DR MARWANI’S SHEET

FOR PEDIATRICS
Residents CLINICAL
EXAMINATION –
RETYPED

* FOR ECG + COMMUNICATION PART PLEASE REFERE TO THE

ORIGINAL SHEET

*This sheet is NOT enough to study from

*Typos & mistakes are possible ☺
 1- CNS:
-CSF Interpretation *
Rewritten by Shima Alahmadi
- Neonate with seizure + bad APGAR score.
Rewritten by Khulud AlSaedi
- Floppy infant *
Rewritten by Khulud AlSaedi
-GBS *
Rewritten by Shima Alahmadi
-Paresthesia + unsteady gait.
Rewritten by Khulud AlSaedi
-Facial palsy.
Rewritten by Khulud AlSaedi
-Acute ataxia.
Rewritten by Shima Alahmadi
-Acute hemiplegia.
Rewritten by Khulud AlSaedi

* Reviewed by Dr. Reham Fallatah

Q: CSF Interpretation:

Normal Bacterial Partially Viral TB

meningitis treated meningitis meningitis
Appearance Clear Turbid Clear Clear Fibrin-web
Not clear
Pressure 50-80 High Normal Normal High
mmHg
WBC 0-100 PT 100-60 1-10 Up to 1000 Up to 1000
0-15
neonate
0-10 infant
0-5 child
PMN% Zero Up to 50000 Up to 1000 Early then Early then
Lymphocyte 60-70% Few Predominant Monocellular Lymphocyte
predominant
Culture -ve +ve Sterile No growth ZN stain for
Acid Fast
Bacilli (AFB)
Protein g/L 1-4 for PT 1-5 1-2 <1.5 1-6
0.3-2 in
neonate
0.2-1 in
infant
0.2-04 in
child
Glucose 2/3 of <40% or < Normal or Normal but < 50 very
serum 2/3 blood decrease decrease in low
glucose Mumps and
HSV

-Traumatic LP \ Bloody CSF:

Corrected WBC (CSF) = WBCCSF – WBC blood x RBC CSF
RBC blood
Ratio (almost) 1:500
-Cerebral abscess " sterile tap " high protein, lymphocytosis, has similar picture like
T.B
- Leukemia: lymphocytosis > low glucose, +ve blood film
-HSV Meningitis (hemorrhagic encephalitis) – high Erythrocyte has involvement of
temporal and frontal lobe

Causes of high CSF Protein:

1. Infection: TB Meningitis, Bacterial meningitis (pneumococcal, H.Influinza), viral,
neurosyphalis
2. Inflammation: GBS, MS, peripheral neuropathy, subdural hematoma
3. Tumor: cerebral hemisphere, spinal cord, acostic neuroma
4. Vascular: cerebral hemorrhage, stroke
5. Degenerative: white matter disease
 6. Metabolic: uremia
7. Toxin: lead.

Oligoclonal band in CFS:

1-Sarcoidosis
2-MS,
3-SLE
4-Subarachnoid hg
5-Neurosyphalis
6-Subacute Sclerosing Panenchephalitis “SSPE”
Q: One-day old with bad APGER score, developed seizure at 1st day
Approach:
1-ABC
2-Seizure is still active or not?
3-If active seizure " control seizure by (phenobarbital, phenytoin)
4-Send for lab work: *Glucose check
*U&E (ca, mg, phos)
*CBC
*Blood c/s

HIE criteria:
• PH arterial <7 (34wks)
• Base: 12 or less (34wks)
• Encephalopathy (seizure, sensorium change??)
• Fetal distress (monitoring, acidosis)

**No seizure " review history

1- Is it seizure or jitteriness?
2- Details of seizure (duration, type, associated symptoms, pre/post ictal symptoms)
3- Term or not?
4- Mode of delivery, O2 sat.
5- Antenatal history
6- Relation to feeding
7- Family history of seizure

Examination:
Full neonatal Exam

Lab work:
1-CBC
2-Electrolytes
3-LFT
4-RFT
5-Blood c/s
6-Uric acid (H) in HIE, (L) in metabolic disease
7-CT brain
8-EEG
Q: Approach to a floppy infant

Usually present with: floppy on handling, delayed motor development, or

recurrent chest infection.

History:
-Onset, progression
-Antenatal: Fetal movement, polyhydromnios
-Natal: APGAR score, Birth weight
-Postnatal: NICU admission, Infection, Trauma, Seizure, chronic illness
-Family history of death, neuromuscular disease
-Developmental history
-Course of the hypotonia: regression, progression
-Improving hypotonia like: congenital myopathy, prader willi, cerebellar hypotonia

Examination:
-Vital signs
-Growth parameters
-Inspection: *posture
*Dysmorphic features
*Alertness “central or peripheral”
*Spontaneous movements
*Tongue fasciculation
*neurocutanous manifestation
-Palpation: -Tone: *Head lag
* Sitting
* Ventral
* Vertical
*Scarf sign
- Power
- Reflexes
-Other systems
*Chest: SMA "bell shape chest"
*CVS: pompe disease
* Abdomen: HSM, Hernia
* Genitalia
Q: GBS (Guilian Barre Syndrome)
What is GBS:
It’s a post infection polyneuropathy involve (Motor –Mainly, Sensory, Autonomic)
-All ages affected
-Most patients have a demyelinating neuropathy, but some have axonal degeneration.

Causative agents:
- GIT (campylobacter jejunum, helicobacter pylori)
- Respiratory (Mycoplasma Pneumonia)
- West Nile virus, CMV, EBV, Hep A-B, Herpes virus
- Following administration of vaccines (Rabies, influenza, oral polio, conjugated
meningeococcal)

Clinical manifestation:
- Usually appear by 10 days post viral infection
- Weakness\paralysis begin in LL > trunk > UL > Bulbar muscles (landry
ascending paralysis)
- Proximal and distal muscles involvements symmetrical (asymmetrical in 9% of
pts)
- Ms tenderness common in initial stage
- Affected child is irritable
- Weakness > inability to walk > flaccid paraplegia.
- Parasthesis occur in some cases
- Bulbar involvement 50% > respiratory insufficiency
- Dysphagia + facial weakness < signs of impending respiratory failure.
- Facial nerve may involve
- Extra ocular muscles involvement > rare
• Miller- Fisher syndrome: external ophthalmoplegia (occulomotor), ataxia,
areflexia.
- Papilledema (some cases), but no visual imparements.
- Urinary incontinence or retention 20% (transient)
- Tendon reflexes absent (usually early, sometime later)
- Autonomic N involvements:
• Liability of BP, HR: postural hypotension, profound brady\tachycardia,
Asystole.
• **Don’t give anti HTN

GBS Classification\ Variant:

- Acute inflammatory demyelination polyradiculoneuropathy
- Acute motor & sensory axonal neuropathy
- Acute motor axonal neuropathy
- Acute sensory axonal neuropathy
- Acute pandysautonom
- Regional variant
- Oropharengeal
- Overlap
- Fischer – Guillain-Barri overlap syndrome
Lab findings:
1- CSF Study (Essential for diagnosis)
• Protein x2 twice normal
• Glucose Normal
• Cells no pleocytosis < 10 cell\mm3
• Cultures –ve , viral culture rarely isolate organism.

**THE DISSOCIATION BETWEEN HIGH CSF PROTEIN AND LACK OF CELLULAR

RESPONSE IN PT WITH ACUTE OR SUBACUTE POLYNEUROPATHY IS DIAGNOSTIC FOR
GBS **

2- MRI Spine:
• Findings: thickening of cauda equina: intrathecal nerve roots with
gadolinium. Sensitive & present > 90% of pt
3- Nerve conduction velocity (NCV)- Slow
4- Electomyography (EMG) – Denervation of muscles.
5- Ck- mild elevated-Normal
6- Anti ganglioside antibody GM1& 8GD1 elevated
7- Muscle biopsy not required
8- Sural nerve biopsy tissue not indicated
9- Serology (campylobacter, Helicobacter)
10- Stool CS – rarely positive.

Management:
- Admission for close observation
- Respiratory effort monitoring (spirometry, FVC)
- Pt with slow progression: observe A- stabilization, B spontaneous remission
without treatment
- Pt with slow progression:
A- IVIG:
-Recommended protocol: 0.4g\kg\day for 5 days
-Mechanism of action: uncretine, ? Suppression of inflammatory & immune
processes.
B- Alternative if IVIG not effective: Plasmaphoresis, immunosuppressive.
- Steroids not effective
- Combined IG + interferon are effective in some pts.
- Supportive care: Resp. support, prevent decubiti in flaccid pt.
- Treatment of secondary bacterial infection

Reasons for PICU Admission:

- Flaccid quadriplegia
- Rapid progressive weakness
- FVC < or equal to 20ml\kg
- Bulbar palsy
- Autonomic CVS instability
Prognosis:
- In general good, benign clinical course.
- Majority 90% of pt recover completely 2-3 weeks
- Bulbar function 1st to recover
- Tendon reflex last to recover
- 3 clinical features associated with poor outcome:
• Cranial N involvements
• Intubation
• Maximum disability at time of presentation
- The electro physiologic feature of conduction block predictive of good outcome
- The most common chronic symptoms is: easy fatigability
- Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and
recurrent GBS 7% associated with residual weakness.
Q: 6 years old boy with parasthesia of hand & feet, became unsteady then
unable to walk

Approach

History:
-Site of weakness *Symmetrical (distal or proximal)
*Asymmetrical
-Static or progressive (ascending or descending)
-Diurnal variation – MG
-Sensory symptoms
-Back pain
-Signs of ICP
-History of URTI, AGE (diarrhea)
-GI symptoms (constipation, heavy ingestion, canned food)
-Sphincter control (urine/stool incontinence)
-History of trips (tick paralysis)

Examination:
-Full neurological exam
-Sensory, motor
-Respiratory , CVS exam
-other

Lab
-Neuroimaging
-LP
-NCS

Treatment:
According to underlying cause

Parasthesia
Quadriparesis Paraparesis
Central Peripheral Central Peripheral
-HIE -Spinal cord: TM -Sagital sinus -Spinal problems
-Nerve: GBS thrombosis
-NMJ: Tick, MG, -Trauma
Botulism -Tumor
-Muscle: Myositis -Infection
Q: 7 year old with ear pain & droopy mouth on same side (Facial Palsy)

Approach:

History:
Ask about
-Infection (OM, herpes in ear canal)
-Trauma
-HTN (bleeding to facial canal)
- 1st time or not (recurrence)
-Ability to close eye (Upper Vs Lower Motor)
-Other cranial nerve involvement
-Sphincter control

Examination:
-Full CNS exam
-ENT exam

Lab:
No lab (Bell’s Palsy)

Treatment:
1-Supportive – artificial tears
2-Steriod (Decrease duration of recovery)
Prednisolone 1mg/kg/day for 1 week then taper over 1 week
3-Acyclovir: can help to complete recovery with steroid
4-Physiotherapy

Prognosis:
85% " complete recovery
10% " Mild residual weak nerve
5% " Permanent sever weak nerve

Q:CT indications?
A: search for it ☺
Q: 4 years old boy with acute ataxia
Differential Diagnosis:
1- Acute cerebellar ataxia
2- Drug intoxication (anti histamine, anti epileptic, anti depressant, organophosphourus
poisoning)
3- Posterior fossa tumor
4- GBS
5- Basilar migraine
6- Benign paroxysmal vertigo
7- Neuoroblastoma

History:
- Trauma
- Infection
- High ICP sign
- Headache, vomiting
- Et loss
- Drug ingestion
- Family history of migraine

Examination:
- Growth parameters
- Vitals signs
- Skin exam (ataxia telengectasia)
- Full neurological exam (hypotonia – cerebellar, hypertonia- hydrocephalus\ ----- on
brain stem)
-
Lab works:
- CT Brain
- CBC, Diff
- +- LP
- Drug level
-
Treatment:
Depending on underlying causes.
In tumor: AVS, Avoid over hydration, EVD, ………..
Q: 3 year old with acute hemiplegia

Approach:

History:
Ask about
-Infection (OM, tonsillitis)
-Skin rash
-Seizure
-Level of consciousness
-Trauma
-Diarrhea
-DM, DKA
-CVS disease
-Blood disease
-Signs of high ICP

Examination:
-Well or unwell?
-Vital signs
-Growth parameters
-Pupil exam
-Full CNS exam
-Skin rash
-Other systemic exam – CVS, ENT

Causes:
A- Vascular
• Infarction: Idiopathic
• Thrombosis: Polycythemia, DKA, SCA, DIC
• Embolism: CHD, Arrhythmia
• Spasm: ???
• Hypoxia: Epilepsy, Arrest
• Bleeding: AV malformation, HTN
B- Infection: encephalitis
C- Tumor
D- Trauma
Site of lesion:
1- Leg > Arm " Ant. Cerebral artery
2- Arm > Leg " Middle cerebral artery
3- Arm = Leg " Internal carotid
Internal capsule
All down: Brain stem
Pons
Medulla
Spinal cord

**Internal Capsule:
- Cotralateral hemiplegia
-UMNL
- Cranial nerves

**Brain stem:
- Cotralateral hemiplegia
- Ipsilateral LMN of 3rd

**Pons:
- Cotralateral hemiplegia
- Ipsilateral LMN of 7th

**Medulla:
- Cotralateral hemiplegia
- Ipsilateral LMN of 12th

**Spinal cord:
- Ipsilateral hemiplegia
- Loss of sphincter control
- Sensory level
Site of lesion:
1- Leg > Arm " Ant. Cerebral artery
2- Arm > Leg " Middle cerebral artery
3- Arm = Leg " Internal carotid
Internal capsule
All down: Brain stem
Pons
Medulla
Spinal cord

**Internal Capsule:
- Cotralateral hemiplegia
-UMNL
- Cranial nerves

**Brain stem:
- Cotralateral hemiplegia
- Ipsilateral LMN of 3rd

**Pons:
- Cotralateral hemiplegia
- Ipsilateral LMN of 7th

**Medulla:
- Cotralateral hemiplegia
- Ipsilateral LMN of 12th

**Spinal cord:
- Ipsilateral hemiplegia
- Loss of sphincter control
- Sensory level
 2- Nephrology:
- Neonate with hydronephrosis *
Rewritten by Khulud AlSaedi
- Red urine *
Rewritten by Ebtihal AlQulaisy
- Microscopic hematouria.
Rewritten by Khulud AlSaedi
- Nocturnal enuresis *
Rewritten by Shima Alahmadi
- Hypertension
Rewritten by Khulud AlSaedi
- Proteinuria*
Rewritten by Ebtihal AlQulaisy
- Nephrotic syndrome*
Rewritten by Ebtihal AlQulaisy
- Girl with recurrent UTI.
Rewritten by Khulud AlSaedi

* Reviewed by Dr. Reham Fallatah.

Q: Neonate with Antenatal hydronephrosis confirmed postnatally

Approach:

History:
-Sex (male/female)
-History of oligohydromnios
-Respiratory problems
-Urine color, volume, stream, dripping
-Unilateral Vs bilateral
-Mild or sever
-Family history of renal disease

Examination:
-Vital signs – BP “on which centile”
-Growth parameters
-Dysmorphic features (flat face, club foot)
-Face (potter face)
-Chest deformity
-Abdominal exam “prune belly”
-Genitalia

Lab:
1-Renal function (U&E)
2-Urinalysis, culture “at risk of UTI”
5-MCUG
6-DTPA (Diethyl-enetriaminepenta acidic acid) 3months

Treatment:
1- If VUR: * Prophylaxis is controversial “decrease the incidence of infection not the
scar”
*Reassessment after DTPA result “looking for renal scar”
2-To rule out PUJ obstruction: US at 4-6wks
3-If mild hydronephrosis (unilateral): repeat US after 3months

Hydronephrosis:
Incidence (Antenatal) 1%
 Red urine

UDS
-ve
false
RBC’S Blood /No
RBC's - Urine crystal (Urate).

