestinal obstruction in children.
Risk factors
● Intussusception most commonly occurs between 5 and 10 months of age and
is also the most common cause of intestinal obstruction in children 3 months to 6
years old
○ 80% of the cases occur before 2 years of age
● In younger infants, intussusception is generally idiopathic and responds to
nonoperative approaches.
● Known medical predisposing factors:
○ Polyps
○ Meckel diverticulum
○ Henoch-Schönlein purpura
○ Constipation
○ Lymphomas
○ Lipomas
○ Parasites
○ Rotavirus
○ Adenovirus
○ Foreign bodies.
● Intussusception may also be a complication of CF.
● Children older than 3 years are more likely to have a lead point caused by polyps,
lymphoma, Meckel diverticulum, or Henoch-Schönlein purpura; therefore, a
cause must be investigated.
Symptoms
● The classic triad for intussusception, intermittent colicky (crampy)
abdominal pain, vomiting, and bloody mucous stools, are present in
fewer than 15% of cases
● Paroxysmal, episodic abdominal pain with vomiting every 5 to 30 minutes.
o Vomiting is nonbilious initially
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Some children do not have any pain.
Screaming with drawing up of the legs with periods of calm, sleeping, or lethargy
between episodes.
Stool, possibly diarrhea in nature, with blood (“currant jelly”).
A history of a URI is common.
Lethargy is a common presenting symptom.
Fever may or may not be present; can be a late sign of transmural gangrene and
infarction.
Severe prostration is possible
Evaluation
● Observe the baby's appearance and behavior over a period of time; often the child
appears glassy-eyed and groggy between episodes, almost as if sedated.
● A sausage-like mass may be felt in the RUQ of the abdomen with emptiness in
the RLQ (Dance sign); observe the infant when quiet between spasms.
● The abdomen is often distended and tender to palpation.
● Grossly bloody or guaiac-positive stools.
Diagnostic labs/Studies
● Abdominal ultrasound is very accurate in detecting intussusception and is the
test of choice
● Abdominal Flat plate x-ray is only accurate ~60% of the time
● An air contrast enema is both diagnostic and a treatment modality
Differential diagnoses
● Incarcerated hernia
● Testicular torsion
● Acute gastroenteritis
● Appendicitis
● Colic
● Intestinal obstruction
Treatment
● Radiologic reduction using a therapeutic air contrast enema under
fluoroscopy is the gold standard
● Emergency management and consultation with a pediatric radiologist and a
pediatric surgeon is recommended
● Rehydration and stabilization of fluid status; gastric decompression
● IV antibiotics are often administered to cover potential intestinal perforation.
● A period of observation following radiologic reduction is recommended (12 to 18
hours)
Cardiac - PEDS
Fetal Circulation:
-Oxygenation of the blood occurs in the placenta, not the lungs
-Fetal pulmonary vascular resistance is high, and systemic vascular resistance in low (High
pressure on the right side of the heart, low pressure on the left)
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-The foramen ovale, the opening in the septum between the two atria, permits a portion of the
blood to flow from the right atrium to the left atrium
-A patent ductus arteriosus provides a connection between the pulmonary artery to the aorta
and bypass the fetal lungs
-Fetal circulation is best described as two parallel circuits, with the left ventricle supplying blood
to the upper extremities and the right ventricle serving the lower extremities and the placenta.
-At the time of transition to extrauterine life, these separate blood flow circuits become a
serial circuit.
(See Burns pg. 756 for full description of circulation)
Congenital heart disease
Understand fetal circulation and how blood bypasses the lungs
●
Risk factors:
Perinatal:
-Maternal infections and exposures- CMV, rubella, other viral syndromes
-Maternal use of tobacco, alcohol, street drugs, retinoic acid,lithium, valproates,
ibuprofen, naproxen, ACE inhibitors, tricyclic antidepressants, sulfonamides,
sulfasalazine, and hydantoins.
-Maternal chronic disease- CHD, lupus, insulin-dependent DM, phenylketonuria
-Maternal age- increased risk of chromosomal abnormalities after 40 years old
-Maternal pregnancy hx-excessive weight gain, gestational DM
Neonatal:
-fetal or newborn distress- hypoxia, aspiration
-prematurity
-Presence of associated anomalies- genetic or chromosomal abnormalities and
syndromes
-Neonatal infections (GBS)
-Birthweight- term infants <2500grams, SGA < two standard deviations from the mean
for gestational age
Newborn:
-murmur at birth or early infancy
-HTN at birth or beyond
-Feeding difficulty
-Cyanosis
-Tachypnea
Toddler, School aged, Teens:
-deviation from individuals normal growth pattern
-frequent respiratory tract infections
-prior murmurs, blue spells
-documented GABHS infection
-HTN
-SOB with exertion
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-CP with exertion
-syncope, dizziness
-Tachycardia, bradycardia
Family HX:
-CHD (especially 1st degree relatives)
-Sudden death or premature MI
-SIDS
-HTN
-Rheumatic fever
-Genetic syndromes
-Hypercholesterolemia
●
Etiology: Caused by an alteration in development of or failure of the embryonic heart to
progress beyond an early developmental stage. Occurs in the 2nd to 8th week of
gestation due to genetic, environmental, or multifactorial influences.
-Most cases have NO identifiable cause
-2-4% caused by teratogens (lithium, ACE inhibitors, tricyclic depressants, sulfonamides,
sulfasalazine, tobacco, alcohol, cocaine, marijuana, antiepileptics, retinoic acid,
ibuprofen, naproxen, maternal conditions, environmental influences (organic solvents,
pesticides, air pollution)
-Maternal illnesses (DM, connective tissue disorders, phenylketonuria, rubella, febrile
illnesses- especially influenza
-Genetic abnormalities
●
s/s of:
-Infants: Tachypnea, Tachycardia, Rales, Wheezing, Cardiomegaly, Hepatomegaly,
Periorbital edema, Poor feedings, Tires easily from feedings, Poor weight gain,
Diaphoresis. Cyanosis around the lips
-Children/Teens: Tachypnea, Tachycardia, Rales, Wheezing, Cardiomegaly,
Hepatomegaly, Orthopnea, SOB or dyspnea on exertion, Peripheral edema, Poor growth
and development.
Work-up for a heart murmur
● Innocent: (Heard in 80% of children)
-Usually grade I-III/VI in intensity and localized
-Changes with position
-May vary in loudness or presence from visit to visit
-May increase in intensity with fever, anemia, exercise, anxiety, tachycardia
-Systolic in timing (except for venous hum, which is continuous), peaking in first half of
systole
-Musical or vibratory in quality, sometimes blowing
-duration is short
-Best heard in LLSB or pulmonic areas (except for venous hum)
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-Rarely transmitted
-May disappear with Valsalva maneuver, position, or gentle jugular pressure- laying
down
-Vital signs= normal
-ECG= normal
-General health status = good
Examples: Stills murmur, Venous hum, Pulmonary flow murmur of infancy, Pulmonary flow
murmur of childhood, Aortic systolic murmur, Peripheral pulmonary stenosis, Mammary artery
souffle
Seven “S” of innocent murmurs:
-SYSTOLIC (apart from venous hum)
-SMALL (limited area)
-SOFT (low amplitude)
-SHORT
-SINGLE (no clicks or gallops)
-SWEET (never harsh except systolic flow)
-SENSITIVE (to posture or with respiration)
Diagnostic testing and indications for referral:
● Systolic Murmurs:
-Midsystolic - what is the significance of midsystolic murmur
-Grade 2 or less
-Asymptomatic and no associated symptoms or signs -> No further work
up! But if uncomfortable, have another coworker listen, or if not one else is able to help, refer to
cardiology
-Symptomatic or other signs of cardiac disease ->Refer
-Early systolic, late systolic, holosystolic -> Refer
-Grade 3 or more ->Refer
-Diastolic and continuous murmurs ->Refer
* No need for chest xray (Unless concerned for CHF) (won’t help you diagnose structural
abnormality of the heart) or ECG (unless you notice dysrhythmia)
● pathologic
-A murmur in a child with a syndrome associated with CHD (ex. Trisomy 21)
-Any diastolic murmur
-Any systolic murmur associated with a thrill
-Pansystolic murmurs- what is significance of pansystolic murmur?
-Continuous murmurs that cannot be suppressed
-Systolic clicks
-Opening snaps
-Fixed splitting of the second heart sound not associated with BBB
-An accentuated S2
-S4 gallops
-Not positional
-Grade III/VI or higher
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-Harsh quality
Causes of Pathologic murmur: Ventricular septal defect, Atrial septal defect, Patent ductus
arteriosus, Tetralogy of fallot, Pulmonary stenosis, Coarctation of the aorta (MUST check
FEMORAL pulses. In newborns and infants they may present with CHF and in older children
they are usually asymptomatic or they may complain of leg pain), Aortic stenosis, Tricuspid
atresia, Total anomalous pulmonary venous connection, Transposition of the great arteries.
Diagnostics:
● Chest X-ray- to visualize cardiac size, size of specific chambers and great
vessels, cardiac contour, status of pulmonary blood flow, status of lungs and
other surrounding tissue.
● ECG: monitors electrical activity of the heart from different locations in the
different planes of the body and gives information about forces of ventricular
contraction, hypertrophy, chamber dilation, and rhythm.
● Echocardiogram: Detects intracardiac structures and their motion, detects
arrhythmias and hemodynamic changes
● CBC: Rules out severe anemia or polycythemia as a cause of the murmur
● Other Diagnostics include: MRI (shows heart structures, and information about
chamber volumes and function), Hyperoxia test (supplementation with 100% O2
that results in pinking and increased O2 saturation when the disease is primarily
pulmonary), exercise testing (determine cardiac output in response to exercise
for endurance and capacity) and Cardiac Cath (shows vascular resistance,
cardiac output, heart anatomy, response of the heart to exercise and
medications)
Coarctation of the aorta
Narrowing of a small or long segment of the aorta
-Caused by a disturbance in the development of the
aorta or secondary tot of the ductus arteriosus.
- Newborns and infants may present with CHF, while older
children are usually asymptomatic or may have leg pain or
weakness
- Higher incidence in females with Turner Syndrome
- Associated with bicuspid aortic valve
Hx:
-COA not always apparent until ductus closes and
decreases blood flow to the lower body.
- complaints of tachypnea, poor feeding, cool lower
extremities.
-older children may complain of headaches, leg pain with
exercise
Physical:
-Systolic ejection murmur heard best over interscapular
region, normal S1S2, decreased or delayed femoral
pulse,have have increased left ventricular impulse
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-upper extremity hypertension with lower extremity hypotension (>20mmHg difference)
-bounding brachial, radial, carotid pulses
-signs of CHF
-delayed timing and absent or weak arterial and other distal arterial pulses
Work up:
-Chest Xray: normal to slightly enlarged heart and normal to increased pulmonary vascular
markers, rib notching may be seen
-ECG: depend on severity of lesion and age of child. In infants- hypertrophy may be seen. In
older children-LVH develops secondary to HTN
Echocardiogram: helpful in confirming dx and locating the constricted aortic segment. May also
show associated cardiac abnormalities.
MRI: Can define location, severity, and anatomy of the aortic arch
Patent ductus arteriosus
-A blood vessel in the developing fetus connecting the trunk of the pulmonary artery to the
proximal descending aorta. It allows most of the blood from the right ventricle to bypass the
fetus's fluid-filled non-functioning lungs.
Normal functional closing occurs 12-72 hours after birth.
-Permanent closure at 2-3 weeks.
-Patent ductus arteriosus is the failure of ductus closure causing a connection between the aorta and
pulmonary artery. Aortic blood is shunted into the pulmonary artery and recirculates through the
lungs.
Hx:
-Infant or child may be asymptomatic if the PDA is small.
-Increasing signs of CHF may appear in the first weeks of life in larger PDAs.
-PDA usually evident by 3 months.
Physical:
-In immediate postnatal period- murmur is soft, systolic, and heard along the left sternal border,
under the left clavicle, and in the back.
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-After the first weeks of life- typical grade II to V/VI, harsh, rumbling, continuous “machinery
murmur” is heard in the left infraclavicular fossa and pulmonic area with a thrill at the base.
-Physical findings of CHF may be present with a large shunt.
Work up:
Chest Xray: small to moderate shunt- heart is not enlarged. Larger shunts- both left atrium and
left ventricle can show enlargement.
ECG: large shunts show LVH, QRS axis is normal or rightward
Echocardiogram: shows patent ductus and usually enlargement of left atrium
Work up and clearance for Sports physical
●
Contraindications:
○ Recurrent episodes of upper extremity pain or weakness
○ Severe hypertension- >160/100.
○ Sickle cell disease - increased rate of rhabdo and increased risk of sudden
cardiac death
○ Suspected CAD
○ Active myocarditis or pericarditis
○ Acute enlargement of liver or spleen
○ Eating disorder
○ Hx of recent concussion and sx of post concussion syndrome- have to by
symptom free for 1 week in order to return to sports.
○ Hypertrophic cardiomyopathy
○ Long QT
○ Poorly controlled seizure disorder
● See table 13-6- conditions of absolute contraindications
Evaluation:
● PMH positive for following requires follow up questions (helpful to have parent in room
for PMH):
○ Syncope/near syncope - vasovagal not as worrisome as other etiologies
■ Need to r/o wolff-parkinson white syndrome, long QT syndrome, and
hypertrophic cardiomyopathy - get EKG
○ Heart murmur
○ Elevated BP
○ Prior cardiac testing
○ Prior restriction from sports participation
○ Eating disorders - prevalent in weight sensitive sports (gymnastics, wrestling,
dance)
○ Psych disorders - are they stable?
○ Drug abuse
○ Anemia - work pt up for sickle cell, fatigue, heavy menses in females-> check
CBC
● Family history positive for following may require follow up:
○ Premature sudden death <50 years old
○ Disability from CV disease <50 years old
○ HCM, dilated cardiomyopathy, long QT, Marfan
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ROS:
○ Asthma - asymptomatic @ rest and exertion = cleared
○ Derm - open wounds, infections, tinea, herpes = ok to play but educate re:
preventing spread
■ Musculoskeletal - confirm no sequelae to hx of injury
■ Neuro - hx of seizure - may not want to clear for water sports (higher risk
of death if seizure during activity)
● Concussion - should NEVER return to play until asymptomatic
○ Physical exam red flags:
■ Tachycardia
■ Elevated bp
● <160/100 = ok to play, but counsel and monitor pt
● >160/100 = not cleared
■ Arrhythmia - get EKG
■ Murmur - assess sitting, lying, standing, squatting, during valsalva, after
activity
● Systolic murmur most worrisome >> if increases with valsalva
and decreases with squatting = hypertrophic cardiomyopathy
= most common cause of sudden cardiac death
● Benign murmurs will not change with squatting
■ Marfan syndrome - refer if 2 or more of below are noticed:
● Height > 5’10” (females) or 6’0” (males)
● Kyphoscoliosis-> side to side curve and a front to back curve
● Pectus excavatum-> breast bone is indented
● Arm span > height
● Moderate - severe myopia
Cardiac - Adult
s/s cardiac disease in adults
Utilizing testing appropriate to diagnosis
Appropriate referral for CAD, CHF, and arrhythmias
Education of s/s of heart disease
What populations tend to have less obvious symptoms? What are atypical signs and
symptoms?
Tests/diagnostics/labs and the info they provide
Coronary Artery Disease:
●
Risk Factors:
○ Obesity
○ HTN
○ Elevated cholesterol (esp. LDL)
○ DM
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○ Smoking
○ Age
○ Family Hx (1st degree relative age 55 for men, age 65 for women)
○ women- hx of preeclampsia/eclampsia
Patho of CAD
●
Classification of chest pain:
○ Typical Angina: Substernal chest discomfort, caused by exertion or emotional
stress, relieved by rest or nitroglycerin
○ Atypical (unstable) Angina: More often in women, 2 of the 3 characteristics
above, and nondescript symptoms such as SOB, fatigue.
○ Non-cardiac chest pain: Has one or more of the characteristics above.
●
Unstable Angina:
○ Rest Angina: occurs at rest, usually prolonged for more than 20 minutes, these
characteristics occur within 1 month of initial presentation
○ New onset Angina: Angina of at least CCS Class III severity with onset within 2
months of initial presentation
○ Increasing Angina: Angina that occurs more frequently, longer duration or with
less effort.
What is the difference between unable angina and STEMI?
Test to evaluate heart disease and info they provide- ECHO, EKG, TROP, STRESS
TEST, HEART CATH
●
EKG:
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Show nonspecific ST segment and T-wave abnormalities in pt with severe CAD.
■ This can have false positives in cases with LVH, digoxin intake, electrolyte
imbalances, or conduction anomalies like BBB or pre-excitation syndromes.
Echocardiography:
○ Done in new or worsening HF or new MI to assess LV function and regional wall motion.
Exercise Treadmill testing:
○ Based on the pt ability to exercise
○ Measures the presence of ischemic ST segment changes, reproducibility of CP,
arrhythmias, changes in BP and HR and functional capacity.
○ Sensitivity: 68%, specificity: 77%
○ Early positive result in the first two stages of the test can indicate a worse prognosis, and
is considered a high risk finding.
○ If the pt experiences CP and -1 mm ST segment depression during exercise the test can
be 90% predictive of the presence of CAD.