- Drug (rifampin).

Myoglobinuria , - Food.
hemoglobinuria
- Chemical.
Glomerula
r
RBC cast, cellular cast
Non-Glomerular
No cast

Dysmorphic RBC No Dysmorphic RBCs

Proteinuria No Proteinuria

Urine brown in color Red Urine

No clot’s there are clots

Renal Multisystem

C3 C3 Renal Urinary tract

-Intestinal Nephritis -UTI

N - SCA - Stone
N
- DKKD - High Ca
- Hydronephrosis - VUR
IgA SLE
- AV malformation - Trauma
PSGN Nephritis HSP
MPGN Alport HUS
SHUNT Syndrome Goodpasture
Nephrit Thin BS
is Rapid
Progressive
GN.
Q: 5 years old with microscopic hematuria

Approach

History:
-History of URTI, infection of throat or skin
-History of trauma
-UTI symptoms
-Loin pain, stone
-Hearing/Vision problems
-History of renal disease or hematuria before
-Systemic review (skin rash, arthritis, SLE)
-Hematological disease (SCA)
-Renal impairment, HTN

Examination:
-Vital signs - BP
-Growth parameters
-Systemic exam (Skin, throat)
-Abdominal exam (mass, HSM)
-Genitalia
-Signs of HF
-Urine dipstick

Lab
1-CBC
2-Chemistry & renal function (U&E)
3-Urinalysis
4-Urine c/s
5-C3, C4
6-ASO titer
7-Kidney US

*If all are negative do:

-Urine calcium/creatinine ratio
-Urine analysis for all family members
-ANA (connective tissue)
Q: 10 year old boy with Nocturnal Enuresis:

Definition of Enuresis:
-Normal void occur at a socially unacceptable time or place
-Positive family history in 50%
-Male more than females.

Classification:
A- Primary: incontinence in child who has never achieved dryness at least for 6
month
B- Secondary: who has been dry for at least 6 months.
Each can be either: Nocturnal, Diurnal, or both.

Approach:

History:
- Primary or secondary
- Diurnal (daytime) or nocturnal (night time)
- Number of wetting & amount
- UTI Symptoms
- History of weight loss, thirsty, polyuria, polyphagia (DM,DI)
- History of constipation or stool incontinence
- Spinal problem or trauma
- Headache, vision abnormality
- Sleep history (dream, tremor, obstructive sleep apnea)
- Using in\out catheter (Neurogenic bladder)
- Family history of similar problem in the family
- Social affect on (patient, parents, siblings), Abuse.

Examination:
- General exam (vital signs, growth parameters, developmental assessment)
- Local exam (genetalia, bladder, anal tone)
- Lumbosacral spinal exam (sign of spinal dysfunction)
- Systemic review (Abdominal, CVS, Respiratory)

Investigation:
- Urine analysis, Culture
- Urine for specific gravity
- Chemistry, osmolarity
- Random blood glucose
- X-Ray Spine
- +\- US Kidney + MCUG
Differential diagnosis:
- UTI
- DM - DI
- Fecal impaction “constipation”
- Surgical like: ectopic ureter, neurogenic bladder, bladder calculus , foreign body

Treatment:
Depends on the age of the patient
- Dry bed training
- Void before sleep
- Do not drink before sleep
- No punishment
- Enuresis Alarm > 7 years (success 75%)
- Medication: (success 50%) the symptom may relapse if stopped
- DDAVP (Desmopressin). S\E Hyponatremia, Headache, BP Fluctuating
- Imipramine (TCA). S\E cardiac conduction problem (arrhythmia) agitation,
sleep disturbance
-Oxybutarine. “ Anti cholenargic.” S/E dry mouth, flushing, constipation.
Q: BP 170/100mmHg (Hypertension)

Approach:

History:
-Check 3 readings, make sure of cuff size & site
-If confirmed, is it acute or chronic
-Symptoms of ICP (headache, blurred vision, flashing & sweating)
-PMHx, known to have chronic illness or syndrome
-Family history of HTN, renal disease or cardiovascular disease
-Drug history, steroid use
-Past history of UTI
-History of UVC, UAC insertion
-History of systemic review of target organs (CVS, Renal, Endocrine, Eye)

Examination:
-Growth parameter
- 4limb BP (right arm)
-Pulse (Radio-Femoral delay)
-Signs of CRF, CHD
-Eye exam (papilledema)
-Abdominal exam
-LL edema
-Back exam

Q: How is hypertension defined in children?

A: The diagnosis of hypertension is made on the basis of comparison with the
normative distribution blood pressure of healthy children of similar age, gender, and
height. (This information is available in the 2004 article cited below as well as a more
recent simplified approach.)

- Hypertension: Average systolic and or diastolic blood pressure is 95th percentile or

higher on three or more occasions
- Prehypertension: 90th percentile or higher, but less than 95th percentile; as with
adults, adolescents with blood pressure of 120/80 mm Hg or higher should be
considered prehypertensive
KEY POINTS: HYPERTENSION
1. Common cause of artifactual elevation: Blood pressure cuff is too small
2. Essential (no detectable cause): Often a strong family history
3. Secondary (detectable lesion) hypertension: More likely with higher blood
pressures and in younger children
4. Most cases of secondary hypertension in children caused by renal disease (renal
anomalies, renal parenchymal disease, renal vascular abnormalities)

Q: How do you determine the optimum cuff size for obtaining a blood pressure?
A: The length of the inflatable bladder inside the cuff (easily palpated) should almost
completely encircle the arm and will overestimate the blood pressure if it is too
short.
Additionally, the height of the cuff should be the largest that comfortably fits from
the axilla to the elbow. A cuff that is too small can produce falsely elevated blood
pressure readings.

WAYS TO AVOID MISDIAGNOSING HYPERTENSION

1. Properly sized cuff (age-dependent) with arm supported and raised to heart level
2. Quiet room, quiet patient
3. Repeated measurements over time and the use of averaged values
4. Get rid of the white coat
5. Sit at child level when taking the measurement

Q: When should hypertension be treated in the neonate?

A: Hypertension is defined as a blood pressure higher than 90/60 mm Hg in term
neonates and higher than 80/45 mm Hg in preterm infants. A sustained systolic
blood pressure of more than 100 mm Hg in the neonate should be investigated and
treated.

Q: What are the indications for the pharmacologic treatment of hypertension in

older children?
- Symptomatic hypertension
- Secondary hypertension
- Hypertensive target-organ damage (e.g., left ventricular hypertrophy on
echocardiogram)
- Diabetes (types 1 and 2)
- Persistence despite nonpharmacologic measures
Q: During the evaluation of a child with elevated blood pressure, what risk factors
should be considered for identification and/or reduction?
A: Important risk factors for hypertension in children include family history (if one
parent has hypertension, the risk is about 25%; if both parents have hypertension,
the risk is 45%), other genetic factors including race (blacks have twice the incidence
of hypertension compared with whites, beginning in adolescence), obesity, history of
renal disease, and dietary factors (mainly salt intake). More recently, a history of
prematurity has been recognized as a risk factor.

**Remembering that hypertension is a critical risk factor for cardiovascular disease,

the important risk factors for this largest cause of mortality should also be
addressed. These include diet and its effect on serum lipids, tobacco use, and lack of
exercise.

Q: What historical information suggests a secondary cause of hypertension?

History Suggests

Known urinary tract infection; recurrent Renal disease

abdominal or flank pain with frequency,
urgency, dysuria; secondary enuresis

Joint pains, rash, fever, edema Renal disease, vasculitis

Complicated neonatal course, umbilical artery Renal artery stenosis

catheter
Renal trauma Renal artery stenosis

Drug use (e.g., sympathomimetics, anabolic Drug-induced hypertension

steroids, oral contraceptives, illicit drugs)

Aberrant course or timing of secondary sexual Adrenal disorder

characteristics; virilization
Q: What are the categories of antihypertensive medications used for outpatient
management of hypertensive children?
- ACE inhibitors
- Angiotensin receptor blockers (ARBs)
- Calcium channel blockers
- a-Blockers and b-blockers
- Central a-agonists
- Vasodilators
- Diuretics

Q: What are the most common causes of hypertension in various age groups?

Age Range
First year of life Secondary (99%)
-Coarctation of the aorta
-Renovascular*
-Renal parenchymal disease
-Miscellaneous causes
-Neoplasia (4%)
-Endocrine (1%)

1-12 yr Secondary (70%-85%)

-Renal parenchymal disease
-Coarctation of the aorta
-Reflux nephropathy
-Renovascular
-Endocrine
-Neoplasia
-Miscellaneous
Primary (essential) (15%-30%)

12-18 yr Primary (essential) (85%-95%)

Secondary (5%-15%): Same causes as 1-12 yr

Q: Why should patients with hypertension and/or those using diuretics avoid
licorice?
A: (pediatric secrets 5th ed, Ch13, pg492-496)
Q: List the features on physical examination that suggest a secondary cause of
hypertension.

Physical Finding Possible Secondary Cause

Blood Pressure
>140/100 mm Hg at any age Multiple secondary causes

Leg < arm blood pressure Coarctation of the aorta

Adenotonsillar hypertrophy Obstructive sleep apnea

Muscle weakness Hyperaldosteronism

Joint swelling Systemic lupus erythematosus, collagen

vascular disease

Poor growth Chronic renal disease

Short stature, features of Turner Coarctation of the aorta
syndrome
Multiple cafe´-au-lait spots or Renal artery stenosis,
neurofibromas Pheochromocytoma

Decreased or delayed pulse in leg Coarctation of the aorta

Vascular Bruits

Over large vessels Arteritis

Over upper abdomen, flank Renal artery stenosis
Flank or upper quadrant mass Renal malformation, renal or adrenal
tumor
Excessive virilization or secondary sex Adrenal disorder
characteristics inappropriate for age
Edema Renal disease
Excessive sweating, increased resting Pheochromocytoma
heart rate
 Proteinuria

Fixed

False Transient Orthostat

ic
At standing
Blood -Fever
Bacteria -Exercise
Anti-septic -Cold
Drug -SZ
(phenothiazine) -CHD
Long standing -Dehydration

Tubulu-
Glomerular intestinal

2ry
1ry Fanconi sy.
Infection
MCNS Cystionosis.
Vascular
FSGS VUR.
Drug
MGN Other
Ischemic
d

*Urinalysis twice a day for 1week, a weeks a part; If both +ve, then R/o transient and
false causes.

*Early morning urinalysis; If +ve; then R/o orthostatic

*Urine analysis if Hematuria, Edema; then R/o tubule –interstitial.

Q: Nephrotic syndrome (NS)
Is characterized by 4 components:

1-proteinuria

>40 mg /m/HR or 1g/kg/24HR

Urine protein: creatinine ratio >200 mg /mmol.

2-Hypoalbuminemia

Serum albumin <25g/L.

3- Hypercholesterolemia

Serum cholesterol > 200m 5/dl. Or 5.17mmol/L.

4-Edema.

Other characteristics finding:

Ca: <2.25 mmol/L (9.0mg/Dl).

K: Over 5.0 mmoL/L.

Na: <135 mmoL/L.

Hypercoagulability PTT

Etiology:

1-Idiopatic nephrotic syndrome (minimal change disease)-INS

-The mast common cause of NS

-INS 80-90%

- Age; 2-5yr; male>female.

- Cause: unknown.

-Clinically: Hematuria occurs in 10%

-Most INS responds to steroid

-Up to 80% have frequent relapse.

2-Focal segmental glomerulosclerosis (FSGS)

-The most common progressing glomerular disease in children

-The 2rd most common cause of ESRD

-It may be A. inherited (AR, AD), B. idiopathic, or C. Secondary to post infectious GN,
obstruction uropathy, systemic disease (SCA,SLE)

-Often in child who has CRINS.

3-mesangial proliferative glomerulonephritis

-This is usually idiopathic

Chronic infection bacterial or viral
May secondary to SCD
SSLE

Renal, BM transplant

4- Membranous glomerulonephritis *Glomerulonephritis:

- Idiopathic -Older children (6-15y)

-Systemic disease (SCA, SLE) -Age variable

-Drug (NSAID, captopril) -Clinically usually

-Toxins (heavy metals) -Hematuria present

-Infection (hepatitis B,C) -High blood pressure

- Low Renal function

-Not respond to steroid

Meningeal PGN FSGS

SLE
MGN

-Clinically more likely to present with hematuria nephritis.

-Persistent low complement c3.

Complication of NS

#1 Infection:

1-The most common organism: Encapsulated bacteria (pneumococuo, homophilus, E-

coli)

2-The most common type of infections: Cellulitis, peritonitis, UTI, septicemia, and
meningitis.

3-Factors increased risks of infection are:

-Urinary loss of immunoglobulin IgG.

-Loss of factor B & D of element complement activation path.

-Loss of transferrin.

-Alter T-Cell Function.

-Impair ability to make antibodies.

-Loss of opsonizing factor.

-Burden of steroid therapy &immunosuppressive drug.

- Presence of edema &ascites.

#2 Edema:

How occur?

Decrease of oncotic pressure " Fluid more " intravascular space.

Jinterstitium Hypervolemia (OLD)

Now; due to

1-Defect in Na excretion.

2- Excess of vasopressin.

Edema can lead to:

• Anasarca
• Scrotal / edema >> Difficulty walking
• Respiratory distress with effusion
• Sever Ascites
• Tissue breakdown and cellulitis.
 *All of those are indications of Albumin infusion followed by Lasix

#3 Thrombosis & Embolisms:

It happens due to:

-Increased plasma fibrinogen, clotting factors "2.5.7.8.9.10,13" , blood viscosity ,

hyperlipidemia

-Decreased plasma anti thrombin 3 , protein S , blood flow

** Risk of thrombosis 2-5%

Most common vessels affected:

Renal vein, sagittal sinuses , DVT, Pulmonary, IVC, Femoral/iliac artery , cerebral artery,
meningeal artery mesenteric vein, hepatic vein

^^SLE, Nephrotic syndrome, and antiphospholipid syndrome can implicate thrombosis

Complications of thrombosis:

1-PE

2-Bilateral renal vein thrombosis usually with secondary nephrotic syndrome in the
form of ARF

*Thrombosis more common in CRINS

Risk factor of Thrombosis:

Diarrhea, Vomiting , use of diuretic immobilization , and indwelling cath

Treatment of thrombosis: LMW heparin

#4 Hyperlipidemia +CVS disease:

-Usually reversible within 4-6weeks

-May be persistent hyperlipidemia to adulthood >> increased risk of coronary vascular

disease

#5 Growth disturbance:

-Due to urinary loss of protein "IGF"

-Use of GH not yet proven

#6 Hypocalcemia:

-Due to loss of vit-D binding protin in urine>> demiralizaton of bone

6-Hypothyroidism:

-Due to urinary loss of thyroid binding protin usually in congenital nephrotic syndrome

#7 ESRD:

-8-10%

-Affect steroid resistant FSGN

#8 Negative nitrogen balance

Management of NS:

**Investigations:

1-Urine:

-Hyaline/waxy cast >>INS

-Cellular cast >>other GN

-Microscopic hematuria >> If transient" is steroid sensitive NS

If persistent is steroid resistant NS

-Urine Protein/Cr ratio >0.02mg/mmol

2-Blood:

-Do U&E, CBC , albumin, c3,4 and hepatitis serology : Hep B in membranous nephritis ,
Hep C in mes PGN

-Do cholesterol, Triglyglycerid

-ANA if SLE suspected

3-Renal biopsy

Indications:

1* Age<1Y

2* Nephritis feature "HTN, Hematuria"

3* Renal impairment "High Cr"

4* Persistent low c3

5* Steroid resistant

Treatment:

1/ Corticosteroid

-Dose: 2mg/kg

-Mainstay of therapy

-Total course of 7m

2/cychlophosphamid:

-Dose: 2mg/kg/day for 8-12weeks

-Prolonged remission and # of relapse

-SE:

*Short term: BM suppression "need weekly CBC "increase risk of viral infection specially
varicella and mussels

*Long term: Hemorrhagic cystitis carcinogenesis, gonadal toxicity

3/cyclosporine:

-Dose: 2-5mg/kg/day

-SE: nephrotoxic, HTN, gingival hypertrophy, hypertrichosis

4/levamisol:

-Effective in steroid dependent

-Decrease need to steroid by 50% and decrease relapse by 50%

-SE: neuropenic, vasculitis, liver toxicity, convulsion.