○ A 2mm ST segment depression + CP is indicative of the presence of obstructive CAD.
○ The presence of anti-ischemic agents (Nitrates, BBs, and CCBs) can reduce sensitivity
and should be withheld 2-3 days prior to the test for long acting drugs and 24 hrs for
short-acting drugs- IF the intent is to dx the presence of obstructive dz.
○ ABSOLUTE CIs to treadmill stress tests: decompensated CHF, symptomatic AVS,
ongoing resting CP, recent MI (w/in the past wk), severe HTN, and intractable
arrhythmias.
○ Nuclear stress tests and Stress Echos are the alternatives in this case.
Stress myocardial perfusion imaging: Nuclear stress test:
○ More accurate to dx obstructive CAD
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Sensitivity (88%) and specificity (72%)
Best ordered in those with intermediate likelihood of obstructive CAD
Adenosine and Dobutamine commonly used.
■ Adenosine dilates the coronary arteries and shunt blood away from
abnormalities.
● Can cause bradycardia and high degree AV block.
■ CI: in those w/ hyperactive airway dz (asthma)
■ NO CAFFEINE 12-24 hrs prior
■ Excellent choice for those who cannot walk on the treadmill
■ Dopamine increases HR and contractility and therefore increases myocardial O2
demand.
■ Reserved for those who cannot walk or the treadmill and those with a CI to
Adenosine.
Stress Echo:
○ Similar to nuclear stress test, but sensitivity is slightly lower.
○ Performed by obtaining initial resting echo images of the heart
○ Assesses LVEF, wall motion characteristics and cavity size.
■ 25% of pt may be difficult to obtain images: severe COPD and morbid obesity.
○ Pt then exercise on the treadmill to a limited protocol to a target HR of 85% of maximum
predicted for age.
○ Once HR is met, post-stress images are obtained at target HR.
MI: Acute mismatch of myocardial O2 supply and demand.
○ Classic presentation of acute MI: substernal chest pain radiating to the left arm,
neck and jaw and interscapular area. Associated with SOB, nausea and
diaphoresis
○ CPR and defibrillation if needed. Administer aspirin, and provide O2 if sat <90%> only if hypoxemia. (increases SVR, coronary vasoconstriction and increased
oxidative stress) Consider the use of nitrates and analgesics.
○ Obtain a 12-lead ECG and note ST elevation. Mobilize hospital resources to
respond to STEMI. Complete a fibrinolytic checklist if it’s indicated.
○ Check for contraindications for fibrinolytic therapy if indicated, and obtain initial
cardiac marker labs, coagulation studies, and electrolyte panel.
■ Absolute contraindications to fibrinolytic:
● Hx of intracranial hemorrhage, structural cerebrovascular lesion,
intracranial neoplasm, ischemic stroke </= to 3 months except for
acute ischemic stroke within 4.5 hours, suspected aortic
dissection, active bleed/bleeding diathesis, significant closed
head/facial trauma within 3 months, intracranial/intraspinal surgery
within 2 months, and/or severe uncontrolled HTN not responding
to therapy.
■ Relative Contraindications:
● Chronic, severe, poorly controlled HTN; syst BP >180 +/- DBP
AAA>110; ischemic stroke >3 mo. or dementia, known intracranial
pathology not covered in absolute contraindications, CPR >10
minutes or major surgery <3 weeks; internal bleeding within 2-3
weeks; noncompressible vascular punctures; pregnancy; active
peptic ulcer; and/or warfarin therapy
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If O2 sat <90%, start O2 at 4L/min. Administer 160 to 325 milligrams of aspirin.
Administer nitrates for chest pain if indicated. If the pain persists, consider the
use of analgesics (morphine is 1st line) to manage the patient’s pain.
ECG interpretation. Classify the patient as: ST-elevation myocardial infarction
(STEMI); non-ST-elevation (NSTEMI); or low to intermediate risk acute coronary
syndrome.
Echocardiogram to look for wall motion abnormalities that indicate ischemia
STEMI:
■ New ST elevation at the J point:
● > 2mm (0.2mV) in leads V2-V3 (men)
● > 1.5 mm (.15mV) in leads V2-V3 (==)
● > 1 mm (0.1mV) in 2 or more other contiguous chest leads or limb
leads
■ Special Cases:
● ST depression > 2 mm in V1-V4 => transmural Posterior Wall MI
● Multi-lead ST depression AND ST elevation in AVR => Left Main
or Proximal LAD occlusion
● Aspirin is the very first drug to be administered
○ MONA:
■ Morphine (ONLY when NTG doesn’t work):
● Initial dose 4-8mg, then 2-8IV q5-15min
■ O2: only in those with sat <90
■ NTG:
● SL: 0.4mg q5min x3
● Spray: 1-2 sprays under the tongue
● IV only if no SL or spray- 12.5-25mcg
● DO NOT GIVE if suspected right ventricular
infarct (ST elevation in inferior + V4R) OR if
pt has used a phosphodiesterase inhibitor
for erectile dysfunction (sildenafil or
tadalafil)- leads severe hypotension
■ ASA- ASAP! 162-325mg chewed or crushed buccal membranes work more rapidly. Maintenance
dose 81mg indefinitely.
● Loading dose of a P2Y12 receptor inhibitor as soon as possible:
○ Clopidogrel (Plavix) 600 mg po
○ Prasugrel (Effient)
60 mg po
○ Ticagrelor (Brilinta) 180mgpo
● Fibrinolytics in STEMI only when anticipated time to PCI exceeds
120 min
○ Tissue Plasminogen Activator (t-PA; Alteplase)
○ Recombinant Tissue Plasminogen Activator (Reteplase)
○ TNKase (Teneceteplase)
● Tissue Plasminogen Activator (t-PA) Dosing
○ “Front-loaded” or Accelerated
○ 15 mg IV bolus over 2 – 3 minutes
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■
■
■
○ 0.75 mg/kg over the next 30 min. (Max. 50 mg)
○ 0.50 mg/kg over the next 60 min. (Max. 35 mg)
○ Total dose 100 mg max
● Recombinant t-PA (Reteplase)
○ Third generation plasminogen activator
○ Has a moderately short half-life (13 –16 min.)
○ Non-antigenic
○ Dose: 10 Units IV over 2 minutes
○ Repeat in 30 min.
● Time from onset of symptoms < 12 hours. If the time from onset of
symptoms is 12 hours or less, proceed with reperfusion therapy. If
the time from onset is greater than 12 hours, treat as a troponin
elevated or high-risk patient.
Reperfusion goals. The door to balloon inflation goal for PCI is 90
minutes. The door to needle goal for fibrinolysis is 30 minutes.
Anticoagulation with fibrinolytics:
● Heparin (unfractionated) wt adj, to PTT of 1.5-2 times control for
48hrs or until revascularization.
○ Bolus 60u/kg (max 4000)
○ Infusion at 12u/kg/hr (max 1000)
● Enoxaparin:
○ <75 yrs- 30mg bolus, after 15 mins- 1mg/kg sc q12hr
○ 75 of older- no bolus- 0.75mg/kg sc q12hr
● Fondaparinux- initial 2.5mg bolus, then 2.5mg sc q24hr, CI in
those with CrCl <30mL/min
NSTEMI:
● Horizontal or downsloping (>0.5 mm)
● T wave inversions (symmetrical; >2mm)
● Use TIMI (thrombolysis in Myocardial Infarction) The
thrombolysis in myocardial infarction (TIMI) risk score is a tool
used to predict the chances of having or dying from a heart event
for people with unstable angina, non-ST-segment elevation
myocardial infarction (NSTEMI)
○ risk score: >= 3 will benefit from LMWH, GP IIb/IIIa
inhibitors, or invasive strategies like cath and/or stenting
● GRACE risk score:
○ 0-100 is low risk;
○ >140 should go to cath lab w/in 24hrs.
○ 109-140 (or TIMI >=2)- should have a delayed invasive
strategy got to cath lab 25-72 hrs after presentation of MI
● FIBRINOLYTICS contraindicated in NSTEMI
●
Nondihydropyridine calcium channel blockers (eg. verapamil,
diltiazem) and nitrates may be helpful for ongoing ischemia
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○
○
Troponin elevated or high-risk patient. A troponin elevated or high-risk patients
should be considered for early invasive strategy if they are experiencing
refractory ischemic discomfort, recurrent ST deviation, unstable blood pressure,
ventricular tachycardia, or signs of heart failure. Administer nitroglycerin and
heparin as indicated.
Biomarkers for Infarction:
■ Myoglobin
● Non-specific- found in skeletal muscles
● Rises quickly (1-4 hrs)
■ CK-MB
● More specific
● Rises in 3 – 12 hrs
■ Troponin I and Troponin
● Highly specific
● Rise in 3 – 12 hrs; Elevated 7 – 10 days
● Only marker used to dx. CAD
●
Treatment of patients diagnosed with coronary disease
○ Lifestyle modification (diet, weight loss, physical therapy)
○ ASA 75-162 mg daily or Clopidogrel 75mg daily (if ASA intol)
○ Moderate to high dose statin -> atorvastatin/rosuvastatin
○ HTN control
○ DM- glycemic control
○ Smoking cessation
●
Diet:
○
○
Reduced saturated fats (<7% of total calories, transfats. <1%, chol <200mg/d)
Mediterranean or DASH diet
●
Weight control:
○ Optimal weight: BMI 18.5-24.9
○ Waist circumference- Men <40, women < 35
○ Assess at every visit
■ Initial weight loss goal 5-10% of baseline weight
●
BP Control: GOAL <130/80
○ Lifestyle
○ Na reduction
○ Medications
■ ACE inhibitors
● Anterior MI, HF, EF </= to 40%.
■ Beta blockers (if previous MI or ACS, LVEF <40% with HF)
● No beta blockers if signs of HF, severe bradycardia, low output
state, increased risk for cardiogenic shock, conduction
disturbances (PR interval prolonged, heart blocks), active
asthma/reactive airway disease.
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■
■
●
● Decrease myocardial O2 consumption and reduce anginal pain
Thiazide diuretics
Calcium Channel blockers (long acting verapamil, diltiazem)
● Decrease myocardial O2 consumption by dilating coronary
arteries, decrease contractility, and increase coronary BF
Followup:
○ See patients annually to assess for:
■ Symptoms
■ Complications (new HF, MI, arrhythmia)
■ Adherence to medication and lifestyle changes
■ Development of comorbid conditions (DM, CKD, Depression)
■ Resting EKG > 1 year in stable patients
■ Evidence not well established for annual stress testing
Chest pain pertinent H&P:
How to differentiate between chest pain and costochondritis or pleuritic pain?
Heart Failure:
●
●
●
●
Pathogenesis
Risk Factors:
○ ***HTN
○ DM
○ MI
○ CAD
○ Alcohol use
○ Tobacco use
○ Obesity
○ Sleep apnea
○ Valvular heart disease
○ Congenital heart defects
○ Arrhythmias
○ Medications such as NSAIDs, anti-arrhythmic drugs, and so on
○ Infections affecting the heart
Signs & Symptoms:
○ Fatigue
○ Weakness
○ Shortness of breath
○ Edema in the extremities=
○ Rapid or irregular heartbeat
○ Rapid weight gain
○ cough, wheezing, pink tinged sputum
HF Contraindicated medications: NSAIDs (due to sodium retention) and Ca Channel
blockers (due to decreased contractility of the heart)
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●
Treatment:
○ Stage A:
■ ACEI or ARB in appropriate pts for vascular dz or DM
■ Statins as appropriate
○ Stage B:
■ ACEI or ARB as appropriate
■ BB as appropriate
■ In select pts: ICD and revascularization
○ Stage C: with reduced EF (HFeEF)
■ ACEi or ARB and BB and diuretics - guideline directed
■ In black patients: isosorbide dinitrate
■ In those with an EF =<35%: ICD and/or cardiac revascularization
○ Stage D:
■ Palliative care
■ Transplant
■ LVAD
■ Investigational trials/studies
Heart Sounds
S1- closing of the mitral and tricuspid valves at the transition from diastole to systole
S2- Closing of the aortic and pulmonic valves at the transition from systole to diastole
S1
-Intensity predominantly determined by mitral valve component
-Loudest @ the apex
-Intensity related to speed with which the mitral valve closed
-Associated with the strength of LV contraction at the moment of closure
What are normal variations of heart sounds in children? What are abnormal variations?
Abnormalities of S1:
● LOUD S1: Short PR interval, mild mitral stenosis, hyperdynamic states
● SOFT S1: Long PR interval, severe mitral stenosis, LBBB, COPD, Obesity,
pericardial effusion
● VARIABLE S1: AV dissociation, A-fib, Large pericardial effusion and severe LV
dysfunction (auscultatory alternans- alternates loud and soft)
S2:
-Easiest to hear at the upper sternal border
-Normally split during inspiration (Contributions from aortic and pulmonic valves are not
simultaneous)
-Intrathoracic pressure decreases during inspiration and leads to increased right
ventricular preload, then increased right ventricular systole, delaying P2
-Decreased LV preload during inspiration leads to shorter LV systole, earlier A2
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Abnormalities of S2:
● WIDE SPLIT: S2 mildly split during expiration and more dramatically split during
inspiration
○ Caused by anything that delays RV contraction and thus P2 which makes LV
contraction in A2 premature, increasing RV afterload or decreasing LV
afterload
○ RBBB, pre-excitation of LV (Wolff- Parkinson White Syndrome), pulmonary HTN,
massive PE, severe mitral regurgitation, constrictive pericarditis.
● FIXED SPLIT: S2 split equally in inspiration and expiration
○ Common in atrial septal defect or severe RV failure
● REVERSED SPLIT: Split heard on expiration, not inspiration (inverse of wide split)
○ LBBB, pre-excitation of RV (RV pacing, Wolff-Parkinson White Syndrome), aortic
valve disease, LV outflow tract obstruction
● ABSENT A2: Severe aortic valve disease- seen in elderly
● FUSED A2P2: Occurs throughout respiration cycle-> Absent split
○ VSD in Eisenmenger syndrome, single ventricle- seen in pediatrics[
● LOUD P2: Suggestive of pulmonary HTN- heard at apex.
S3: -low pitched, early diastolic sound -Easiest to hear at apex when patient in left lateral
decubitus position
-Although occasionally heard in young healthy people and pregnant women-> in those over
40 years old = usually pathologic and indicative of LV failure
-”Ventricular Gallop”
S4:
-low pitched, late diastolic sound (pre-systolic)
-Always pathologic, though to be caused by atrial contraction into a stiff and non-compliant
ventricle
-Has been described in patients with afib and aflutter but the mechanism for this has yet to be
explained.
-”Atrial Gallop”
Summation Gallop= S3 +S4 are superimposed during tachycardia
Gallops: Usually originate from the left side of the heart, but can occur from right side
-Left sided (ex. CHF)- Softer with inspiration
-Right sided (ex. Massive PE)- louder with inspiration
Clicks:
● Aortic Ejection Click: early is systole, opening of aortic valve, high pitched, heard
everywhere if audible at all, not affected by patient standing
○ Indicated pathology of aortic valve
● Mitral Valve Prolapse Click: Occurs during mid-systole, caused by prolapse of one of the
mitral valve leaflets, high pitched, audible only at apex, occurs earlier in systole when
standing
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Split S1
● Normal split of S1, very narrow and not appreciable
● Causes○ S1 is actually split: tricuspid valve closure delayed relative to the mitral valve
closure for some reason (RBBB, pre-excitation, idioventricular rhythm from left
ventricle
○ 1st component of S1 is actually S4
○ 2nd component of S1 is actually aortic ejection click
● True split S1:
○ Both components high pitched, heard best at LLSB
● S4 mimicking Split S1:
○ First component low pitched, second component is high pitched, heart best at the
apex
● Aortic Ejection Click:
○ Both components high pitched, heard equally everywhere
Significance of split S2 murmur?
Grading of Murmurs:
●
●
●
●
●
●
Grade I. Barely audible and may require several cycles to detect
Grade II. Soft, but easily audible
Grade III. Moderately loud murmur without a thrill- about as loud as the S1 heart
sound
Grade IV. Loud murmur with a thrill
Grade V. Loud murmur heard with the stethoscope barely off the chest
Grade VI. Loud murmur heard without the stethoscope touching the chest
Benign murmurs:
●
●
Vibratory Still's Murmur:
○ most common innocent murmur in children.