Q: 4 years old girl with recurrent UTI

Approach:

History:
-All UTI (when, how, treatment, lab, prophylaxis, admissions)
-Why recurrent: *voiding dysfunction
*constipation
*Anatomical problem (neurogenic bladder, vesicouretric reflux)
-Renal symptoms: HTN, hematuria, proteinuria
-Current UTI symptoms
-Nocturnal enuresis
-Antenatal US

Examination:
-Vital signs - BP
-Growth parameters
-Systemic exam (Abdominal, CNS)
-Genitalia
-Back exam
-Urine dipstick

Lab
1-Renal functions (U&E)
2-Urinalysis
3-Urine c/s
4-Kidney US
5-MCUG
6-DMSA

**If all are negative, start prophylactic Abx (for 6m to 1y) then stop and see
**If any is abnormal start prophylaxis & Repeat MCUG at 1 year

Indication of prophylaxis:
1- Infant/child with UTI " 10 days antibiotic??????
Workup not ,,,, finished??
2- Urological problems (voiding dysfunction, VUR)

** Do urine c/s 7days after starting antibiotics

** US age of 2y????

#Referral to nephrologist:
1-High BP
2-Alteration of renal function
3-Obstructive uropathy
4-VUR grade 4
5-Not responding to antibiotics
Indication of MCUG:
1-Male 1st time
2-Recurrent UTI
3-Younger than 2y
4-Renal impairment
5-Unusual organism
6-Abnormal US
 3- Hematology:
- HB Electrophoresis*
Rewritten by Shima Alahmadi

- Neonatal thrompocytopenia
Rewritten by Khulud AlSaedi
- ITP
Rewritten by Khulud AlSaedi
- Approach to thromppocytopenic pt
- Rewritten by Khulud AlSaedi
- Thalassemia*
Rewritten by Shima Alahmadi
- SCA with splenic crisis.
Rewritten by Khulud AlSaedi
- Hemophilia A
Rewritten by Hamad Altruif
- Tumor lysis syndrome
Rewritten by Khulud AlSaedi
- Down syndrome with CBC
Rewritten by Khulud AlSaedi

* Reviewed by Dr. Reham Fallatah

Q: Interpretation of Hemoglobin Electrophoresis

Hb Electrophoresis:
It is the single most important investigation in the diagnosis of hemoglobinopathies
At birth: HbA 20% HbF 80%

Normal:
HbA 95%
HbA2 2-3.5%
HbF 0.5%

Sickle cell disease:

HbS 90%
HbF 10%
HbA2 2%
HbA 0%

Sickle cell trait:

HbS 40-45%
HbA 50-55%
HbA2 2%
HbF 0%

**Sicklthal**
Less sever than SCA
They have microcetic anemia

Sickle cell B+ thalassemia:

HbS 65%
HbA 15%
HbF 10%
HbA2 3%

Sickle cell B0 thalassemia:

HbS 75%
HbF 15%
HbA2 3%
HbA 0%

Sickle SC disease:
HbS 50%
HbC 50%

Thalassemia:
1- B thalassemia Major:
HbF 90-95%
HbA2 2-5%
HbA 0% (absent)
 2- B thalassemia Minor:
HbA 90-95%
HbF 1-3%
HbA2 4-7%

*Alpha thalassemia:
-4 genes on chromosome 16, the pathology is due to deletion of this genes.
-Alpha thalassemia causes microcytic anemia, diagnosed by specific genetic test.

1 gene deletion" Silent carrier

2 genes deletion" Alpha thalassemia trait
3 genes deletion" (Hb H disease) – Anemia + Splenomegaly
4 genes deletion" Hb barts – hydropsfetalis – still born
Q: Approach to Neonatal Thrombocytopenia
-First:
Patient: stable vs unstable

History:
- Current history
- Antenatal: Maternal fever, URTI, Preeclampsia, IUGR
- Prenatal: Term, delivery, APGAR score, Birth weight
- Postnatal: NICU admission, UVC, UAC, RDS, Sepsis, exchange
- Mother PLT, auto-immune disease

Examination:
-Well Vs sick
-Vital signs
-Growth parameters
-Dysmorphic features
-Eyes – cataract (TORCH)
-Hand & toe exam (Absent radius or thumb)
-Hemangioma
-Skin bruising
-Systemic examination – cardiac

Causes:
Neonatal Thrombocytopenia
Sick Well
-Preterm -Dysmorphic -No dysmorphism
-Medical complication -Signs -No signs

-Asphyxia -TAR -Occult infection

-Cold injury -Fanconi -Auto-immune TP
- Preeclampsia -Trisomy -NATP
-Sepsis -Kasabach-merritt -Amegacaryocytic TP
-DIC syndrome -WAS
-RDS
-NEC
-Thrombosis
-Exchange transfusion
-BM suppression
LAB:
Depends on Hx & Ex:
1-CBC & Diff
2-PLT size
3-Peripheral blood film
4-CBC mother (PLT)

Treatment:
1-Auto-immune Thrombocytopenia
-IVIG 1gm/kg if PLT < 20 OR clinical bleeding
-Response 80%, resolve within 2-3 montha
-PLT transfusion " No benefit EXCEPT CNS bleeding

2-Neonatal Allo-immune Thrombocytopenia

-As Rh disease; Baby has antigen from the father; which is not present in the mother "
mother forms Antibodies against it " destruction of fetal PLT

Characterized by:
*Sever thrombocytopenia
*50% at first pregnancy
*CNS bleeding 20-25% in utero
*Mother Ab (antiplatelet antibody????)
*Recurrence rate 75%

Management:
-CBC daily
-Brain US to rule out ICH
-Washed maternal PLT
-IVIG can be used
-Family counseling regarding next pregnancy IF previous baby is severely affected ICH
-To administer corticosteroid/ IVIG +/- PLT transfusion to the fetus through US guidance
during the 3rd trimester
Q: Idiopathic (Autoimmune) Thrombocytopenic Purpura

**The most common cause of acute onset thrombocytopenia in an otherwise well child is
ITP

Pathogenesis:
-It is an autoimmune disease (why?) cause is unknown
Postviral infection (50-65%)
-The most common viruses associated with ITP:
1-EBV
2-HIV (usually chronic ITP)
3-H.pylori
4-MMR vaccine (rare)

Clinical Presentation:
*Classic presentation of ITP
-Age: 1-4y , male > Female
-Onset: sudden generalized patechiae/purpura
(often) with gum & mucus membranes bleeding (PLT<10g/l)
-Preceding viral infection (1-4wks)
-Slenomegaly, LN, bone pain, pallor (RARE)
-Presence of HSM, LN enlargement, Bone and joint pain with Insidious onset suggest other
Diagnosis " leukemia

*Classification of ITP:
-No symptoms
-Mild symptoms: bruising, patechiae, minor epistaxis
-Moderate: Sever skin & mucosal bleeding, major epistaxis & menorrhagia
-Sever: bleeding episodes (epistaxis & menorrhagia, melena) needs hospitalization

Lab Findings ???

-PLT < 20,000 (common)
-Hb: normal unless there is significant bleeding
-WBC & differential: normal
-BM ex: Normal granulocyte & erythrocyte series with MEGAKARYOCYTES
-ANA: to rule out SLE (adolescent / new onset ITP )
-Coombs test: to rule out Evan’s syndrome (unexplained anemia)

Indications to BM
1-Abnormal WBD & diff
2- Unexplained anemia
3- Hx & Ex suggest BM failure
Differential Diagnosis:
1-Drug induced
2-Splenic sequestration (portal HTN)
3-Aplastic (Fanconi) anemia
4-Congenital thrombocytopenia (TAR, MYH9 – thrombocytopenia)
5-Increased PLT destruction (HUS, DIC)
6- Hypersplenism (Liver disease, DVT)
7-Autoimmune thrombocytopenia as an initial manifestation (SLE, HIV infection)
8-Wickott-Aldrich- Syndrome (WAS)

Treatment:
1-No Therapy:
-Mild-Moderate symptoms
-Family education & counseling

2-IVIG
-Dose: 0.8-1gm/kg/day
-MOA: Down regulation of FC-mediated phagocytosis in splenic macrophage of Antibody
coated PLT
-Response: within 48-72hr, PLT > 20 in 80-90% of pts
-S/E: Headache, vomiting (aseptic meningitis)

3-IV Anti-D
-Dose: 5-70gm/kg
-For Rh +ve patients
-MOA: RBC-Antibody complex bind to macrophage FC receptor & interfere with PLT
destruction
-S/E: May indue mild hemolytic anemia

4-Prednisone:
-Dose: 1-4mg/kg/24hr
-Continue for 2-3wks PCT > 20
-BM examination should be performed before prednisone - to rule out other causes (ALL) -is
controversial

5-PLT transfusion (contraindicated) Unless:

Life threatening bleeding (i.e intracranial bleeding)

6-Splenectomy:
A) Age > 4y + sever ITP > 1y
B) Life threatening hemorrhage (intracranial) in acute ITP
S/E:
-Overwhelming infection (encapsulated organism)
-Pulmonary hypertension (adulthood)
Prognosis:
-Sever bleeding is rare <3%
-70-80% of acute ITP spontaneously resolve by 6m
-1% " intracranial hemorrhage
-20% " will have chronic ITP
-ITP in younger child most likely to resolve
Q: Approach to patient with low platelets (Thrombicytoenia)

History:
-Well Vs ill
-Onset: Acute vs chronic
-URTI symptoms or history
-Drugs (phenytoin, valproic acid…)
-Bruising, purpura, patechiae
-Weight loss, sweating, fatigability, bone & joint pain
-Liver disease
-Autoimmune disease
-CNS symptoms

Examination:
-Vital signs
-Growth parameters
-Pallor, jaundice, hemangioma, skin rash
-Lymphadenopathy
-Hepatosplenomegaly
-Bone tenderness
-Evidence of autoimmune disease
-Stigmata of CLD

LAB:
-CBC & diff
-Peripheral blood film

Treatment:
-Admission to hospital
- Avoid trauma
- Avoid NSAID (can use celecoxib-choline if febrile/headache)
-IVIG:1gm/kg (blocks FC receptor in solenic macrophages)
CBC after 24h, if no response; give 2nd dose
-If no response: Steroid 2-4 mg/kg/??? (after doing BM aspiration or biopsy)
-IV anti-D for Rh +ve patients

Chronic ITP 12m or more:

New definition:
3/12 " acute
3m-1y " Persistent
1y " chronic
 **When to treat acute ITP ??
1-PLT < 20,000
2-PLT 20,000-30,000 & symptomatic (bleeding)

#If PLT> 20,000 with No bleeding " No treatment

-Age 1-4y
-Viral illness " Ab+PLT # destruction of Fc receptor
-Prognosis: 80% " spontaneous relief
20% " chronic ITP
-CNS bleeding: give PLT, IVIG, Steroid, splenectomy

**Chronic ITP treatment:

Medical:
-Same as acute ITP
-Rituximab
Surgical:
-Splenectomy (successful complete remission 65-88%)

Differential Diagnosis of Thrombocytopenia :

Well
-Large PLT -Small PLT
-Normal CBC, Hb -(H) MCV
Immune Non-immune Congenital Acquired
-ITP -TAR -Toxins
-2ry to SLE, HIV -WAS -Medications
-Drug induced -Amegakaryocytes -Radiation
-NATP -Fanconi anemia

ILL
Large PLT Small PLT
(L) Fibrinogen HSM
(H)FDP
Consumption Sequestration Decreased synthesis
-Microangiopathy -Hemangioma -Malignancy
-HUS - RDS -Hyperslenism -Storage disease
-TTP - Thrombosis
-DIC - Sepsis
-UAC - Viral infection
-NEC
Q: Approach to thalassemia

-Microcytic hypochromic anemia

-Autosomal recessive
-It can be alpha or beta thalassemia

History:
- Anemia symptoms
- Consanguinity
- Family history of thalassemia
- Drug, food
- Urine color
- Diagnosis (transfusion program, chelating agent)
- Vaccination “regular and extra”

Examination:
- General, vital signs
- Growth parameters
- Pallor, jaundice, ……….
- Hepatosplenomegaly
- Dysmorphic fetures (Thalasemic face)
- Leg ulcers
- Scars (splenectomy, gall bladder stones)
- CVS
- Tuner stage

Investigation:
- Not on transfusion:
- CBC, diff
- Retics, LFT
- HB Electrophoresis
-Blood film
- On transfusion:
- CBC, diff
- Retics
- Gene study
- Parents HB Electrophoresis

Treatments:
1- Counsel family: genetics
2- Support ineffective erythropoiesis by chronic transfusion program:
- 10-15 ml\kg every 3 weeks
-Aim: Hb> 9g\dl (before), > 11-12g (after)
- Ferritin level after 1 year>1000
 3- Chelating agent:
A-Desferal:
-Dose: 20mg\kg SC over 12h, 5-6 days\week
-S\E: 1-local irritation
2- Sensorineural hearing loss
3- retinal changes
4- bone abnormalities (psudo-reckits)
5- alter renal function
B- Oral:
-Deferiprone TID:
- S\E neutropenia
-Ex Jaid OD:
-S\E: 1- Renal impairment.
2- elevated LFTs.
3- GI Upset.
4- Auditory toxicity
5-cataract
4- Cardiac follow up: T2- MRI

Complication:
- Anemia: Expand BM, Thin bone, short stature
- Hypersplenism
- Iron overload: Endocrine (DM, HTN, Gonads in form of delays sexual maturation
and 2ry infertility, Hypopituitarism), Heart, Liver.

Causes of death:
1- CHF, arrhythmia
2- Sepsis
3- Organ failure.