○ typically audible in children between ages 2 and 6
○ may be present as late as adolescence or as early as infancy
○ low to medium in pitch, in early systole
○ Normally grade III (range I-III)
○ Heard maximally at the LL sternal edge and extending to the apex
○ Loudest in supine
○ changes in character, pitch and intensity with upright positioning
○ Characteristic: vibratory, musical, harmonious, like twanging string
○ Quality: rough or noisy
○ d/t physiologic narrowing of the left ventricular outflow tract
Pulmonary Flow Murmur
○ heard in children, adolescents, and young adults
○ crescendo- decrescendo, loudest in early- to mid-peaking ejection systolic
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○
●
●
●
●
At the second and third interspaces at the left sternal border, radiates to the
pulmonary area
○ Low intensity: grade II-III
○ rough and dissonant without the vibratory musical quality
○ best heard in the supine position and is exaggerated by the presence of a
pectus excavatum
Peripheral Pulmonary Arterial Stenosis Murmur
○ frequently in newborns and in infants younger than 1
○ audible turbulence of peripheral branch pulmonary arterial stenosis, angulation,
or narrowing
○ Grade I or II
○ Low to mod pitch, begin in early to mid systole, occasionally just after S2
○ May be associated with URI in infants, in the recovery phase
○ best heard peripherally in the axillae and back
Supraclavicular or Brachiocephalic Systolic Murmur
○ systolic crescendo-decrescendo murmur may be heard in children and young
adults
○ audible maximally above the clavicles and radiates to the neck but may be
present to a lesser degree on the superior chest
○ Low to med pih, abrupt onset and maximal in the first half or ⅔ of systole
○ Present in supine and sitting, varies with hyperextension of the shoulders
Aortic Systolic Murmur or “Athlete’s Murmur”
○ arise from the outflow tract in older children and young adults
○ may arise secondarily to extreme anxiety, anemia, hyperthyroidism, fever, or
any condition of increased systemic cardiac output
○ ejection in character, confined to systole, and audible maximally in the aortic area
○ In trained athletes, slower heart rates with increased stroke volume may give rise
to short crescendo-decrescendo murmurs of low to medium pitch
○ These murmurs must be distinguished from the systolic murmur of hypertrophic
cardiomyopathy
■ presence of a family history of hypertrophic cardiomyopathy or a family
history of unexplained death in a young individual- especially w/ activity
■ systolic murmur that gets louder with Valsalva maneuver and is
considered almost diagnostic of hypertrophic cardiomyopathy with
systolic anterior motion of the mitral valve
■ rapid squatting improves venous return; the left ventricular chamber
size is enlarged, the mitral valve and septum are farther apart, and the
murmur of hypertrophic cardiomyopathy gets softer
Venous Hum
○ Normal continuous murmur.
○ most common type of continuous murmur heard in children
○ most audible on the low anterior part of the neck just lateral to the SCM but
often extends to the infraclavicular area of the anterior chest wall
○ Normally louder on the right than on the left, is louder when the patient is sitting
than when lying down, and is accentuated in diastole
○ From faint to grade III
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○
○
○
●
Variable in character
Always low pitched- “rumbling”, “roaring”, or “whirring”.
Best elicited with the patient in a sitting position and looking away from the
examiner
○ resolves or changes in character with lying down and may be eliminated or
diminished by gentle compression of the jugular vein or turning the head
toward the side of the murmur
○ D/t turbulence at the confluence of flow as the internal jugular and subclavian
veins enter the thoracic inlet or perhaps from angulation of the internal jugular
vein
Mammary artery soufflé
○ High-pitched systolic murmur that can extend into diastole
○ best heard along the anterior chest wall over the breast
○ Rare in adolescence
Pathologic murmurs:
●
●
●
●
Ventricular septal defect
○ In 20-25% of children with CHD
○ Small defects: usually asymptomatic
○ Medium or large defects: CHF, symptoms of bronchial obstruction, frequent
respiratory infections
○ Small defects: loud holosystolic murmur at LLSB (may not last throughout
systole if defect is very small)
○ Medium and large defects: increased right-to- left ventricular impulses; thrill at
LLSB; split or loud single S2; holosystolic murmur at LLSB without radiation;
grade 2 to 5; may also hear a grade 1 or 2 mid-diastolic rumble
Atrial septal defect
○ In 8-13% of children with CHD
○ Usually asymptomatic and incidentally found on physical examination or
echocardiography; large defects can be present in infants with CHF
○ Grade 2 or 3 systolic ejection murmur best heard at ULSB; wide split fixed S2;
absent thrill; may have a grade 1 or 2 diastolic flow rumble at LLSB
Patent ductus arteriosus
○ In 6-11% of children with CHD
○ May be asymptomatic; can cause easy fatigue, CHF, and respiratory symptoms
○ Continuous murmur (grade 1 to 5) in ULSB
○ (crescendo in systole and decrescendo into diastole); normal S1; S2 may be
“buried” in the murmur; thrill or hyperdynamic left ventricular impulse may be
present
Tetralogy of Fallot
○ In 10% of children with CHD
○ Onset depends on severity of pulmonary stenosis; cyanosis may appear in
infancy (2 to 6 months of age) or in childhood; other symptoms include
hypercyanotic spells or decreased exercise tolerance
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○
●
●
●
●
●
●
Central cyanosis; clubbing of nail-beds; grade 3 or 4 long systolic ejection
murmur heard at ULSB; may have holosystolic murmur at LLSB; systolic thrill at
ULSB; normal to slightly increased S1; single S2
■ Ventricular septal defect
■ Pulmonary Valve stenosis
■ Misplaced aorta
■ R ventricular hypertrophy
Pulmonary stenosis
○ In 7.5-9% of children with CHD
○ Usually asymptomatic but may have symptoms secondary to pulmonary
congestion.
○ Systolic ejection murmur (grade 2 to 5); heard best at ULSB radiating to
infraclavicular regions, axillae, and back; normal or loud S1; variable S2; systolic
ejection click may be heard at left sternal border and may vary with respiration
Coarctation of the aorta
○ In 5.1-8.1% of children with CHD
○ Newborns and infants may present with CHF; older children are usually
asymptomatic or may have leg pain or weakness
○ Systolic ejection murmur best heard over interscapular region; normal S1 and
S2; decreased or delayed femoral pulse; may have increased left ventricular
impulse
○ This is why it is so important to check the femoral artery pulses!
Aortic Stenosis
○ In 5-6% of children with CHD
○ Usually asymptomatic; symptoms may include dyspnea, easy fatigue, chest pain,
or syncope; newborns and infants may present with CHF
○ Systolic ejection murmur (grade 2 to 5) best heard at upper right sternal border
with radiation to carotid arteries; left ventricular heave; thrill at ULSB or
suprasternal notch
Transposition of the great arteries
○ In 5% of children with CHD
○ Variable presentation depending on type; may include cyanosis or CHF in first
week of life
○ Cyanosis; clubbing of nail beds; single S2; murmur may be absent or grade 1 or
2 nonspecific systolic ejection murmur; may have a grade 3 or 4 holosystolic
murmur at LLSB and mid-diastolic murmur at apex
Total anomalous pulmonary venous connection
○ In 2-3% of children with CHD
○ Onset of CHF is 4-6 wks of age
○ Grade 2 or 3 systolic ejection murmur at ULSB; grade 1 or 2 mid-diastolic flow
rumble at LLSB; wide split fixed S2
Tricuspid atresia
○ In 1.4% of children with CHD
○ Early-onset cyanosis or CHF within the first month of life
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○
Cyanosis; clubbing of nail beds; normal pulses; single S2; holosystolic murmur at
LLSB or midsternal border; murmur may be absent; mid- diastolic flow murmur at
apex may be present
MURMUR PNEUMONIC:
Systolic murmurs: MR Peyton Manning AS MVP
●
Mitral Regurgitation, Physiologic Murmur, Aortic Stenosis, Mitral Valve
Prolapse
Diastolic murmurs: ARMS
●
●
● Aortic Regurgitation, Mitral Stenosis
Another:
MR. ASS (Mitral Regurgitation, Aortic Stenosis, systolic) heard in S1
MS. ARD (Mitral stenosis, aortic regurgitation, diastolic), heard in S2
Exam findings for aortic insufficiency and mitral valve disorder
Endocarditis:
●
Causes: Inflammation of the endothelium of the heart most likely due to microorganism.
-Endothelium is connected to the valves and leads to cardiac output problems due to
valvular involvement
-cause extra heart sounds or murmurs (AV blocks)
-most commonly bacterial
-Most common pathogens from normal flora of mouth or skin (Strep + Staph)
Risk Factors:
-IV drug abusers
-Male>female
-Dental work
-Artificial heart valve
-Congenital heart defects
-Hypertrophic cardiomyopathy
●
Indications for Prophylaxis:
-Prosthetic cardiac valves, including transcatheter-implanted prostheses and
homografts
- Prosthetic material used for cardiac valve repair, such as annuloplasty rings and
chords -Previous endocarditis
-Congenital heart disease (CHD) only in the following categories:*
–Unrepaired cyanotic CHD, including those with palliative shunts and conduits
–Completely repaired congenital heart defect with prosthetic material or device, whether
placed by surgery or catheter intervention, during the first six months after the procedure
–Repaired CHD with residual shunts or valvular regurgitation at the site or adjacent to
the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
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-Cardiac transplantation recipients with valve regurgitation due to a structurally
abnormal valve
●
Treatment for disease and prophylaxis:
Treatment:
-Antibiotic therapy, prolonged, at least 6 weeks, IV, Bactericidal, high dose (Ex.