Indications of splenectomy:
1- Adolescent with hypersplenism
2- Persistence increase in blood transfusion requirements by 50%
3- Annual PRBCs > 250ml\kg\year (180-200)
4- Large spleen causes discomfort.
Q: Approach to SCA with Splenic Sequestration Crisis

Treatment:
*Acute
-This is an actual emergency
-Make sure about ABC
-Close monitoring in PICU
-CBC, x-matching, blood g… screening
-Give: PRBC 5ml/kg (simple transfusion) with close monitoring

*Chronic
-Educate the family how to palpate the spleen
-Long term plan for splenectomy in 3-4y
-Chronic blood transfusion monthly
-Aim: to decrease HbS to 30% or less
-Vaccine: for pneumococcal, H.influenza
-No role for exchange transfusion

**2cm spleen enlargement BCM – drops Hb by 2gm/dl

Indications for exchange transfusion:

1- Stroke
2- Priapism (painful erection > 30min)
3- Before major surgery
4- ACS
5- Sever infection

**It’s better to read management of SCA from Dra.Fatma AlZahrani’s sheet

Q: Approach to patient with Hemophilia A

History:
-Natal: circumcision
-Children: Bruising, hematoma, hemarthrosis (target joint)
-CNS bleeding - ICH
-GI bleeding
-Spontaneous bleeding Vs after trauma
-Admission (hospital, PICU)
- Medications: type (blood product or not)
-Social impact on child, parents and sibling
-Complications: -Infection, transfusion related
-Arthropathy (disability)
-Development of inhibition for factor 8 " 25-35%
-Immunization: HBV, HCV, HIV
-Family history of hemophilia

Examination:
-Vital signs
-Growth parameters
-Skin bruising
-Examination of ALL joints
-Systemic examination

Classification:
Mild >5%
Moderate 1-5%
Sever <1%

LAB:
-CBC
-PT, PTT
-Factor Assay
-Mixing study (If not corrected with mixing " inhibitor)

Management:
-Family counseling
-Avoid NSAID, trauma, IM injection
-Vaccination
Prophylaxis
*Desmopressin for mild hemophilia A
* Regular transfusion, blood or non-blood product
-Factor:
*In mild & moderate should rise 30-50%
*In major & life threatening bleeding in 100%
-Monitoring complications
-Psychological support
Injectable vaccines can be given:
1-Same
2-Deep SC
3-Compress for 10min after injection

Dental extraction:
-Transexemic acid – 4hr
-Factor 8 – 1hr

Calculation of dose:
Factor 8 (%desired x wt x 0.5)
Factor 9 (%desired x wt x 1.5)
Sever (50-75 unit/kg )
Q: Approach to Tumor Lysis Syndrome

Definition:
Metabolic complications occur as a result of rapid lysis of large tumor burden

Causes:
Bulky tumors especially:
1- Burkitt lymphoma
2- T-cell Leukemia
3- Lymphoma

Triad of TLS
1-High uric acid
2-Hyperkalemia
3-Hyperphosphatemia

Treatment:
This is an acute emergency!!
(involve heam/onco and nephrology team from the beginning)
1-ABC
2-Close cardio-pulmonary monitoring
3-PICU admission
4-IV fluid (10% deficit) 3000ml/m2/day
Aim: good urine output (>3ml/kg/hr)
5-Alkalization by bicarbonate To avoid uric acid precipitation in the kidney; but may lead to
ca/phos precipitation
6-Allopurinol Vs resburicas (preferred)
7-Aluminium hydroxylase to decrease PO4
8-Do not correct hypocalcemia UNLESS patient become symptomatic
Q: 10 Days old with trisomy 21, CBC showed:

WBC 76,000 " 40%blast

Hb 15mg/dl
PLT 560,000
What is the diagnosis?

Transient myeloproliferative syndrome " Transient leukemia in Down syndrome (up

to 3m)

Treatment:
Depends on the general condition
1-Well
2-No stasis
3-No cholestasis
" It will improve with time, counsel family about this condition

** 20% of trisomy
-80% Resolve
-20% AML (M7) in 2-3y old

Leukemoid reaction:
WBC > 50,000/mm3

Causes:
1-Bacterial sepsis
2-Tuberculosis
3-Congenital syphilis
4-Congenital/acquired toxoplasmosis
5-Erythroblastosis fetalis
6-Down syndrome
 4- Toxicology:
- Paracetamol ingestion*
- Iron ingestion*
- Organophosphate poisoning

All Rewritten by Khulud AlSaedi

* Reviewed by Dr.Reham Fallatah
Q: Name the toxicology ‘time bombs’?
A: ‘time bombs’ are medications that lack symptoms early after ingestion but later have a
profoundly toxic course
1- Acetaminophen (delayed hepatic injury)
2- Iron (delayed cyanosis and profound metabolic acidosis)
3- Alcohols- methanol (delayed acidosis), ethylene glycol (delayed nephrotoxicity)
4- Lithium
5- Anticonvulsants – Phenytoin (Dilantin), carbamazepine
6- Time-release medications
(pediatric secrets 5th ed, Ch5, pg181)

Q: What is gastrointestinal decontamination?

A: Gastrointestinal decontamination refers to a variety of medications that may be
administered and techniques that may be used to decrease the absorption of ingested
poisons. Methods of gastrointestinal decontamination include; activated charcoal, whole
bowel irrigation and gastric lavage.
(pediatric secrets 5th ed, Ch5, pg181)

Other Q:
1-How dose a single dose of charcoal work & when should it be considered?
2-For what substances is charcoal NOT recommended?
3-When is gastric lavage indicated?
4-What are the indications for whole bowel irrigation (WBI) in acute ingestions?
5-How can pupillary findings assist in the diagnosis of toxic ingestion?
6-When can a toddler who swallowed some multivitamins be discharged home?
 Table 63-2 Selected Historical and Physical Findings in Poisoning

SIGN TOXIN

ODOR
Bitter almonds Cyanide
Acetone Isopropyl alcohol, methanol, paraldehyde, salicylates
Alcohol Ethanol
Wintergreen Methyl salicylate
Garlic Arsenic, thallium, organophosphates, selenium

OCULAR SIGNS
Miosis Opioids (except propoxyphene, meperidine, and pentazocine),
organophosphates and other cholinergics,
clonidine, phenothiazines, sedative–hypnotics, olanzapine

Mydriasis Anticholinergics (e.g., antihistamines, TCAs, atropine),

sympathomimetics (cocaine, amphetamines, PCP)
postanoxic encephalopathy, opiate withdrawal

Nystagmus Anticonvulsants, sedative–hypnotics, alcohols, PCP, ketamine,

dextromethorphan

Lacrimation Organophosphates, irritant gas or vapors

Retinal hyperemia Methanol

CUTANEOUS SIGNS
Diaphoresis Cholinergics (organophosphates), sympathomimetics, withdrawal
syndromes
Alopecia Thallium, arsenic

Erythema Boric acid, elemental mercury, cyanide, carbon monoxide,

disulfiram, scombroid, anticholinergics, vancomycin

Cyanosis (unresponsive to Methemoglobinemia (e.g., benzocaine, dapsone, nitrites,

oxygen) phenazopyridine), amiodarone, silver

OTHER SIGNS Reference: Nelson 20th edition (Pg450)

 Q: Approach to Paracetamol Ingestion:

-Minimum Toxic dose: 150-200 mg/kg

PHASE/S Time After Signs & Symptoms Lab Changes

TAGE Ingestion
1 First 24h -Asymptomatic Normal EXCEPT for
-Occasional Anorexia –Nausea – vomiting acetaminophen level
-Malaise –Pallor - Diaphoresis

2 24-72h *Resolution of earlier symptoms -High bilirubin

-RUQ abdominal pain & tenderness -High hepatic enzymes
-Prolonged PT, INR
-Oliguria
3 72-96h -Fulminant hepatic failure PEAK liver function
-Multisystem organ failure (encephalopathy, abnormalities
cardiomyopathy, coagulopathy, hepatic
failure/necrosis, renal failure)

4 4d-2wk ** Clinical recovery PRECEEDS histologic Resolution of liver function

recovery or Death abnormalities

LAB:
1-CBC
2-Chemisrty (renal profile)
3-LFT
4-PT, aPTT
5-Drug level (4h post ingestion)
**Recheck lab q12-24h

**If suspected toxicity; acetaminophen level should be measured 4h AFTER reported time of
ingestion.
**Patients presenting to medical care >4h, a STAT acetaminophen level should be obtained.
**Acetaminophen levels obtained <4h after ingestion are DIFFICULT to interpret & can NOT
be used to estimate the potential for toxicity.

Management:
-ABC
-Activated charcoal; 1-2h of ingestion ((MOST USEFUL))
-ANTIDOTE: N-acetylcysteine (NAC)
-Drug level 4h
-Plot on nomogram (no hepatic toxicity, possible hepatic toxicity, probable hepatic toxicity)
-consider co-ingestion
-Toxicology consultation

HEPATOTAXICITY > 150mg/kg

ALT > 1000 (marker of sever liver injury)

**High risk group hepatotoxicity:

-DM
-Viral infection
-Malnourished
-cytochrome P-450 drug (phenytoin, carbamazepine, rifampicin)

N-acetylcysteine (NAC)
MOA: Increase hepatic GLUTATHIONE stores & conjugates toxic metabolites.
Indication: (to start immediately)
1-Single ingestion > 150mg/kg – 7.5 gm (by history)
2-Unknown time of ingestion & drug level > 10mcg/L
3-Sever clinical symptoms
4-Abnormal liver function
5-Chronic ,subacute ? overdose with risk
6-“ possible hepatic toxicity’ on nomogram

*When to use:
1-Within first 24h post ingestion
2-Most effective if used in the first 8hrs

*Side effects:
-Anaphylactic reaction
-Bronchospasm
-Angioedema

#How to manage anaphylactic reaction (non IgE mediated) :

1- STOP the infusion
2- Treat with diphenhydramine, albuterol, and/or epinephrine as indicated
3- Restart the infusion at a slower rate once symptoms have resolved

Q: What breath odor is associated withN-acetylcysteine ingestion?

A: Rotten eggs odor (pediatric secrets 5thed, Ch5, pg185)

***Cytochrome P-450 ---metabolite--- Paracetamol" depletion of glutathione " hepatic

stores -" decrease glutathione 70% ---metabolite--- hepatic ?? "causes live necrosis
NOT SURE IF I GOT THIS SECTION RIGHT!!
Cytochrome P-450 interactions (selected)

Indusers (+) Substrates Inhibitors (-)

1-Chronic Alchohol use 1-Anti-epileptica 1-Acute AlchoholAbuse
2-St. john’s wort 2-Theopphylline 2-Ritonavir
3-Phenytoin 3-Warfarin 3-Amiodarone
4-Phenobarbital 4-OCPs 4-Cimetidine/Ciprofloxacin
5-Nevirapine 5-Ketoconazole
6-Rifampin 6-Sulfonamides
7-Griseofulvin 7-Isoniazid (INH)
8-Carbamazepine 8-Grapefruit juice
9-Quinidine
10-Macrolide (except
azithromycin)

ChronicalchoholicsSteal Always Think When Outdoors AAA RACKS IN GQ Magazine

phen-phen&Never Refuse
Greasy Crabs
** FIRST AID FOR THE USMLE STEP 1- 2016 Page 254
 Q: Approach to A Patient with Iron Ingestion:

-Toxic dose: 20-30 mg/kg

*Pediatric patients who ingest >40 mg/kg of elemental iron should be referred to
medical care for evaluation, although moderate to severe toxicity is typically seen with
ingestions of >60 mg/kg.

The severity of an exposure is related to the amount of elemental iron ingested.

• Ferrous sulfate contains 20% elemental iron. (one tablet of 200mg contains 65
mg elemental iron)
• Ferrous gluconate 12%
• Ferrous fumarate 33%.
Multivitamin preparations and children’s vitamins rarely contain enough elemental iron
to cause significant toxicity.

Oral toxic serum iron concentration of

• 350 µg/dL" minimal toxicity
• 500 µg/dL" moderate toxicity
• 1000 µg/dL" sever toxicity

PHASE/ST Time After Signs & Symptoms

AGE Ingestion
1 30min-6 hr -Profuse vomiting -diarrhea (often bloody) - abdominal pain
“GI phase” - Significant volume losses leading to potential hypovolemic shock
2 6-24 hr -GI symptoms typically have resolved.
“relative -However, careful clinical exam can reveal subtle signs of
stability hypoperfusion, including tachycardia, pallor, and fatigue.
phase”
3 12-36 hr -Multisystem organ failure –shock
“systemic -Hepatic and cardiac dysfunction
toxicity -Acute lung injury or acute respiratory distress syndrome (ARDS)
phase” -Metabolic acidosis.
**Death occurs most commonly during this stage.
4 4-6 wk -Formation of stricture
“GI scaring -Signs of GI obstruction.
phase”

*Symptomatic patients and patients with a large exposure by history should have serum iron
levels drawn 4-6 hr after ingestion
LAB:
1-CBC (leukocytosis> 150,000/mm)
2-Chemisrty (renal profile)
3-LFT
4-PT, aPTT, INR
5-Serum glucose level (hyperglycemia > 150mg/dl)
6-ABG (metabolic acidosis w/ increase anion gap)
7-Serum iron level (4h post ingestion)
8-Abdominal x-ray might reveal the presence of iron tablets (though not all
formulations of iron are radiopaque).
9-Endoscopy ?

Management:
Close clinical monitoring + aggressive supportive and symptomatic care, is essential to
the management of iron poisoning.
-ABC
-Activated charcoal does NOT adsorb iron
-WBI (whole bowel irrigation) remains the decontamination strategy of choice. “C.I if
airway is compromised”
- ANTIDOTE: IV Deferoxamine (specific chelator of iron).
-Vigorous hydration

*Observation/ no treatment if:

- Asymptomatic
- Less than 40mg/kg ingestion

Deferoxamine
Indications:
1- Moderate to sever symptoms regardless of serum iron concentration.
2- Serum iron concentration >500 µg/dL.
3- High anion gap metabolic acidosis.
4- Significant number of pills on x-ray.
5- Signs of organ failure.

Dose:
Preferably given via continuous IV infusion at a rate of 5-15 mg/kg/hr
(max, 6g/24h)
*Therapy is typically continued until clinical symptoms resolve.

Side effects:
1-Hypotention
Managed by slowing the rate of the infusion and administering fluids and/or
vasopressors as needed.
2-Tachycardia
4-Diarrhea / GI upset
5-Urticaria
6-Fever
7-Hearing loss
**Prolonged deferoxamine infusion (>24 hr) has been associated with:
-Pulmonary toxicity (ARDS) and
-Yersinia sepsis.
# The deferoxamine–iron complex can color the urine reddish (“vin rosé”), although
this is an unreliable indicator of iron excretion.

Contraindications:
?? Renal impairment " hemodialysis
*Hemodialysis if:
-More than 1000µg/dL
-Renal impairment

Q: Which ingestions are radiopaque on abdominal radiograph?

A: the mnemonic CHIPS indicate possible suspects:
Chloral hydrate
Heavy metals (arsenic, iron, lead)
Iodides
Phenothiazines, psychotropics (cyclic antidepressants)
Slow release capsules, enteric coated tablets
(pediatric secrets 5thed, Ch5, pg184)
Organophosphorous Poisoning

Inhibition of cholinesterase enzyme " Accumulation of Acetylcholine " Over stimulation

of muscarinic & nicotinic receptor.

Signs & Symptoms:

Muscarinic Effects Nicotinic Effect CNS Effect

Eye: Miosis & Lacrimation CNS: Muscle weakness, Agitation, delirium ,
Oral: Salivations, Oral & tracheal fasciculations, tremors, seizures and coma.
secretions hypoventilation (diaphragmatic
CVS: Bradycardia paralysis)
RESP: Bronchospasm/Bronchorrhea
GIT: Vomiting (emesis), Cramping, CVS: HTN, Tachycardia &
Defecation/Diarrhea dysarrythmias.
RENAL: Urination
" Pulmonary edema >>?
MNEMONIC:
*DUMBBELS *SLUDGE

SEVER CASES:
Coma, seizures, shock, arrhythmias & respiratory failure.

*History:
1- Source
2- Site
3-Methode of exposure ( inhalation, absorbtion, ingestion..)
4-Amount
5- Witness

*Examination:
1-General exam
2-Vital signs
3-Level of consciousness
4-Eye " miosis
5-Systemic exam (Resp & GI)

*Lab Tests:
1-CBC
2-U&E
3-LFT & Amylase
4-Blood Gas
5- RBC & plasma cholinesterase level***
6- CXR
7- ECG
*Management:
-ABC:
1-Maintain airway (secretion, patency ) " intubation
2-Breathing (signs of bronchospasm)
3-Circulation (HR, BP) bradycardia &HTN
4-Connect to cardiopulmonary monitor

-DECONTAMINATION:
1-Remove clothes
2-Clean the patient with soap & water
3-Wash the eye with NS

-TREATMENT: (antidots)
1- ATROPINE
DOSE: 0.05-0.1mg/kg IV/ET q5-10min as needed
Until –airway becomes dry
-Mydriasis (early indication of atropine use)

MOA: Competitive on acetylcholinesterase receptor (muscarinic )

SE: Mydriasis & tachycardia

2-PRALIDOXIME (2PAM)
DOSE: 25-50mg/kg over 5-10 min IV/IM (loading)
(max dose 200mg/min), can be repeated after 1-2h (for 2 doses), then q10-12h as
needed.
OR start infusion at 10mg/kg/hr
Indication: To reverse the muscle paralysis.
Until – Muscle paralysis relived.