Penicillin G +Gentamycin + Cefazolin) Azithromycin if allergy to PCN
-Possible valve replacement or repair
-Coumadin or LMW heparin to prevent clot formation
-Teach prevention: good oral hygiene (Gingivitis most common source of
spontaneous bacteremia)
Prophylaxis: For dental procedures.
Aortic Aneurysm screening:
PRESENT WITH EPIGASTRIC PAIN- may radiate to the back
AAA: Is an abdominal aortic dilation 3cm or greater.
● Risk factors:
-MAIN RISK FACTORS: Male sex, >65 years old, smoking history
-OTHER RISK FACTORS: family hx of AAA, CAD, HTN, PAD, previous MI,
cerebrovascular disease, atherosclerosis, other vascular aneurysms,
hypercholesterolemia, obesity.
Screening Recommendations:
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-One-time screening for AAA with ultrasonography should be performed
in men 65 to 75 years of age who have smoked 100 cigarettes or
more in their lifetime.
B
-One-time screening for AAA with ultrasonography should be selectively
offered in men 65 to 75 years of age who have never smoked, but
have risk factors for AAA.
B
B
-AAA screening should not be performed in women who have never
smoked.
●
●
●
B
Cardiac Tests
What tests are done to evaluate cardiac structure and function and what information
do these tests provide you with? When would you order these diagnostic tests or
labs?
EKG:
○ Show nonspecific ST segment and T-wave abnormalities in pt with severe CAD.
■ This can have false positives in cases with LVH, digoxin intake,
electrolyte imbalances, or conduction anomalies like BBB or preexcitation syndromes.
Echocardiography:
○ Done in new or worsening HF or new MI to assess LV function and regional wall
motion.
Exercise Treadmill testing:
○ Based on the pt ability to exercise
○ Measures the presence of ischemic ST segment changes, reproducibility of CP,
arrhythmias, changes in BP and HR and functional capacity.
○ Sensitivity: 68%, specificity: 77%
○ Early positive result in the first two stages of the test can indicate a worse
prognosis, and is considered a high risk finding.
○ If the pt experiences CP and -1 mm ST segment depression during exercise the
test can be 90% predictive of the presence of CAD.
○ A 2mm ST segment depression + CP is indicative of the presence of obstructive
CAD.
○ The presence of anti-ischemic agents (Nitrates, BBs, and CCBs) can reduce
sensitivity and should be withheld 2-3 days prior to the test for long acting drugs
and 24 hrs for short-acting drugs- IF the intent is to dx the presence of
obstructive dz.
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○
●
●
ABSOLUTE CIs to treadmill stress tests: decompensated CHF, symptomatic
AVS, ongoing resting CP, recent MI (w/in the past wk), severe HTN, and
intractable arrhythmias.
■ Nuclear stress tests and Stress Echos are the alternatives in this case.
Stress myocardial perfusion imaging: Nuclear stress test:
○ More accurate to dx obstructive CAD
○ Sensitivity (88%) and specificity (72%)
○ Best ordered in those with intermediate likelihood of obstructive CAD
○ Adenosine and Dobutamine commonly used.
■ Adenosine dilates the coronary arteries and shunt blood away from
abnormalities.
● Can cause bradycardia and hig.h degree AV block.
● CI: in those w/ hyperactive airway dz (asthma)
● NO CAFFEINE 12-24 hrs prior
● Excellent choice for those who cannot walk on the treadmill
■ Dopamine increases HR and contractility and therefore increases
myocardial O2 demand.
● Reserved for those who cannot walk or the treadmill and those
with a CI to Adenosine.
Stress Echo:
○ Similar to nuclear stress test, but sensitivity is slightly lower.
○ Performed by obtaining initial resting echo images of the heart
■ Assesses LVEF, wall motion characteristics and cavity size.
● 25% of pt may be difficult to obtain images: severe COPD and
morbid obesity.
○ Pt then exercise on the treadmill to a limited protocol to a target HR of 85% of
maximum predicted for age.
○ Once HR is met, post-stress images are obtained at target HR.
Sensory:
Visual changes associated with aging:
● Glaucoma
group of diseases that damage the optic nerve
○ People who are high risk should have an exam every 2 years
■ (AA >40,
■ all adults >60 especially Mexican Americans,
■ those with a family history of glaucoma)
○ No acceptable test to accurately detect
■ Risk assessment for Open Angle Glaucoma:
● Increased IOP, older age, family history, AA
● Acute onset of severe eye pain. Accompanied by HA, n/v, halos
around the lights, and decrease vision. Mid-dilated pupil that is
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■
■
■
oval shaped, cornea appears cloudy, and fundoscopic exam
reveals cupping of the optic nerve.
● This is an emergency.
OAG- may be asymptomatic initially, peripheral and central visual field
loss with progression
● Common signs = optic nerve cupping, visual field changes
● Tx- pressure lowering medications, laser or surgery
Acute Glaucoma= marked blurring, photophobia, cloudy cornea, elevated
intraocular pressure, diffuse conjunctival injection,and severe pain with
possible nausea or vomiting.
Starts with gradual changes in peripheral vision and then central vision.
● Cataracts:
○
○
○
a clouding of the lens; leading cause of vision loss in the US
Symptoms: blurry, hazy, glare, halos around lights and blurred vision
Tx: surgery when symptomatic
●
Macular Degeneration:
○ Major risk factors include: age, race (Caucasians), smoking, hereditary
○ Macular retinal changes such as blurred central vision or a blind spot in the center of the
visual field
○ early= asymptomatic
○ Late= central vision loss (gradual or sudden)
○ Tx: Laser treatment, photodynamic therapy
○ Requires yearly eye examinations
●
Diabetic Retinopathy:
○ Risk factors: hyperglycemia, worse with HTN
○ Common signs: retinal edema, microaneurysms, hemorrhages, exudates
○ Symptoms: asymptomatic, gradual vision loss, or sudden vision loss, cotton wool spots
(fluffy yellow-white patches on the retina).
○ Tx: Glycemic and HTN control, laser surgery: hyper
○ Yearly eye examinations
Acute problems in vision changes in aging:
● Iritis:
○
blurred vision, moderately severe pain/intermittent stabbing, moderate
photophobia, no discharge, circumcorneal conjunctival injection, clear
appearance of the cornea, constricted pupil size, normal or low IOP
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● Conjunctivitis:
○
normal vision, no pain, no photophobia, usually significant discharge with
crusting of lashes, diffuse conjunctival injection, clear appearance of the cornea,
normal pupil size, normal IOP
● Foreign Body/Corneal Abrasion:
○
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pain, gritty feeling in the eye, tearing, redness, sensitivity to light, H/A, visualizing
the cornea under cobalt-blue filtered light after the application of fluorescein will
confirm the diagnosis
○ Always ask patient if they wear contacts.
○ Acute onset of severe eye pain with tearing.. Foreign body sensation on the
surface of the eye.
Acute symptoms to be concerned about and require a referral – decreased vision, eye
pain, drainage or redness of the eye, double vision, floaters, circles/halos around light
sources, flashing lights
With all of the above, check for the following symptoms or signs
○ Reduced vision, pain, photophobia, corneal staining, corneal edema, unequal
pupils, elevated IOP
■ Refer to ophthalmologist if any of these are present
● If none are present the above is probably conjunctivitis
○ Triad of red eye, pain and loss of vision should always
alert the examiner to a potentially blinding condition
Visual changes for pediatrics (amblyopia)
● Occurs when the eye experiences a blurred and normal view, but the brain only
processes the normal view.
● Causes:
○ Deprivational (ptosis, cataract, nystagmus)
○ Strabismic (strabismus or lazy eye)
○ Refractive (myopia, hyperopia, astigmatism, anisometropia) <-most common
visual disorder in children
● Patching of the dominant eye can allow for the weaker eye to become stronger
● Refer to ophthalmology
● Untreated or insufficient treatment in young childhood results in irreversible and
lifelong vision loss
Visual changes for adults (presbyopia)
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Presbyopia is caused by a loss of elasticity of the lenses which makes it difficult to focus
on near or close objects. Onset in the early to mid-40’s. Can be remedied with reading
glasses or bifocal lenses.
■
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Conductive hearing loss:
● Failure of normal transmission of acoustic energy of sounds through the middle ear
(conductive part of the canal) BC>AC
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Not as common- 10%
Associated with cholesteatoma, cerumen impaction, foreign body in ear canal,
ossicular problems, OM with effusion, otosclerosis, retracted TM (Eustachian
tube dysfunction), tumor of ear canal/middle ear, TM perforation,
tympanosclerosis
Txt: Abx, or sx.
Sensorineural hearing loss:
● Hearing loss caused by damage to the inner ear or the nerve from the ear to the brain;
permanent; in adults it’s caused by aging and prolonged exposure to loud noises, in
children it’s caused by congenital abnormalities or infections
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Occurs 95% of the time
Not easy to treat=hearing aid is usually treatment (very expensive)
Associated with acoustic neuroma, DM, hereditary (congenital) loss, idiopathic
loss, Meniere’s disease, multiple sclerosis, noise-induced loss (noise at or above
80 decibels), ototoxicity, perilymphatic fistula, presbycusis, syphilis
Hearing changes:
● Congenital:
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present at birth. It can include hereditary hearing loss or hearing loss due to
other factors present either in-utero (prenatal) or at the time of birth
1 out of 2 cases of hearing loss in babies is r/t genetic causes, might have a
family member with hearing loss too, about 1 out of 3 babies with genetic hearing
loss have a syndrome (Usher syndrome, down syndrome)
● Acquired
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appears after birth; can occur at any time in one's life as a result of an illness or
injury or genetic factors
● Cerumen Impaction:
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causes conductive hearing loss
Speech evaluation- when to be concerned:
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Hearing loss in children- affects the ability to develop speech, language and social skills.
The earlier the intervention, the better the prognosis
Red flags of partial/complete hearing loss: babies
○ Does not startle to loud noise
○ Does not turn to sound at 6 months of age
○ No single words by 1 (mama, dada)
○ Turning head when sees parent/name is called but does not turn head when
name is called- sometimes thought as not paying attention or ignoring
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○ Seems to hear some sounds but not others
Red flags of partial/complete hearing loss: children
○ Delayed speech
○ Don’t follow directions -sometimes thought as not paying attention or ignoring
○ Unclear speech
○ Says “Huh” often
○ Turn TV up loud
○ Not reaching milestones
Risk indicators that if positive, prompt referral to audiologist
○ Caregiver concern about hearing, speech, language or development
○ Family history of permanent childhood hearing loss
○ NICU for >5 days
○ In utero infections- CMV
○ Craniofacial abnormalities
○ Physical findings such as white forelock
○ Syndromes associated with hearing loss or progressive or late onset hearing loss
○ Neurodegenerative disorders
○ Culture positive infections associated with sensorineural hearing loss
○ Head trauma, especially basal skull or temporal bone fracture
○ Chemotherapy
All babies should have a hearing screen no later than 1 month. Often this is done in the
hospital after birth. If they fail, they should have a follow up/repeat no later than 3
months of age.
Children should have a hearing test before they enter school or anytime there is a
concern for hearing loss. If they don’t pass, they need a full work-up/audiology referral
Peds Ortho
Know difference between legg-calve-perthes and slipped capital femoral epiphysis
Slipped capital femoral epiphysis:
● Posterior displacement of capital femoral epiphysis from femoral neck through the
cartilage growth plate
● More common in males and occurs bilaterally 25% of the time
● Most commonly occurs at puberty in obese children with delayed sexual maturation
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Physical Exam Findings
Classic presentation: painful limp with/without a history of recent trauma
Typically overweight and adolescent age years
If a patient reports knee pain, always examine the hip, because knee pain may be referred
pain from the hip via the obturator nerve.
Patients often hold their affected hip in passive external rotation.
Determine the patient's ability to bear weight (stable vs unstable).
If the patient is ambulatory, determine his or her gait pattern:
○ Antalgic – Shortened weight bearing phase on the affected side and longer swing
on the affected side
Out-toeing
Always examine both hips.
○ Assess the active and passive range of motion in both hips.
○ In patients with unilateral complaints, this comparison allows the clinician to
compare the affected and unaffected sides for differences.
○ Internal and external rotation are best tested with the patient in the prone position
with the knees flexed to 90 o.
If SCFE is present, the lower extremity may externally rotate and abduct with gentle
passive hip flexion.
Internal rotation is decreased in nearly all hips with SCFE → painful!
○ Internal rotation is often painful
Slight shortening of the involved lower extremity is observed in some patients
May walk with a limp that involves swinging the affected foot outward
SCFE is a Salter-Harris fracture type 1
Needs xray
Treatment involves pinning or screws placed in surgery
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Legg-Calves-Perthes
● Avascular necrosis of the capital femoral epiphysis
● Physical Exam Findings
○ Unilateral involvement is the rule
■ If bilateral case is suspected some form of epiphyseal dysplasia must first
be ruled out
● Xray will look different than SCFE, growth plate will appear crushed
History
There can be an acute or chronic onset with or without a history of trauma to the hip, such as
jumping from a high place.
● The most common presenting sign is an intermittent limp (abductor lurch-trendelenburg
gait caused by weakness in the gluteal muscle), especially after exertion, with mild or
intermittent pain.
● The most frequent complaint is persistent pain in the groin, anterior hip region, or
laterally around the greater trochanter.
● Pain may be referred to the medial aspect of the ipsilateral knee or to the anterior thigh.
● Some children may report limited range of motion of the affected extremity.
Physical Examination.
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Antalgic gait with limited hip movement
Trendelenburg gait resulting from pain in the gluteus medius muscle
Muscle spasm
Atrophy of gluteus, quadriceps, and hamstring muscles
Decreased abduction- harder to move outward, limited and painful internal
rotation, and extension of the hip
Adduction flexion contracture
Pain on rolling the leg internally
Leg length inequality due to collapse of the femoral head
Short stature: This result from deformity of the femoral head.
Roll test:
○ With patient lying in the supine position, the examiner rolls the hip of the affected
extremity into external and internal rotation. This test should invoke guarding or
spasm, especially with internal rotation.
Trendelenburg sign:
○ While standing, the patient lifts one leg up at a time; owing to muscle weakness
on the affected side, the pelvis drops to the opposite side
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Diagnostics
● Routine AP pelvis and frog-leg lateral views are used to confirm the diagnosis, stage the
disease, and follow disease progression and response to treatment.
● Ultrasound can be helpful early in the disease
○ Useful in the preliminary diagnosis; capsular distention can be seen on
sonographic images.
How to assess a hip complaint in a child:
Three Causes of Intoeing
1. Femoral anteversion
2. Metatarsus adductus
3. Internal tibial torsion
Rotational profile
Hip and Tibial alignment
Determining alignment of hip and toes
Gait
Femoral anteversion (Pigeon Toe)
Can be viewed as a normal finding of the lower extremity positioning in the developing child
As the child ages, the femoral neck usually remodels to a position of slight anteversion and
normal alignment of the lower extremity
In children with delayed rotational correction, a persistent in-toeing can occur
Position is generally bilateral and not associated with any other musculoskeletal problems
Physical Findings
● Child stands with thighs, knees, and feet turned inward
○ Increase in internal rotation over external rotation is apparent on assessment of
ROM of the hip
● Unsightly gait
● Kissing patellas
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● Kicking of the heels
● Tripping on walking or running
● May be a history of sitting on the floor with knees bent and lower legs turned outward in
a reversed taylor position
● Gradually resolves by the age of 10
Assessment
● Internal and external rotation
○ Normal internal rotation 20-60 degrees and external rotation 30-60
○ Severe if greater than 90 degrees
■ FA: Usually have increased internal rotation greater than 70 degrees and
decreased external rot less than 20
● Serial measurements
● Emphasize flexibility of the hip
Referral
● If External rot is less than 10 in a child greater than 8-10 years of age
Internal Tibial Torsion
Nonpathologic finding in the normal development of children younger than 5
Thought to be a rotational deformity resulting from internal molding of the foot and
leg in utero
CC: concern about prominent intoeing on walking and frequent tripping or falling
Assessment
● Assess gait
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○ Hips and knees are normally aligned and the patellas are facing anteriorly
Assess thigh foot angle
○ 0-20 degrees is normal
○ -10 degrees or less = tibial torsion
Examine the lateral and medial malleolus
○ Drawing a line across they should be in equal position
○ ITT: medial malleolus will be posterior to the lateral malleolus
Generally unilateral
Lower legs and feet are rotated inward
Associated Condition
DDH
Metatarsus adductus
Treatment
Avoid sleeping in prone position
Referral
○ Over the age of 6
○ Significant functional def
○ Thigh foot angle is greater than 3 STD
Metatarsus Adductus
Metatarsals are deviated medially with normal hindfoot alignment!