MOA: Restore the acetylcholinesterase activity

SE: Nausea, dizziness, headache, tachycardia, muscle rigidity and bronchospasm
(rapid administration)

-FOLLOW UP:
1-Close observation 12h PICU
2-Admission for 48h (risk of respiratory failure)
3-Toxicology consultation

-EDUCATION:
1-Counseling of the family to prevent further episodes
2-??

Q: What breath odor is associated with organophosphate insecticide ingestion?

A: Garlic odor (pediatric secrets 5th ed, Ch5, pg185)
5- GIT:
- Neonatal jaundice*
Rewritten by Khulud AlSaedi
- Neonatal cholestasis
Rewritten by Khulud AlSaedi
- Neonatal diarrhea
Rewritten by Khulud AlSaedi
- FTT
Rewritten by Raneem Abushanab
- Rectal bleeding
Rewritten by Khulud AlSaedi
- Chronic diarrhea
Reference Uptodate, Nelson text book
Done by Nouf Nosani
- Cholestasis in children*
Rewritten by Khulud AlSaedi
- Milk Formulas
Rewritten by Khulud AlSaedi

* Reviewed by Dr. Reham Fallatah

Q: Approach to Neonatal Jaundice:

* History:
Jaundice:
- When was noticed
- Increasing or not
- Color of urine or stool
- Blood group (baby & mother)
- Rh incompatibility + anti D
- Feeding-amount
- Hx of fever “suspecting infection”
- Cephalhematoma
Prenatal;
- Maternal infection
- DM
- US abnormality
Natal:
- Gestational age
- Birth wt.
- APGAR score
- Type of delivery - Instrumental “for birth defect”

Signs of kernicterus (bilirubin enchephalopathy)

- Basal ganglia
- Deep jaundice
- Sleepy
- Seizure
- Irritable
- Stuper
- Coma

Family hx of blood disease or splenectomy, feeding, activities

* Examination:
- Well or ill, Signs of kernicterus
- Dysmorphic or not
- Any hematoma or birth injury
- Eye exam: (cataract) TORCH , galectocemia , congenital rubella
- CVS: heart murmur
- Abdomen: Liver, spleen, hernia, large tongue
- Urine & spleen inspection
- Skin: looking for petichiae or congenital infection”

* Diagnosis:
Most common cause is physiological jaundice

* Lab work:
- Bilirubin: total, direct
- Blood group, DCT
- G6Pd, retics
- CBC
- Blood film
-
* Treatment:
- IV hydration
- Phototherapy

Prolonged jaundice:
>10days in term
>2week in preterm
Q: Approach to Neonatal Cholestatic Jaundice:

-1st make sure patient is stable

-If stable " detailed history

History:
1- Antenatal (fever, US, mother illness, treatment)
2-Perinatal (term/preterm, delivery, APGAR score, Birth wt)
3-Postnatal(NICU admission , cause of admission - sepsis, asphyxia): Hx of UVC, UAC-
NEC, TPN, surgery)
4- Present illness (Jaundice, when did it begin, Progressed or not, Stool &Urine Color)
5- Associated symptoms, seizures, respiration, constipation)
6- Fhx of liver disease
7- Drug Hx
8- Nutritional Hx ( breast Vs formula )

Examination:
-Well or ill
-Vital signs
-Growth Parameter
-Pallor, jaundice
-Eye exam (cataract )
-CVS: heart murmur
-Abdomen: Hepatosplenomegaly
-Stigmata of CLD

LAB:
-CBC & diff
-U&E
-Glucose level
-LFT, alpha GT
-Bilirubin (TBIL, DBIL)
-Coagulation profile
-TFT
-Urine c/s
-Urine reducing substance
-Abdominal US
-Intra-operative-cholangiogram

Treatment:
According to underlying disease
Abdominal US:
Hepatocyte Biliary
(H) ALT & AST (H) GGT & ALP

Serology virus/ TORCH US (normal)

Metabolic/ Endo
HIDA scan
Not clear
Liver biopsy
Liver Biopsy

Neonatal hepatitis

Cholestasis + Hypoglycemia:
-Fulminant hepatic failure
-Metabolic- Galactosemia
-Panhypopitutarism
-Neonatal hemochromatosis
-Sepsis

Treatment:
-Biliary Atresia --> Kassi Op (hepato-Porto-enterotomy)
-Success ? 80-9-% in first 8/52
-Choledocal --> excretion
-Stone --> remove
-Paucity--> transplant
 Cholestasis
A) Biliary B) Heptocellular
-Acholioc stool -Preterm
-Prutitis -Small for GA
-Term
-Appropriate for GA

**Extrahepatic **Intrahepatic Neonatal Hepatits

1-Biliary atresia 1-PFIC -Idiopathic 80% - good prognosis
2-Choledocal cyst 2-Cystic fibrosis -Hereditary 20% - bad prognosis
3-Stone 3- Caroli Disease
4-Inspisciated bile 4-Paucity *Syndrome: Metabolic
5-Neonatal sclerosing Alligile -AA: Tyrosinemia
cholengitis *Non-CMV -Carbohydrate: Galactosemia / GSD / Heridatory
fructose intolerance
-Lipid: Neimanbeck (A,B,C) / Gaucher disease /
Wolman disease

Infection
-Viral: CMV / HAV / HBV / Enterococcus
-Bacterial: TORCH / Brucellosis / UTI / Sepsis
-Parasite: Toxoplasmosis

Drugs Endocrine
-Sulfa -Panhypopitutarism
-INH -Hypothyroidism
-Anti-epileptic -CAH

Others
-Alpha-1- anti trypsin -CF
-Wilson -SLE
-TPN -Cardiac
-Neonatal hemochromatosis -Down syndrome
-Zellweger
Q: Approach to Neonatal Diarrhea

Differential Diagnosis
1- Chloride loosing Diarrhea
2- Sodium loosing Diarrhea
3- Microvillus inclusion disease
4- Cow’s milk Allergy
5- Tought?? Enteropathy

History:
*Antenatal: polyhydromnious
*Natal: Symptoms (diarrhea in details + associated symptoms)
Feeding
Sepsis

Examination:
1-General/ Signs of dehydration
2-Growth parameter
3-Full systemic exam

LAB;
1-CBC
2-U&E, Glucose check
3- Stool (PH, electrolyte) c/s
4-Urie electrolytes

Treatment:
1-Correct dehydration
2-Correct electrolyte abnormalities
3-Treat underlying cause
4-GIT Consultation
Q: Failure to thrive:

Definition: it is a description not diagnosis

Suboptimal weight gain of infant and toddler.
- Wt. < 3rd percentile > 2 occasion
- Cross 2 major centile down
- Child wt. < 80% of ideal wt. for ht.

Measurements:
1- Gomez classification: weight for age: Actual wt. for age
------------------------ X 100 Ht. For age
Standard wt. =
Actual ht.
Wt. for age Grade --------------X 100
Standard ht.
> 90% N
<95. Mild
75-89% Mild <90%. Moderate
< 85% Sever
60-74% Moderate
<60% Sever

2- Waterlow Classification: Weight for hight: Actual ht. /ht.

--------------------- X 100
Standard ht. / ht.

Wt. for ht. Grade

> 90% N
80-89% Mild
70-79% Moderate
<70% Sever

3- Welloome Classification:

60-80% Exp. wt. < 60% of expected wt.

No edema Under wt. Marasmus

Edema Kwashirkor Marasmus
Kwashirkor
Treatment:
1- Correct water and electrolytes
2- Treatment chronic disease
Organic
Non- organic - multidisplanary
3- Catch up:
Recommended daily allowance (RDA) : of 50% of wt.
for age then give 60% if
RDA
------- 110. 1y
KCL 100 1-3 y
90. 4-6 y
Nutrional requirment : ideal wt.
------------ * RDA
Actual wt.

Then give 60% - carbohydrate 50% = 1Gm = 4 kcal

Protein 15% = 1Gm= 4 kcal
Fat 35% = 1Gm= 7 kcal

Instructions:
1- Meal time 30 min.
2- Solid food first
3- Eat with others, decrease distraction
4- High calorie food

Q. If you are in desert what to do?

1- Each 100 ml of milk add 1/2 spoon of MCT oil or polycarb
2- Put 1 scoop in 50 ml instead of 1scoop in 60 ml of water
1ml MCT / 7 kcal Poly carp 1ml / 2kcal. Oz ( 30 ml ) 1 ml = 20 kcal 0.67 kcal

Complication
- Refeeding syndrome
- CHF
- Hypothermia
- Vit deficiency
- Hypoglycemia
Approach to FTT

History:
- Birth : wt - complication - IUGR - anomalies - GI malformation
- GIT symptoms:
Diarrhea , vomiting , loss wt. , steatorrhea , choking , anal problem
- Other Symptoms :
Joint pain, skin rash
- Nutritional hx in details
Deit , who ----- , how ---
- Systemic review
- Psychosocial

Examination:
-Growth parameter
Acute = wt. ⬇, ht. N
Chronic. = wt. ⬇, ht. ⬇, ratio N
Acute on chronic = all ⬇
-Vital signs
-Dysmorphic feature
-CLD stigmata
-Nutritional assessment

Lab with significance:

- CBC
- U&E
- Bone profile
- LFT, S. ALB
- Coagulation
- Zinc level
- Stool analysis, c/s
- Tissue transglutaminase IgA, Karyotype in firl
- CRP, ESR, ferritin
- Immunoglobulins, sweat test and chest x-ray, TFT
 FTT

1) Inadequate intake “most common cause”:

*Organic < 5%: impaired sucking “cleft lip, CP”, chronic illness lead to anorexia
“Chron’s, CF, liver disease
*Non-organic: inadequate available food, psychosocial deprivation, neglect or child
abuse
2) Inadequate retention: GERD, Vomiting
3) Malabsorption: short bowel, CF, celiac
4) Failure to utilize nutrition: chromosomal disorder, metabolic disorder
5) Increased requirement: Thyrotoxicosis, CF, malignancy, chronic infection
 CRONIC DIARRHEA
! WHO Defines: Increase in fluidity, volume and frequency of stools relative to the
usual habits of an individual.

! The great majority of diarrhea episodes last less than one week.

When diarrhea persists for more than 14 days, it is called persistent, intractable, or chronic
diarrhea
! Introduction Sequelae:

! Dehydration.

! Marked weight loss and malnutrition.

! FTT.

! There are Five basic pathophysiological categories of diarrhea:

! (1) Osmotic Diarrhea

! (2) Secretory Diarrhea

! (3) Inflammatory Diarrhea

! (4) Diarrhea due to Motility Disorders

! (5) Decrease intisnital surface area

! Causes of Chronic Diarrhea

! Infections:

! Viral: Rota / adenovirus / Post infectious secondary lactase deficiency.

! Parasitic Giardasis Most Common for chornic onset /Ascaris / Amoeba /

Ankylostoma.

! Bacterial mainly acute diarreah and bloody Salmonella/ Campylobacter.

! Antibiotic induced: C. difficile.

! Endocrin: Hyperthyroidism increasing motaliti / Adrenal insufficiency.

! Malabsorption:

! Carbohydrates :Lactase deficiency / Glucose-glactose malabsorption.

! Fat Malabsorbtion.

! Protien Malabsorbtion.

! Immune defects Agammaglobulinemia / IgA deficiency / AIDS.

! Metabolic defects: Familial chloride diarrhea.

! Pancreatic enzymes: Cystic Fibrosis

! Small intestine: Celiac disease

! Auto- Immue Inflamatory: IBD crohns Vs UC

! Chronic nonspecific diarrhea.

! History

! Patient profile Age, known case?

! Duration: Sudden, progressive, On and OFF ,Past history of similar attack? How
frequent?

! Character Consistency? Blood? Mucus? Pus? Offensive?

! Associated symptoma:

Vomiting? Fever? Abdominal pain? Tenesmus? Convulsion? Cough? Appetite?

Weight loss? Height intolerance? Tremorr?
! Type and quantity of milk?
 ! Alleviating and aggravating factor Relation to Food?

! Past Medical and Surgical Histoty?

! Allergy to food?

! Family hx of a similar condition?

! Social history Living conditions? Pets ?

! Drug history?

! Travel history?

! Physical examination:

! General appearance and mental status

! Vital signs

! Growth Parameters: FTT???

! Hydration assessment.

! Orthostasis- volume depletion,autonomic dysfunction

! Exophthalmos Thyroid Examinations (hyperthyroidism)

! Hyperpigmentation (Addison's disease)

! Aphthous ulcers (IBD and celiac disease)

! Lymphadenopathy (malignancy, infection or Whipple's disease)

! Clubbing (liver disease, IBD, laxative abuse, celiac disease,)

! Dermatitis herpetiformis (celiac disease)

! Erythema nodosum and pyoderma gangrenosum (IBD)

Abdominal Examination/ PR examination:

! Surgical scars / Abdominal tenderness / Masses

! Hepatosplenomegaly

! Auscultation: bacterial overgrowth / obstruction, or rapid intestinal transit.

! PR examination for Ulcers / fissures/ abscesses /Fistulas

! Chest Examinations: Cystic firosis

! Joints: Arthritis: (IBD, Whipple's disease)

Investigations are directed by clinical findings:

! CBC U&E

! Stool culture Electrolytes/ ph /Trace elements (carbs malabsorbtion High)

! RFTs.

! endoscopy, clonoscopy,

! TFTs,

! Antibody test for celiac disease.

! Sweat chloride test.

! Trial of lactose restriction? Lactose breath hydrogen.

Q: Approach to cholestasis in children

DDX:
1-Infection: Viral hepatitis, EBV, CMV
2-Obstruction: Stone, mass, LN
3-Autoimmune hepatitis
4-Metabolic: Wilson Disease, Lipodosis, GSD, Tyrosinemia
5-Syndrome of intrahepatic cholestasis
6-Alpha-1-Antitrypsin deficiency
7-Toxin: Drugs
8-Other: IBD, CHD, TPN, CF

History:
Detailed history

Examination:
-Vital signs
-Growth parameters
-Eye exam – Wilson
-CVS: heart murmur, Alagille syndrome
-Abdominal exam
-Stigmata of CLD

Lab:
1- CBC & differential
2- ESR
3- LFT, GGT
4- Hepatitis serology
5- Abdominal US
6- Urine copper, ceruloplasmin
7- Antibody (Anti-liver-kidney microsomal Ab, ANA, Anti-smooth muscle Ab)

Treatment:
According to underlying cause

Cause of cholestasis:
**Obstructive
Biliary atresia, primary sclerosing cholangitis, choleducal cyst
**Cholestasis
Ductal paucity, Allagile, ispisated bile
**Hepatocellular cholestasis:
Hepatitis, alpha one anti trypsin deficiency, TPN associated, PFIC
Q: Approach to Patient with rectal bleeding

1st : Make sure patient is stable

IF stable, start with history

History:
-Fresh or melena
-Painful or painless
-PR bleed (amount, relation to stool)
-Other symptoms (Constipation, diarrhea, tenesmus, abdominal pain, vomiting, weight loss,
jaundice, skin rash, arthritis, fever)
-Hematological disease
-Family history of bleeding (from rectum or other sites)
-Allergy to food
-Medication history

Examination:
-Vital signs
-Growth parameters
-Pale, jaundice
-Skin rash
-Clubbing, ulcer
-Oral cavity
Abdominal exam
-Per rectum (fissure, fistula, polyp, tag, stool)

Lab
1-CBC
2-U&E
3-LFT
4-Coagulation profile
5-Stool for occult blood

Treatment:
-NPO
-IVF
-NGT
-Endoscopy
Esophageal varices Esophagitis/ Gastritis
1-Sclerotherapy -Take biopsy for H.Pylori
2-Banding -Start PPI
3-Quarty
4-Vassopressin IV
-Avoid steroid, NSAID, Caffeine & spicy food
Q: List the indications for lower gastrointestinal (GI) colonoscopy or endoscopy in
children.
1- Hematochezia in the absence of an anal source
2- History of familial polyposis
3- Chronic diarrhea of unclear etiology
4- Persistent severe unexplained mid- to lower abdominal pain
5- Colitis of unclear etiology
6- Diagnosis and management of inflammatory bowel disease
7- Removal of foreign body
8- Ureterosigmoidostomy, surveillance
9- Abnormality on barium enema
10- Dilation of a colonic stricture
th
(pediatric secrets 5 ed, Ch7, pg258-261)

Q: When is colonoscopy contraindicated?