Result of intrauterine molding and is usually bilateral
Needs to be distinguished from club foot
CC: Baby’s toes are turning in during the 1st year of life
Assessment
● Tickling will move the foot into a normal position
● General pressure on medial forefoot
● With foot braced against flat surface or with patient standing
● Position hindfoot and midfoot straight and the affected forefoot should assume a medial
deviation or varus position
● Skin creases may be located over the medial aspect of the longitudinal arch
● Some patients may have tibial torsion deformities, but their calf muscle remains normal
in size
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Classification
1. Mild: 10-15 degrees correctable past the midline
2. Moderate: 15-25 degrees correctable to midline with some difficulty
a. Stretching with each diaper change, moving the foot into the correct position
3. Severe: minimal correctability and greater than 30 degrees past the midline
a. Refer for possible serial casing and bracing
Club foot
Idiopathic deformity of the foot of unknown etiology
Most common in Polonesian heritage
Talipes equinovarus (clubfoot) has three elements:
1. The ankle is in equinus (the foot is in a pointed-toe position)
2. The sole of the foot is inverted as a result of hindfoot varus or inversion deformity of the
heel
3. The forefoot has the convex shape of MA (forefoot adduction).
**The foot cannot be manually corrected to a neutral position with the heel down**
Management
● X-rays
● Referral to ortho for serial casting using the Ponseti technique
Genu Varum (Physiologic Bowleg)
Normal variation of the lower leg in 1-3-4 year old age group
Evaluation
● Ankles together and make sure feet are pointing forward
● Measure the distance between the knees
○ 5-6 inches or greater is considered pathologic
○ Abnormalities:
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■ Neurofibromatosis (unilateral tibial bowing)
■ Rickets gradually progresses , has short stature, atypical diet, and family
history
■ Tibial torsion
■ Juvenile RA
■ Osteomyelitis
■ Neoplasm
■ Trauma
■ Blount’s disease (unilateral, common in obese, early walkers, Aftrican
American, and Scandanavian children)
Physical Exam
● Diffuse bowing of lower joints
● Internal tibial torsion
● Increased distance between both knees that is accentuated with standing
● Varus positioning of the heel with pronation of the feet may be noted on weightbearing
● Waddling gait and kick the heels on running to clear feet from ground to avoid hitting the
contralateral limb
Treatment
● Rarely indicated because the condition should resolve with growth
○ Serial measurements
● x-Ray:
○ bowing beyond 2 standard deviations for age height less than 25%, increasing
severity, asymmetry of the limbs
● Pathologic genu varum associated with Rickets, dwarfism can be diagnosed with x-rays
● Unilateral bowing warrants immediate evaluation for an underlying disorder
● Persists beyond 7-8 years ortho referral definitely indicated
Genu Valgum (Physiologic Knock-Knee)
Normal variation in lower extremity configuration in children between 3 and 5 (7-8) years of age
Physical Findings
● Increased distance between the feet with the medial aspects of the knees touching each
other
● Ankles may appear to roll in and may correct when the knees are corrected
Assessment
● Measure intermalleolar distance (should be less than 8cm) serially to monitor for
progression
● Unilateral warrants immediate referral
○ Growth plate injury
○ trauma/infection/vascular insult
○ Neoplasm
○ Proximal metaphyseal tibial fracture
○ Benign tumor
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○ Ollier's disease
Management
● Reassurance
● Serial measurement
● Referral for lack of spontaneous resolution by 7-8
Common Fractures: Salter Harris ● Bowing ● Buckle ● Greenstick
Osgood Schlatter’s Disease:
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Often seen in adolescents after going through a rapid growth spurt the previous year.
More frequent in boys
Hx:
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Recent physical activity (running track, playing soccer, or football)
Pain increased during and immediately after the activity and decreased when the activity
is stopped for a while.
● Running, jumping, kneeling, squatting, and ascending/descending stairs exacerbate the
pain.
● Pain is bilateral in 20-50% of cases
● Approximately 25% of patients give a history of precipitating trauma
Physical:
● Pain reproduced by extending the knee against resistance, stressing the quadriceps, or
squatting with the knee in full flexion
● Focal swelling, heat, and point tenderness at the tibial tuberosity
● Full range of motion of the knee
Dx: Based on hx and physical examination. Radiographs are not indicated unless
another pathologic condition is suspected.
Twisted legs
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Congenital Hip Dysplasia
Dysplasia that can be missed
Can result in subluxation and possible dislocation of the hip second to capsular laxity
Instability caused by genetic laxity and intrauterine and post natal malposition
Dysplasia ->dislocation
Anterior-lateral acetabulum
All infants should be screened until walking age (no diapers on during screening)
Risk
Breech
Family history
Female (6:1)
Most common ortho problem in newborns
Left hip most common
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● Bilaterally only 20%
● White, Native Americans, and Laplanders (???) because of tight swaddling keeps hips
adducted
● Oligohydramnios in pregnancy
Diagnosis
● Newborn infant Barlow and Ortolani
○ Barlow first: dislocates an unstable or dislocatable hip posteriorly
■ supine position with knees flexed, the hip is flexed, and the thigh is
brought into an adducted position applying downward pressure.
■ With hip instability, the femoral head slips/drops out of the acetabulum or
can be gently pushed out of the socket; this is termed a positive Barlow.
■ The dislocation should be palpable as this maneuver is performed.
○ Ortolani: Adduct thighs to try and dislocate a dislocatable hip and then abduct
with your fingers pushing toward the midline and thumbs away from the midline
to relocate a dislocated hip
■ A definitive clunk can be audible and felt if the femoral head has been
dislocated and then moved back into the acetabulum
○ Rarely positive after 2 months of age
○ Skin fold examination of thighs should by symmetric anteriorly and posteriorly
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Treatment
Refer to pediatric orthopedics
US/referral
Any risk factors in history -> always refer
Greater than 6 months of age, do x-ray and refer
Pathophysiology of a long bone/growth plate:
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The physeal plate is a cartilaginous plate present in ends of long bones adjacent
to the metaphysis. This is the area that provides longitudinal growth to bones and
eventually matures into bone. During growth, the physeal cartilaginous plate is
weaker than the surrounding bone and often weaker than the ligaments and
tendons that attach nearby, causing it to fracture before other areas. The SalterHarris classification system describes these injuries
Growing Pains:
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occur in the evening or late in the day - may awaken child from sleep
gone by the morning with no limitation of activity
poorly localized and bilateral
Occur commonly in the front of the thighs, shins, in the calves, and behind the knees
transient and occur over a period of time as long as several years
not associated with a limp or disability
no fevers or swelling
no recent or remote trauma
Fractures
1. The skeletal system of children is anatomically, biomechanically, and physiologically
different from that in adults. The presence of growth plates (or physes) in the
pediatric skeleton is one major difference. The growth plate is composed of cartilage.
It can be thought of as the "weakest link" in the pediatric bone. It may separate before an
adjacent joint ligament tears. Injuries to the growth plate may result in deformities
=Salter Harris Fractures
2. Another difference seen in children is a thicker periosteum surrounding the
bones. As a consequence, fractures in children tend to be more stable and less
displaced than those seen in adults. The greater bone-forming potential of the
pediatric periosteum results in faster bone healing in children. Non-unions are rare in
pediatric fractures.
3. A third difference is the increased porosity, due to larger, more abundant
Haversian canals, and decreased density of pediatric bones. This feature makes
children's bones more prone to buckling when compressed, or bowing when bent.
4. Finally, remodeling is more rapid in children than in adults. Imperfect reductions
have been known to remodel into satisfactory alignment. The differences between
pediatric and adult fractures result in different fracture patterns, problems of diagnosis,
and management techniques.
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5.
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Know significance of types of fractures
Salter Haris- growth plate fractures
Bowing - due to increased porosity
Buckle - due to increased porosity
Greenstick
Types of growth plate fractures – 5 categories based on the type of damage caused.
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Type I – Fracture through the growth plate
○ The epiphysis is separated from the metaphysis with the growth plate remaining
attached to the epiphysis.
○ The epiphysis is the rounded end of the long bones below the growth plate and
the metaphysis is the wider part at the end of the long bones above the growth
plate.
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Type II – Fracture through the growth plate and metaphysis
○ Most common type of growth plate fracture. The growth plate and metaphysis are
fractured without involving the epiphysis.
Type III – Fracture through the growth plate and epiphysis
○ The fracture runs through the epiphysis and separates the epiphysis and growth
plate from the metaphysis.
○ It usually occurs in the tibia, one of the long bones of the lower leg.
Type IV – Fracture through growth plate, metaphysis, and epiphysis:
○ Fracture goes through the epiphysis and growth plate, and into the metaphysis.
○ This type often occurs in the upper arm near the elbow joint.
Type V – Compression fracture through growth plate:
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Rare condition where the end of the bone gets crushed and the growth plate is
compressed. It can occur at the knee or ankle joint.
Signs and symptoms of a growth plate injury include:
○ Inability to move or put pressure on the injured extremity
○ Severe pain or discomfort that prevents the use of an arm or leg
○ Inability to continue playing after a sudden injury because of pain
○ Persistent pain from a previous injury
○ Malformation of the legs or arms as the joint area near the end of the fractured
bone may swell
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GU: hernia - worsens with high static demand (ie: weight lifting)
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