1- Suspected perforation
2- Toxic megacolon
3- Recent abdominal surgery
4- Unstable medical illness (abnormal vital signs or severe anemia)
5- Inadequate bowel preparation
6- Coagulopathy
7- Massive lower GI bleeding
th
(pediatric secrets 5 ed, Ch7, pg258-261)

Q:In patients with acute GI bleeding, how may vital signs indicate the extent of volume
depletion?
A:It is important to remember that, when acute bleeding occurs in children, it may take 12
to72 hours for full equilibration of a patient’s hemoglobin to occur. Vital signs are much
more useful for patient management in the acute setting (Table 7-8).
th
(pediatric secrets 5 ed, Ch7, pg258-261)

Q: What is the simplest way of differentiating upper GI from lower GI bleeding?

Nasogastric lavage. After the insertion of a soft nasogastric tube (12 Fr in small children, 14
to16 Fr in older children), 3 to 5 mL/kg of room-temperature normal saline is instilled. If
bright red blood or coffee-ground–like material is aspirated, the test is positive. A pink-
tinged effluent is not a positive test because it can simply denote the dissolution of a clot
and not active intestinal bleeding. By definition, upper GI bleeding occurs proximal to the
ligament of Treitz. If the lavage is negative, it is unlikely that the bleeding is above this
ligament, and this rules out gastric, esophageal, or nasal sources. However, bleeding from
duodenal ulcers and duodenal duplications may sometimes be missed by these aspirates.
th
(pediatric secrets 5 ed, Ch7, pg258-261)
Q: How does the type of bloody stool help pinpoint the location of a GI bleed?
1- Hematochezia (bright red blood): Normal stool spotting on toilet tissue likely suggests
distal bleeding (e.g., anal fissure, juvenile colonic polyp). Mucous or diarrheal stools
(especially if painful) indicate left-sided or diffuse colitis.
2- Melena (black, tarry stools): Indicates blood denatured by acid and usually implies a
lesion, likely before the ligament of Treitz. However, melena can be seen in patients with
Meckel diverticulum as a result of denaturation by anomalous gastric mucosa.
3- Currant jelly (dark maroon) stools usually come from the distal ileum or colon and often
are associated with ischemia (e.g., intussusception).
Because blood is a cathartic, intestinal transit time can be greatly accelerated and makes
defining the site of bleeding by the magnitude and color of the blood difficult. This difficulty
underscores the importance of the initial nasogastric tube insertion.
th
(pediatric secrets 5 ed, Ch7, pg258-261)

Q: What can cause false-negative and false-positive results when stool testing for blood?
Hemoglobin and its various derivatives (e.g., oxyhemoglobin, reduced hemoglobin,
methemoglobin, carboxyhemoglobin) can serve as catalysts for the oxidation of guaiac
(Hemoccult) or benzidine (Hematest) when a hydrogen peroxide developer is added,
thereby producing a color change. Of note, iron does not cause false positive results.
False negatives: Ingestion of large doses of ascorbic acid; delayed transit time or bacterial
overgrowth, allowing bacteria to degrade the hemoglobin to porphyrin
False positives: Recent ingestion of red meat or peroxidase-containing fruits and vegetables
(e.g., broccoli, radishes, cauliflower, cantaloupes, turnips)
th
(pediatric secrets 5 ed, Ch7, pg258-261)

Name the six most common causes of massive GI bleeding in children.

1. Esophageal varices
2. Meckel diverticulum
3. Hemorrhagic gastritis
4. Crohn disease with ileal ulcer
5. Peptic ulcer (mainly duodenal)
6. Arteriovenous malformation
th
(pediatric secrets 5 ed, Ch7, pg258-261)
 Baby Formula:

Cow Soy Partial Elemental Premature Fat modified Metabolic

milk based hydrolyse
based Protein
(stand hydrolysate
erd,
LF, AR,
HA)
Kcal/Oz 20 20 20 20 24 20 Alot
CHO Lactos Sucrose + Corn syrup Glucose Lactose + Sucrose + MSUD "
e corn polymer Glucose corn Ketonex
polymer
Fat LCT LCT LCT MCT + LCT MCT + LCT MCT + LCT MMA "
Protein Cow Soy Protein Protein H. Cow milk Cow milk Propimex
milk hydrolysate + Aminio
Acid Isovaleric
Example -NAN -Isomil -Progestamil Pregestimil -Similac -Portagen academia "
-S26 -Nursoy -Nutramigen -Neocate special care Valex
- -Neosure
Similac PKU "
Indicatio Term *Lactase *Cow milk *Malabsorp Preterm Steatorrhea Phenex
n baby deficiency Protein tion <2kg
*Galactos allergy *Intestinal Homocystinur
emia *Multiple resection ia " Hominex
*Cow food allergy
milk UCD "
Protien Cyclinex
allergy
Children Formula:
Standard Partial hydrolyzed Elemental:
-Nutrient Junior -Peptamen Junior -Vivonex (24/Oz)
-Pediasure -Elecare
-KinderCal -Neocate one plus
6-Endocrine:
-Neonate with hypoglycemia
Rewritten by Ebtihal AlQulaisy.
-Newborn with ambiguous genetalia
Rewritten by Kholoud Hothan
-Neonate with high TSH level.
Rewritten by Kholoud Hothan
-DKA
Rewritten by Kholoud Hothan
-Diabetic pt *
Rewritten by Khulud AlSaedi,
Reviewed by Dr. Reham Fallatah
-Short stature
Rewritten by Kholoud Hothan
 Q: Approach to neonate with Hypoglycemia

Hx
-Event (Diet before event, feed vs. fasting)

-Type of feeding (milk, feature, protein)

-Symptoms of hypoglycemia (sweating, tremor, tachycardia)

Neuroglycemia(Seizure – coma –confusion –lethargy)

-Age of onset

-Antenatal U/S – IUGR.

-Natal (term-wt-GA-apgarscor-hypoglycemia- seizure, UVC)

-FHx: consanguinities, sudden death."??metabolic cause"

Exam
- Vital signs.

- Growth parameter

-Midline defect (endocrine cause)

-Hemi-hypertrophy.

-Ear crease (bickwithwidman syndrome)

-Hypotonia

-HSM-GSD

-Digmentation

-Ambiguous genitalia.

- Urine dipstick
 Causes

ketotic
Non-ketotic

FA oxidation
defect

Dehydration Other
Organic A. Ketotic
SD A.A Endocrine Sepsis
MMA Hypoglycemi
Fructose Tyrosinemia CAH CHF
P PA a
intolerance Shock

Lab
Critical sample

A-Hormone (insulin, GH, cortisone, ACTH, c-peptide)

B-substrate (Glucose, FFA, katon, Loctate, ammonia, carnitine)

C- Urine (reducing substance, katon).

D-Blood gas.
Rx

Correct Hypoglycemia

*Stable conditions give oral.

*Unstable;

- ABC..

- D10; 2-4 ml/kg IV bolus

- Or glucagon IM < 6yr: 0.5mg /20kg

> 6yr: 1mg /20kg

-Infusion glucose: dextrose % *fluid rate * 0.167 = (6-8 mg / kg/ min)

wt
 Q: Approach to newborn with ambiguous genitalia
• This is a social-medical emergency
• Need multidisciplinary approach including: Pediatrician, Endocrinologist, pediatric
surgeon, pediatric urologist and psychologist
• Parent should see the baby
• Make sure patent is stable and examine him thoroughly
• Reassure the parent that the patient is stable, but need time to assign the sex till the
results of the investigations
• Update them with each result

History:
• Antenatal history:
o Drugs (Danazol, Progesteron)
o High androgen symptoms (Irregular menses, voice, hyperpigmentation)
• Presentation:
o Sepsis like (LOC, vomiting seizure decrease activity)
o Signs of hypoglycemia
o Hyperpigmentation
• Consanguinity
• Neonatal death

Examination:
• Well or ill
• Vital signs (maintaining BP)
• Dysmorphic features
• Skin pigmentation
• Genitalia (Phallus):
o Pigment >> CAH
o Gonad >> male pseudo
o Fusion of labioscrotal folds
 Labs: Based on history and examination
o U&E
o Gluco check
o Blood gas
o US (internal organ, gonads)
o Karyotype
o 17. H progesterone (If >2 days) to avoid false negative (Preterm, SGA, sick baby)

Management:
• Family counseling
• Stabilize the patient
• Correct hypoglycemia
• Correct electrolyte disturbance
• If in crisis (adrenal):
o Stress dose of steroid 100mg/m2/dose, then maintenance
o Fludrocortisone
o Anti-hypertensive medications
o Follow up with endocrinology
Q: Approach to neonate with high TSH level

TSH level:
• <30 >> Normal
• 30-60 >> Borderline (Do T4 on same sample, if normal discharge, if low repeat)
• >60 >> confirm, repeat sample

High TSH (Primary hypothyroidism)

• Transient (Maternal):
o Antibodies (hypothyroidism and hyperthyroidism)
o Drug (Antithyroid, antitussive, contrast, Amiodarone)
o Diet (Iodine)
• permanent:
o 85% Structure: (Aplasia, hypoplasia, ectopic)
o 15% Function: Dyshormongenisis (Goiter, no goiter)

History:
• Baby: Antenatal and post-natal (symptoms of hypothyroidism)
• Mother: Medications
• Family history: Pendred syndrome (AR, hypothyroidism, goiter), Thyroid disease,
Goiter
• Diet
• Living area

Examination:
• Well/ill
• Growth parameters
• Dysmorphic
• Thyroid gland
• Signs of hypothyroidism (FTT, dry skin, bradycardia, prolonged jaundice, coarse
features, hypotonia, hypothermia)

Investigations:
• Repeat TFT
• Thyroid scan (Before starting thyroxin *If started will be done t age of 3years)
o Absent >> Neck US:
$ Present >> maternal antibodies, iodine trapping defect
$ Absent >> Agenesis
o Present: Ectopic Vs. non ectopic
• Antibodies if mother has history
• Iodine level in urine of the mother
Management:
• Permanent: Thyroxin for life (Agenesis, ectopic)
• Transient: Thyroxin for 3 years, then stop treatment for one month then repeat TFT, if:
o Normal >> stop treatment
o Abnormal >> This is dyshormonogenesis, continue for life
$ Dose: 10-15 mic/kg OD on empty stomach (fasting)
$ Don’t take with milk, iron, Ca
Q: Approach to a diabetic patient
History:
-Current (DKA, trigger, insulin dose, … )
-Hypoglycemia symptoms, How to treat
-Hyperglycemia symptoms, How to treat
-DM type 2 history, when, where, how – diagnosis
-Admission; ward/PICU, and the cause of admission
-Follow-up; where, when, lab frequency (HbA1C, Urine dispstick, Glu check)
-Insulin; dose, increase with stress?, supply, missed dose, how is it given & where
-Diet
-Exercise
-Association; celiac disease, hypothyroidism
-Complications (systemic review)
-Social impact on (Patient, Parents, Siblings)

Examination:
-Vital signs
-Growth parameters
-Skin- vetiligo
-Site of glucose check & insulin injection site ”atrophy, hypertrophy”
-Eye exam
-Mouth, fingers & toes (candida)
-Thyroid
-Puberty “tanner stage”
-UDS “urine dip stick”

Lab:
Blood Urine
1-HbA1C (3/12) 1-UDS (urine dipstick) if high RBS (random
2-Thyroid blood sugar)
2-Analysis at diagnosis
At Diagnosis: 3-Microalbuminurea
3-Chemisrty?
4-Anti-antobodies
5-Lipid
6-Celiac

Treatment:
1-Nutrition
Carbohydrate 50% (Avoid simple sugar)
Fat 35% (low cholesterol)
Protein 15%
2-Exercise
At least 30 minutes
 3-Insulin
A) Conventional
2/3 morning: 1/3 regular
2/3 NPH

1/3 evening: 1/3 regular

2/3 NPH

B) Multiple dose injection “MDI”

50% Lantose (long acting insulin) OD
50% Aspart (Ultra-short insulin) before each meal

#What to do for any procedure:

Short Procedure Long Procedure
-Fast Or Sliding Scale: A) Will eat immediately
-Omit dose before OR RBS Insulin rate -No regular
-Glu check Q15min 120 0.00 -1/2 dose NPH
120-200 0.03 -IVF D5 1/2NS maintenance
200-300 0.06
300-400 0.08 B)Will not eat immediately
>400 0.1 -IVF D5 1/2NS maintenance
-Regular insulin 50 units + NS 500cc at a rate
RBS Q1Hr of 0.025unit/kg

Complications:
Acute: *DKA
*Hypoglycemia

Chronic: *Microvascular; CNS

Retina
Renal
*Macrovascular; Heart, atherosclerosis
Stroke
Sick day management:

-Basal insulin (Glargine - detemir) should be give at usual dose & time
-NPH decreases by ½ if RBS < 150 mg/dl
-Oral fluids: *Sugar free if BSL > 250 mg/dl
*Sugar containing if BSL < 250 mg/dl

Urine ketone RBS Correction of Insulin Comment

-ve/small Q2Hr Q2Hr if BSL> 250 Ketone every other voiding

Medium/large Q1Hr Q1Hr if BSL> 250 Ketone each void

**Start acting**
When to call the physician or nurse/seek advice?
1-BSL remains elevated after 3 extra doses
2-BSL < 70mg/dl
3-Child not taking orally
4-Signs of dehydration/ emesis
5-Not controlled ketonuria

Hypoglycemia:
Treatment:
1-Carbohydrate containing snack or drink
2-Glucagon IM: Dose; * < 20 kg " 0.5mg
* > 20kg " 1mg
3-IVF, D10 (4ml/kg)
4-Adjustment of carbohydrate intake &insulin

Insulin regimens:
1- Daily (Long acting only – mixed)
2- Twice daily (common)
3- Twice daily with addition of short or ultrashort
4- Basal bolus (common)
5- Pre-mixed (non-compliance, inability to mix insulin)
6- Insulin pumps; very young patient: ONLY intermediate (NPH)/Long acting insulin
 Types of Insulin:

Rapid acting Short acting Intermediate Long acting Biphasic (short 30%,
Ultra-short acting intermediate 70%)
Beginning 5-15 min 30 – 60 min 1-2 Hr 2-4 Hr 30 min
of action
Peak 30 – 120 min 2-5 Hr 4-12 Hr Peak less 1-12 Hr
Duration of 3.5-6 Hr 6-8 Hr 16-24 Hr 20-24 Hr 16 – 24 Hr
action
Brand Insulin Natural Isophane I Lantus Mixtaral
name analogue Requral NPH Glargine
Lispro Aspart Soluble Determir

Points about insulin:

1- Intramuscular (Higher peak, shorter duration) than subcutaneous
2- Best site for insulin absorption;1-abdominal wall, 2-Upper limb, 3-Lower Limb
3- Insulin should not be injected to an area going to exercise
4- Side effects of Insulin
A) Lipohypertrophy (avoided by rotating injection sites)
B) Hypersensitivity; *Local
*Generalized
C) Local insulin resistance "Treatment: Add protease enzyme to insulin
D) Circulating antibodies "Treatment: Increase insulin dose

Target HbA1c: it is age specific

*Preschool: 7.5%-8.5%
*6-12 y: <8%
*13-18y: <7.5%

Target fasting and pre-prandial blood sugar:

*Preschool: 100-180 mg/dl
*School age: 90-180 mg/dl
*Teenagers: 90-130 mg/dl

Target bedtime blood sugar:

*Preschool: 110-200mg/dl
*School age: 100-180mg/dl
*Teenagers: 90-150mg/dl
Somoggi Phenomenon
Definition: Rebound hyperglycemia after an incident of hypoglycemia
Cause: Counter regulating hormones (natural response)
Time: At night (unrecognized, untreated) hypoglycemia “child is asleep”
Diagnosis: Hypoglycemia (2:00-3:00 a.m) followed by Hyperglycemia at 7:00 a.m (several
nights)
Treatment: Type, dose & time of evening insulin might need to be changed

Dawn Phenomenon
Definition: Early morning (5:00-8:00 a.m) Hyperglycemia without preceding hypoglycemia
Cause: 1- Increased cortisol level in the morning (normal)
2- Overnight GH secretion
3- Insulinopenia (length time from last dose)
Treatment: 1- Shifting more aggressive insulin to evening & pre-bedtime Hr
2- Use a type of insulin having long duration
3- Avoid the carbohydrate snack at bedtime
4- Vigorous exercise at evening Hr

Honeymoon Phenomenon
Definition: it is a period of falling or minimal exogenous insulin requirement..
Cause: continuous residual endogenous insulin production
Time: 1-2 week after initiation of insulin treatment
Diagnosis: excellent control of blood sugar
Out of honeymoon: if fasting blood sugar become elevated.
Treatment: decrease insulin dose to avoid hypoglycemia

Management of Hyperglycemia only:

Giving the regular dose and add correcting dose.
Q: Approach to patient with DKA
History:
• DKA symptoms (Abdominal pain, vomiting, dehydration)
• Triggers (Infection, omit dose, stress)
• Full history of
DM
Examination:
• ABC
• Neuro vital examination, LOC
• Vital signs
• Hydration status
• Systemic examination if need PICU
Labs:
• Glu check
• Urine dipstick
• Blood gas
• Chemistry

Management:
• Deal with emergency
• Start with ABC, then:
A) Fluid:
o Bolus NS 10ml over 1 hour
o IVF NS maintenance + deficit 7-10% over 48hr
o Change IVF to D5 ½ NS if RBS ≤250mg/dL, then to D10 ½ NS if RBS ≤150mg/dL
o Maximum IVF 4L/m2/ day
B) Insulin:
o Infusion 0.1unit/kg/day regular insulin (50unit +NS 500ml)
o If no response in 3hours, re check the dose
o Acceptable decrease of glucose is 3-5 mmol/hr
o Shift to SC if HCO3 ≥15
o Give SC dose 30 minutes before stopping insulin infusion
C) KCL/ electrolyte:
o Start initially with 40mmol/1L
o Then follow K level:
• <3.5 >>> 60mmol/L
• 3.5-5.5 >>> 40mmol/L
• >5.5 >>> Hold KCL
D) HCO3/Acidosis
o Don’t give HCO3 unless:
o Symptomatic hyperkalemia
 o Cardiac instability
o Inadequate ventilation compensation

WHY????
HCO3 increase paradoxical in CNS acidosis by increase diffusion of CO2 across blood
brain barrier tissue hypoxia, shift oxyhemoglobin dissociation curve, osmotic change,
increase cerebral edema

% PICU admission indication:

1) <2 years
2) Blood sugar >1000
3) Comatose
4) pH <7.0
5) Shock state
6) Cannot be managed at ward
% Risk of cerebral edema:
1) Increase BUN
2) Decrease pCO2
3) Young <5years
4) Treatment HCO3
5) Lack of increase in Na with treatment
6) Newly diagnosed DM
Treatment of cerebral edema:
• PICU admission
• Mechanical ventilation standby for possible intubation
• Elevate the head of the bed
• Mannitol infusion
Complication of DKA:
1) Electrolyte disturbance
2) Brain edema
3) Pulmonary edema
4) DVT
5) ATN
6) Arrhythmia
7) Pancreatitis
8) Bowel ischemia
Q: Approach to short stature

History:
**First make sure from the readings (measure/ re plot on chart)
• Antenatal: Term, mode of delivery, growth parameters at birth (birth weight),
prolonged jaundice, hypoglycemia
• Shortness: Onset, who noticed, who/what is the concern, change of clothes and shoes
• Recent symptoms: Sign of ICP, hypoglycemia, headache, head trauma, radiation
• Developmental history
• Family history of other short siblings, delayed puberty
• Social impact on child, siblings and family
• Systemic review >> evidence of chronic illness

Examination:
• General:
o Growth parameters
o Growth velocity (5-7cm/year in childhood, 8-14cm/year in puberty
o Measurements
o Dysmorphic features
o Pallor, jaundice or cyanosis
o Hemi hypertrophy
• Thyroid exam
• Breast and genitalia (signs of puberty)
• Signs of rickets
• Systemic exam (CVS, abdomen/celiac)
• Parental height (mid parental height:
o Boys: mother ht +13+ father height/ 2 ± 7.5cm
o Girls: Father ht -13+mother height/ 2 ± 6cm

Labs:
• CBC, ESR
• Chemistry
• Thyroid function test
• Endomysial antibodies (celiac disease)
• JGF, IGFBP3
• Chromosal study in girls
• Bone age
Management:
Growth hormone, indications:
• GH deficiency
• ESRD
• Turner syndrome
• Prader willi syndrome
• IUGR
• Severe familial short stature
Complication of GH:
• Headache (psuedotumor cerebri)
• Hyperglycemia
• Hyperpigmentation
• SCFE
• Increase risk of solid tumors
Arthralgia
• Hyperthyroidism
• Gynecomastia
Stop GH if:
• Ht <1inch/yr
• Bone age 14yrs, 16yrs

Short stature:
• Physiologic:
o Familial
o Constitutional
• Pathological:
o Symmetrical:
$ Prenatal: syndromic, IUGR
$ Postnatal: Endocrine (GH deficiency, hypothyroidism, panhypopitutarism, Cushing),
chronic disease, social
o Non symmetrical:
$ US > LS: Achondroplasia, ricket, hypothyroidism
$ US < LS: Scoliosis, spondylodysplasia, OI, russel silver, klippel-feil
7-CVS:
- Kawasaki disease
Rewritten by Kholoud Hothan
- Rheumatic fever
Rewritten by Omniya Alkhilaiwi
Kawasaki disease
-Mucocutaneous lymph node syndrome/ infantile polyarthritis
-Is an acute febrile vasculitis
-Etiology: Unknown
-Pathology: Vasculitis of medium sized arteries with striking predilection for coronary
arteries

Epidemiology: Is an illness of early childhood

• Median age is 2-3 years
• 80% < 5years
Clinical manifestations:
1) Fever:
o High, unremitting, unresponsive to antibiotics
o Duration: 1-2 weeks >>> persistent 3-4 weeks
o Increase risk of coronary artery disease
2) Conjunctivitis: Bilateral non exudative bulbar conjunctivitis
3) Mucous membranes:
o Erythema of oral and pharyngeal mucosa
o Strawberry tongue
o Dry and cracked lips
4) Skin rash:
o Polymorphus exanthem (maculopapular rash, erythema, multiform,
scarletiform)
o Accentuated in the groin area
5) Cervical LN:
o Unilateral non suppurative
o Size >1.5 CM
6) Change in extremities:
o Acute: Erythema of palms, soles, edema of hand and feet
o Subacute: periungual peeling of fingers, toes (2-3weeks)

Other clinical features:

Musculoskeletal: arthritis and arthralgia
GIT: Diarrhea, vomiting, abdominal pain, hepatic dysfunction 65%, hydrops of gallbladder
GU: Urethritis, meatitis, sterile pyuria
CNS: irritability (infancy), aseptic meningitis, sensory neural hearing loss
Resp: interstitial infiltration, effusion 30%
Other findings: erythema of BCG site, anterior uveitis, desquamation rash in groin

Cardiac findings:
1) Myocarditis and congestive heart failure
2) Pericarditis, pericardial effusion
3) Coronary artery aneurysm 25% (2nd-3rd week if untreated)
 4) Valvular regurgitation (mitral valve)
5) Giant CA aneurysm (internal diameter >8mm) >> rupture >> thrombosis/stenosis >>
myocardial infarction
6) Aneurysm of medium sized non coronary arteries
7) Raynaud phenomenon
8) Peripheral gangrene

Phases of the disease:

1) Acute febrile phase (1-2 weeks)
Fever + other acute sign
2) Subacute phase (4-8 weeks)
Desquamation, thrombocytosis (increase Plt)
Development of CA aneurysm
3) Convalescent phase (6-8 weeks)
When all clinical signs disappear continue till ESR normalized

Lab works:
No diagnostic test for Kawasaki disease
• CBC: leukocytosis, with neutrophilia, normocytic normochromic anemia (common),
thrombocytosis (2nd week), Plt (1000,000/mm3)
• ESR, CRP high
• High ALT, AST, Bilirubin, GGT
• U&E (High Na)
• Urine analysis (Sterile pyuria)
• LP CSF analysis (pleocytosis)
• EHCO: at diagnosis, againat 2-3 weeks, if normal repeat at 6-8 weeks, normal repeat
1 year with lipid profile >> follow Q5years
• If abnormal ECHO >> needs more frequent
Diagnosis: KD is diagnosed clinically
A) Typical KD:
Fever for 5 days or more + 4/5 of the following:
1) Bilateral non purulent conjunctivitis
2) Erythema of mucous membranes
3) Edema of hand and foot
4) Skin rash
5) Cervical lymph adenopathy
B) Atypical KD:
o Fever + less than 4 of the previous criteria
o But the lab works and ECHO consist with KD
o More in infancy
o High risk to develop CAD
Differential diagnosis:
1) Viral infection (Adenovirus, Enterovirus, measles, EBV)
2) Bacterial infection (Scarlet fever, Bacterial cervical lymphadenitis)
3) Rh disease (systemic onset JIA
4) Other (TSS, SSSS, SJS)
5) Drug hypersensitivity reaction
Treatment:
Acute stage:
• IVIG 2g/kg/over 10-12hours:
o When?? As soon as possible after the diagnosis, ideal within 10 days of onset
o Mechanism of action: unknown
o Outcome: 85-90% rapid resolution of clinical signs, CAD risk decrease (2-4%) in first
10 days
• Aspirin 80-100mg/kg/day PO Q6hr until patient is afebrile 48hours
Convalescent stage:
• Aspirin 3-5mg/kg/day OD 6-8weeks, DC if normal ECHO
Long term in CAD:
• Aspirin 3-5mg/kg/day OD
• Clopidogrel 1mg/kg/day
• Warfarin or LMW heparin (High risk of thrombosis)
Acute CA thrombosis:
• Fibrinolytic therapy (tissue plasminogen activator)
IVIG resistant KD:
• 2nd dose of IVIG
• IV methylprednisolone
• Cyclophosphamide and plasma phoresis (less often)
• Infliximab
Complications:
• CAD (Thrombosis and aneurysm)
• Complication of treatment:
o Aspirin >> Reye syndrome >> avoid influenza and varicella vaccine for 5 months
o IVIG >> interfere in immune system
Risk factor for severe outcome:
1-Male gender
2-Age <1year
3-Prolonged fever
4-Recurrent fever
5-Lab (low Hbg, low Plt, High neutrophilia with band, low albumin)

$ Complete recovery & CAD

$ Recurrence rate 1-3%
$ Mortality <0.01% with CAD
$ Coronary aneurysmresolve 50% by 1-2years
$ Giant aneurysm unlikely to resolve >> Thrombosis and stenosis
Rheumatic fever:
Immunologic disaffecting the connective tissues of the; Heart, Joint, CNS?, Suprasternal
nodule? And the Skin.

- One of the most common cause of acquired CVS disease.

- Female more than Male.
- All ages except infancy ( 5 – 15 years )
- 2-4 weeks post infection ( pharyngitis ) , pharyngitis or Tonsillitis.

Etiology:
- Genetic predisposition:
HLA marker.
B-cell alloantigen ( D8\17 )
- Environmental Factor:
2\3 of the patient they had a URTI ( group A – B hemolytic streptococcus )
M type ( 1,3,5,6,18 and 24 ) > more frequent.

Pathogenesis:
- Cytotoxicity Theory:
Group A Streptococcus > extracellular toxin > damage of target organ . ( not explain
latent period )
- Immunological theory:
Cross – reactivity ; Group A Streptococcus have M Protein share A.A this same human (
Brain , Heart , Joint ) attack these tissues.

Pathology:
- Ashoot body ( Myocardium ) is pathognomonic lesion of Rh Fever.
Clinical manifestation:
& Jones Criteria;
- Major:
Carditis , Migratory Arthritis , Chorea , Erythema Marginatum , Subcutaneous nodules.
- Minor:
Fever , Artharlgia , high ESR and CRP ., Prolong P-R interval in the ECG.

Diagnosis:
2 Major or ! major and 2 Minor. > + evidence of Streptococcus infection.

1- Carditis ( 50 – 60 % )
- Can be Asymtomatic.
- May cause insidious carditis > Valvular HD < discover after
- Or acute ( Pancarditis ) = Pericarditis , Myocarditis , Endocarditis.
- Mitral valve ( most common affected )
- Mitral and Aortic affected \ Tricaspid and Pulmonary less involve.

2- Poly Arthritis ( 75 % )
- 2 or more joint should be involved.
- Affected Joint ; Knee , wrist , elbow . ( hand , foot , spine ; uncommon )
- Joint hot , red , swollen , painful , tender , limitation of movement.
- Transient , migratory , not symmetric.

3- Chorea ( 10 – 15 % )
- May be only sing of Rh . fever
- Prolong latent period.
- Un …….. movements , prominent in face , shoulder and trunk .
- Exacerbate by stero and disappear with sleep.
- Hypotonia ( milkmaid grip , Darting tongue, choric hand , ………. )
- Self limited condition subside within week to 1 year.
- Emotional liability.
- Treatment ; Diazepam , Valporic acid , Carbamazpine , phenothiazide, …….
 4- Erythema marginatum ( <3% )
- It is erythematous macular lesion with ….. center .
- Site ; trunk , extremitis ( not on face )
- Accentuated by warm skin.
- Often with chronic carditis.

5- Subcutanous nodules ( < 1% )

- Firm , nontender , small 1 cm .
- Site ; extensor surface of joint near bony prominence ( knee , elbows and spine )
- Usually with significant Rh. Heart disease.

Treatment:
1- Bed rest .

2- Treatment of group AB streptococcus infection , primary and secondry to eradicate

strep from URT.

3- Anti inflammatory ;

& Aspirin ;

- Indication ; arthritis and carditis, NO > Cardiomegaly of HF

Dose ;

100 mg \ kg \ Day Q6hr 3-5 days

then

75 g \ kg \ Day for 4 weeks.

- Gradual Tapring
 & Corticosteroid ;

- Indecation ; Cardiomegaly and Congestive heart failure.

- Dose Predinsolone 2 mg \ kg \ day Q6hr (2-3 weeks )

- + Asporon 75 mg \ kg \ day ( 6 weeks )

- Gradual Tapring for both.

4- Management CHF ; Diuretics.

5- Treatment ………Chorea.

6- Treatment of residual valvular ; Surgery.

Prognosis;
- Recovery 75 % ( Before Prophylaxis )
- 70 % patient with Carditis ( NO ) residual heart disease.
- 20 % patient with chorea develop Rh heart disease with 20 year if not on ………….

Lab work:
1- ESR, CRP
2- ECG (Prolong PR interval) 1st degree heart block
3- Evidence of Group A – Streptococcus infection; Throat culture, Rapid strept antigen
test , ASOT
DDx;

Complication;
1- Acute term; Arthritis and Chorea > Resolved completely without Sequel
2- Long term (limited to the heart);
- Heart Failure.
- Arrythmia
- Infective endocarditis
- Thromboembolism (common with mitral stenosis)
Prevention:
1- Primary:
Antibiotics within 9 days of symptoms of pharyngitis;
- Pnicillin
- Ospen
- Erythromycin
- Other ( ……… Clindamycin )

2- Secondary:
To prevent acute Pharyngitis of patient at Risk of recurrent Rh. Feve;
- Penicillin
- Ospen
- Sulfadiazine
- Erythromycin

Duration:
- Rh fever without carditis; 5 year or up to 21 year
- Rh fever with carditis (No valvular Disease); 10 year or 21 year
- Rh fever with valvular disease; 10 year – until 40% > Life long.
8-ER:
-Drowning pt.
Rewritten by Kholoud Hothan
- Snake bite.
- Scorpion sting.
- Status epilepticus.
- Head trauma.
- Status asthmatucus.
- Septic shock.
- Anaphylaxis shock.

All Rewritten by Khulud AlSaedi

Q: Approach to drowning patient

This is an emergency, so start by Primary assessment (take in consideration neck injury)

Look
*Airway patency by: Jaw
A Airway Listen
thrust, NO head-tilt chin-
Feel lift

RR
B Breathing Effort
Airentry

Consider intubation by Rapid sequence intubation RSI:

1) Pre oxygenation (non rebreather mask 100% x3mins)
2) Medications:
Adjunction (Atropine, Lidocaine)
Sedation (Ketamine, Fentanyl)
Muscle relaxant (succinylcholine, Rocuronium)
3) Cricoid pressure
4) Open mouth by jaw thrust
5) Intubation (Tube size= 4+(Age/4)) Depth= ETT size x 3
6) Check ETT and secure

Perfusion
Pulse *Insert IV line
C Circula•on *Start fluid
BP
Colour

D Disability (CNS GCS

responsivness)
Pupils
 Temperature
measerues
E Exposure
Bleeding

Rewarming

External >32 °C Internal <32 °C

*In each step: Evaluate Identify Interfere

Secondary assessment:
• History: SAMPLE (S: symptoms, A: allergy, M: medications, P: past medical, L: last
meal, E: event)
• Full examination from head to toe
• History of drowning:
o Duration of submersion
o CPR there, duration
o Apnea, cyanosis
o Type of water (fresh water, sea)
o Swimmer or not

Tertiary assessment:
Lab works: CBC with diff, Electrolytes, Glucose, LFT, Blood gas, Chest Xray and CT brain
*Council family the outcomes based on prognostic factors
Poor prognostic factors:
A) IN FIELD:
1. Submersion time >5 mins
2. 10 mins delay of CPR
3. CPR >25 mins
4. Apnea and cyanosis
5. Age <3years
B) ER:
1. GCS <5
2. Fixed dilated pupils
3. Need CPR
C) PICU:
1. Continue GCS <5
2. Apnea
 3. pH <7.1

Preventive measures:
1) Education of parents, patient and physician
2) Fencing pool (4 feet tall) *Both decrease incidence by 80%
3) CPR course for population
4) Swimming programs for parents and children >4 years
5) Supervision by adults all the time
Q: Approach to snake bite

Snake Bite

-Tri-angular head -No Fangs

-Fang marks -No sever local pain
**No symptoms: **No symptoms
-Observe 14H -Observe 2-8H
-Anti-Tetanus

**Symptoms present: **Symptoms present:

Hematologial toxic Neurological toxic
Symptoms Symptoms
-Bleeding, Bruising, Hematuria -Ptosis, ophthalmo…
-Blister -Paralysis of muscles of swallowing (face-
-Swelling tongue)
-Shock -Respiratory problems
-GSS abnormal

Lab
-CBC: (H) WBC & (L)RBC, Hbg, PLT
-U&E: (H) K+
-Coagulation profile: (H) PT, PTT
-(L)Fibrinogen

Treatment: Treatment:
-ABC -ABC
-Polyvalent Snake Anti-venom (5Ampule): -Respiratory observation
*50ml diluted in 250ml NS -Bivalent Snake Anti-venom
*Over 30-60min
*Repeated dose Q4-6H, till symptoms
disappear
Q: Approach to Scorpion Sting

1st : Make sure patient is stable

History:
-Scorpion sting:
• Time
• Site
• Number of bites
• Type of scorpion
-Symptoms:
• Abnormal behavior
• Local pain
• Paraesthesia
• GIT upset (nausea, vomitting..)
• Urine
• CNS (convulsion)

Examination:
-Stable Vs Unstable
-Vital signs (Tachycardic, hypotensive)
-Local exam
-Systemic exam – Respiratiory

Lab:
1-CBC: (H) WBC
2-Chemistry: (L)Na: hyponatremia, (H)K: heperkalemia, (L)Ca: hypocalcemia)
3-Blood Gas: Acidosis
4-CXR: Pulmonary edema
5-ECG

Treatment:
-ABC
-Polyvalent Scorpion Anti-venom (5Ampule/1ml):
*5ml diluted in 50ml NS
*Over 20min
*Repeated dose Q2H, Up to 4 doses
-Observation for 24H

Causes of Death:
-Cardiac
-Respiratory
-Shock
Q: Acute Management of Status Epilepticus

Definition:
Continuous convulsion lasting more than 20-30min
OR
Recurrent seizure activity without regaining consciousness >30min

Management:
*Supportive measures (ABC 0-5)

-Assess airway (keep airway patent, gentle suction of secretions)

-Breathing (administer O2)
-Circulation
-Vital signs
-Correct hypoglycemia

LAB:
-Glucose
-Electrolytes
-Ca,Mg
-BUN, creatinine
-LFT
-CBC
-Blood c/s (if suspecting infection)
-Drug level

*Drugs:
1-Lorazepam
-Benzodiazepine
-Dose: 0.05-0.1mg IV slowly, repeat q5min x3doses
-S/E: less incidence of hypotension & respiratory depression than diazepam + longer
duration

2-Diazpam
-Benzodiazepine
-Dose: 0.3-0.5mg IV slowly / PR 0.5mg/kg
-S/E: hypotension, respiratory arrest

3-Midazolam
-Benzodiazepine
-Dose: 0.15mg/kg IV
-Can be given Intranasal (0.2-0.3mg/kg) & Buccal (0.2-0.5mg/kg)
-S/E: Hypotension, bradycardia, respiratory depression

STILL SEIZING ?! (15-30min)

4-Phenytoin
-Sodium channel blocker
-Dose: Loading (10-20mg/kg) diluted by NS
-Infusion rate 1mg/kg/min
-Maintenance dose
-S/E: phlebitis, systemic hypotension, arrhythmia, bradycardia

5-Fosphytoin
-Same but has advantages:
1-Water soluble
2-Less irritant after IV
3-Well absorbed IM inj.

6-Phenobarbital
-GABA inhibition
-Dose: Loading (10-20mg) IV over 30min
-Infusion rate 1mg/kg/min
-Maintenance dose:
-S/E: hypotension, respiratory arrest

SIEZURE PERSIST??

1-Induction of barbiturate coma – In PICU

-Keep on ventilator
-Connect to continuous EEG monitor
-IV- Thiopental 2-3mg/kg bolus Then titrate dose until burst suppression on EEG
-Barbiturate coma 48h, followed by stopping thiopental
" therapeutic level (20-40mg/ml)
-S/E: hypotension, electrolyte abnormalities

2-General anesthesia
Halothane, isoflurane

3-Valproic acid
-Loading: 25mg/kg IV Then 30-60mg/kg/24h
Q: Approach to patient with Head Trauma

First:
-ABC
-C-Spine Immobilization

Physical Exam:
-GCS
-Vital signs
(Cushing triad: NTN, Bradycardia, Irregular breathing)
-Full neurological exam
-Head Exam;
-Scalp injury
-Raccoon eye (orbit roof fracture)
-Battle sign (ecchymosis behind pinna) – mastoid fracture
-CSF leak (Basilar skull fracture)
-Pupil (size, symmetry, reactivity) - hyphema
-Funduscopy – papilledema – ICP

Re-examination??
- Alter or LOC
- Amnesia
- Behavior change
- Seizure
- Vomiting
- Headache
- Visual change
- Gait disturbance
- Mechanism of injusry

Management:
-Evaluate C-Spine
-CT brain (non-contrast)
-Observation for 4-6h (detect delayed S&S)
-Continue observation at home

Indications for hospitalization:

1-Decreased LOC
2-Neurological deficit
3-Persistant headache or vomiting
4-Seizure
5-CSF leak
6-Battle sign
7-Raccoon eye
8-Skull fracture (linear, compound, depression)
9-Suspecting child abuse
10-Bleeding disorder/ On anticoagulant
Foreign Body Aspiration:

Stable Unstable
-Forceful cough -Unable to speak
-Well oxygenation -Poor air entry
-Cyanosis
-Admit to remove FB Infant Child
by bronchoscopy
Place infant over arm/lap " 5 abdominal thrust (Heimlich
5min back blow maneuver)
" 5 chest thrust

-Open mouth by tongue- jaw lift

-Remove FB (visualized) by finger swab
-Magill forceps if FB in posterior pharynx

" Direct laryngoscopy to remove FB

Complete airway obstruction?

Yes " Needle cricothyrotomy No " Intubate
Q: Approach to Status Asthmaticus

Focused History:
-Onset of current exacerbation
-Frequency and severity of day/night symptoms
-Limitation of activity
-Frequency of bronchodilator use
-Current medications and allergy
-Potential triggers
-Systemic steroid use
-ER visits
-Hospitalization
-PICU admissions
-Intubation
-Life threatening episodes

Examination:
-Growth parameters
-Vital signs (HR, RR, SPo2)
-Use of accessory muscles, muscle retraction
-Peak expiratory flow rate
-Pulsus paradoxus ( >20mmHg difference in systolic BP-Inspiratory Vs Expiratory)
-Dyspnea
-Color
-Aletrtness (LOC)

Treatment:
1-Oxygen by mask/nasal cannula " treats hypoxia
-To maintain O2 saturation >92%
-Cardio-pulmonary monitoring

2-Albuterol/ Ventolin Neb

-Bronchodilator (Short acting B-agonist)
-Dose: 0.15mg/kg " q20min to effect
-S/E: tachycardia, arrhythmia, tremor, hypokalemia, hypoxia (V/Q mismatch)

3-Additional Neb- Ibratropium (Atrovent)

-Anticholinergic
-Mycolytic/ bronchodilator
-Dose: <12y 250mcg " q20min x3 times Then q2-4hr PRN
>12y 500mcg " q30min x3 times Then q2-4hr PRN
-S/E: Anxiety, dizziness, headache, GI discomfort
4-Steroid – Methylprednisolone
-Dose: 2mg/kg IV/IM bolus Then 2mg/kg/day q6hr
OR Prednisolone 2mg PO
-Effect: minimum of 8Hr

5-Epinephrine: (1:1000) – If there is still poor air entry

-Bronchodilator, vasopressor
-Short acting 15min
-Dose: 0.01mg/kg (MAX 0.5mg) q15min – up to 3doses

6-Continous ventolin Neb

-Dose: 4mg/kg diluted in 200cc NS (18-20cc/hr)

7-Magnisium sulfate
-Smooth muscle relaxant " relieve bronchospasm
-Dose: 25-75mg/kg over 20min q4-6hr x3-4 doses
-S/E: Hypotension, Renal insufficiency

8-Turbutaline
-Systemic B-2 agonist
-Dose: 0.01mg/kg SC q15min x2doses
-S/E: tremor, tachycardia, HTN, headache, GI upset

POOR RESPONSE:
1-Blood gas (normal PCo2) " impending respiratory failure
2-Maximize and continue initial management
3-Terbutaline 2-10mg/kg loading dose Then 0.1-1mg/kg/min under cardiac monitoring
4- Helium 70% or more & O2 mixture
5-Amniophylline
6-Non-Invasive ventilator (BiPAP)
7-Intubation (impending respiratory failure)

Indications for Ventilation:

1-Decreased LOC
2-Sever hypoxia
3-Respiratory or cardiac arrest
Q: Management of Septic Shock

1-Recognition? (signs of poor perfusion) (0-5min)

1-Decreased LOC
2-Delayed capillary refill time (CRT)
3-Cold extremities
4-Weak pulse
5-Hypotension
6-Low urine output

2-Assessment ABC (0-5min)

1-Provide O2 100% by high flow rate (15L)
2-Early intubation (neonate-infant)
3-Breathing assistant – Mechanical ventilation

3-IV Access and connect to monitor:

-Insert large pore peripheral line (if difficult) " 10
-Consider lab:
Blood gas, Lactate, Glucose, electrolyte, ionized calcium, CBC and cultures

4- fluid + electrolyte resuscitation:

*Fluid:
-Push 20ml NS - IV/IO - 5-20min or fast
-Repeat 20ml bolus up to 60ml/kg or until clinical symptoms improve
-Fluid may reach to 200ml/kg

*Correct HypoGlycemia
-Glucose 0.5-1g/kg
(D25 2-4ml/kg --- D10 5-10ml/kg )

*Correct HypoCalcemia
-Calcium gluconate 100mg/kg - IV/IO

5-Infection Control: (5-60min)

-Immediate start of antibiotic (ceftriaxone/vancomycin) after collecting cultures

6-Fluid refractory shock (presents after …/kg) (15-60min)

-Continue fluid resuscitation – central line – arterial monitoring
-Start dopamine (10-20mg/kg/min)
-Warm shock Norepinephrine (0.1-2 mg/kg/min)
-Cold shock Epinephrine (0.1-1 mg/kg/min)
7-Shock persistent after inotropic support
-Continue fluid replacement
-Obtain CVP measurement

SVo2 < 70% SVo2 < 70% SVo2 > 70%

Cold Shock Normal BP Warm Shock

Poor perfusion
-Transfusion Hb > 10gm - Transfusion Hb > 10gm/dl -Norepinephrine
-Optimize SpO2 -Optimize SpO2 -Vasopressin
-Epinephrine -Milrinone (0.25-75mg/kg/min)
-Nitruprusside (0.3-5mcg)

8- Fluid refractory & Inotropes – dependent shock (60mins)

-Consider adrenal insufficiency
-Hydrocortisone 2mg/kg (Max 100mg)
-Obtain basal cortisol level

9- Continued shock
-Consider cardiac output measurement- Further theory
-ECMO

10- Supplemental therapies

-Blood Transfusion Hb <10gm/dl
-Oxygenation
-Analgesic
-Sedation
-IVIG

11- Therapeutic end point

Clinical:
-HR normal for age
-CRT < 2sec
-BP normal for age
-Warm extremities
-Normal pulse quality
-UOP > 1ml/kg/hr
-Normal mental status
-CVP > 8mmHg

Lab:
-Decreased lactate
-SVo2 > 70%
Q: Acute Management of Anaphylactic Shock

Definition:
Rapid onset of IgE-mediated systemic allergic reaction

Symptoms & signs:

Cutaneous 90% Respiratory 70% GI 40-50% CVS 3-40%
-Flushing -Laryngeal edema -Vomiting -Tachycardia
-Urticaria -Bronchospasm -Diarrhea -Hypotension
-Pruritus -Wheeze -Abdominal pain -Syncope
-Angioedema -Stridor
-Hypoxia

Management:
1-Remove/Stop exposure to precipitating antigen
2-ABC (airway, O2, IV line, Trendelenburg position)
3-Epinephrine IM (1:1000) – DON’T DELAY !!
-Dose: 0.01ml/kg - MAX 0.5ml
-Site: lateral aspect of thigh

4-Anti-histamine
- H1 Receptor antagonist (Diphenhydramine- IV,IM, PO) 1-2mg/kg –MAX 50mg
- H2 Receptor antagonist (Ranitidine)

5-Corticosteroid
-Methylprednisolone 2mg/kg IV Bolus, Then 2mg/kg Q6hr
-Prednisolone 2mg/kg PO OD

6-Albuterol
For wheezy chest to relieve bronchospasm, q15min as needed

7-Racemic epinephrine 0.5ml (upper airway obstruction)

Discharge patient on:

1-Epi-pen
2-Anaphylaxis action plan