Professional Documents
Culture Documents
Objectives
This work was done by :
Only and only use the objectives , mostly from the references : USMLE Step 2
CK l Pediatrics + Illustrated Textbook of Paediatrics + Nelson Essentials of
Pediatrics 7th Edition
Last update at :
Topics :
Vesicular
Rash
Petechial
Macular and
and
Maculopapul
Purpuric
ar Rash
Rash
Vesicular Rash
Viral Bacterial
Chickenpox shingles
hand-foot-mouth
Syndrome
Varicella “” العنقز Multiple stages of the rashes
-Cause by Varicella Zoster virus , herpes virus
-Clinically : fever, headache , malaise
macules , papules , Vesicles and crusts in Various stages of healing
-Management : Supporative in immunocompetent
Consider Acyclovir , VZIG
-Complications :
Pneumonia
Encephalitis
Congenital varicella
Skin infection
-Management : Supporative
-Complication: Viral Myocarditis
Macular and Maculopapular Rash
Viral Bacterial
Group A
Adenovirus HHV6,7 Parvovirus Salmonella
Streptococcus
Roseola infantum(sixth disease)
-Cause by HSV-6
-Clinically : high fever (40)
After the fever Subsides Pink-colored maculopapular rash appear
-Management : Supportive
-Complications: “ Febrile seizure “
Viral Bacterial
The pattern : of fever in children depending on age and the nature of the
illness:
1. Neonates may not have fever but be hypothermic, despite significant infection.
2. older infants and children younger than 5 years of age may have an
exaggerated febrile response with temperatures of up to 105° F (40.6° C) in
response to either a serious bacterial infection or an otherwise benign viral
infection.
3. in older children and adolescents Fever up to 105° F (40.6° C) suggests a
serious process.
How is fever identified in children? In hospital, it is measured at:
• <4 weeks old by an electronic thermometer in the axilla
• 4 weeks to 5 years by an electronic or chemical dot thermometer in
the axilla or infrared tympanic thermometer.
In general, axillary temperatures underestimate body temperature
by 0.5°C.
Define FWLF (Fever without
localizing focus)
Most febrile illnesses in children may be
categorized as follows:
• Fever of short duration accompanied by localizing signs and
symptoms, in which a diagnosis can often be established by clinical
history and physical examination .
• Fever without localizing signs (fever without a focus) ,
frequently occurring in children younger than 3 years of age, in which
a history and physical examination fail to establish a cause.
• Fever of unknown origin (FUO) , defined as fever for >14 days
without an identified etiology despite history, physical examination,
and routine laboratory tests or after 1 week of hospitalization and
evaluation.
A ‘pustule‘ is a vesicle
A ‘vesicle‘ is a papule containing yellow fluid. This A ‘nodule‘ is a larger
with a fluid-filled centre. fluid usually consists of serum swelling on the skin surface
(blood fluid), white blood (usually more than 5 mm in
Vesicles are typical of cells, and the virus that has diameter). It extends deep
chickenpox rash and caused the original infection. into skin, and is usually firm
‘cold sores’. The presence of a pustule to the touch.
does NOT mean that the rash
has ‘become infected’ with
bacteria; pustules are an
‘expected’ event in many
viral illnesses.
Describe different types of rash
Purpura Petechiae
Check blood pressure and signs of cardiac disease (murmur, femoral pulses,
Marfan syndrome). ( this is clinical not diagnostic study but just for knowledge
).
Understand the short and long term risk associated
with syncope.
Recurrent syncope has serious effects on quality of life. The impairment due to
syncope is comparable with chronic illnesses such as chronic arthritis, recurrent
moderate depressive disorders and end-stage kidney disease.
Morbidity is particularly high in the elderly and includes loss of confidence,
reduced mobility, depressive illness, fear of falling, fractures and subsequent
institutionalisation.
Female gender, a high level of comorbidity, the number of episodes of syncope
and the presence of presyncope seem to be associated with poorer quality of life.
Physical injury: soft tissue and bone injuries may occur. Syncope was found to be
the cause of 21% of road accidents involving loss of consciousness at the wheel,
second only to epilepsy
https://patient.info/doctor/syncope#nav-6
Heart failure
1. Define cyanosis.
2. Classify and enumerate the various causes of cyanosis.
3. Outline methods to differentiate cardiac for non-cardiac causes
of cyanosis.
4. Formulate an appropriate approach to evaluate an infant with
cyanosis.
Define cyanosis
Acrocyanosis or Peripheral cyanosis (blue color of the hands
and feet with pink color of the rest of the body) is common in the
delivery room and is usually normal. may occur when a child is
cold .
Central cyanosis of the trunk, mucosal membranes, and tongue
can occur at any time after birth and is always a manifestation of a
serious underlying condition. cardiopulmonary diseases are the most
common causes .
most common causes of cyanosis in infants admitted to a neonatal
intensive care unit : Respiratory distress syndrome, sepsis, and
cyanotic heart disease .
Differential cyanosis Upper half of the body is pink and the lower
half cyanotic, or vice versa .
https://
www.slideshare.net/sunilagrawal9693/approach-to-a-neonate-with-cyano
sis
Approach to failure to thrive
….
List the important points in the history (risk factors)
Cheilosis
Recognize the difference between
marasmus and dehydration
Marasmus results from the
body’s physiologic response to
inadequate calories and
nutrients.
Loss of muscle mass and
subcutaneous fat stores can be
confirmed by inspection or
palpation .
Dehydration
Dehydration, most
often due to
gastroenteritis is
common in children
Discuss the classification of FTT
Organic failure to thrive .
???
Case#1
A 6 year old boy has been seen for
preschool clinical assessment. Although
previously at the 25th percentile for
height and weight, he is now at the 5th
percentile for weight and has remained
at the 25th percentile for height. How
would you counsel him and his family?
Case#2
An 8-month old has a weight, which is
below the fifth percentile. List five
organic causes of failure to thrive and
diagnostic hints.
Approach to
proteinuria
Qualitative Quantitative
Quantitative assessment
most common method - 24-hour urine collection
Normal protein excretion
Child: < 100mg/m2/day or 150mg/day
Neonates: up to 300mg/m2/day
In children: levels >100 mg/m2 per day (or 4 mg/m2 per hour)
are abnormal
Proteinuria of greater than 40 mg/m2 per hour is considered
heavy or in the nephrotic range
MEASUREMENT OF URINARY PROTEIN
Quantitative assessment
Alternative method - measurement of the total
protein/creatinine ratio (mg/mg) on a spot urine sample .
best performed on a first morning voided urine specimen to
eliminate the possibility of orthostatic (postural) proteinuria
normal protein excretion Ratios
<0.5 in children <2 yr of age
<0.2 in children ≥2 yr of age.
A ratio >2 suggests nephrotic-range proteinuria.
Historical Questions
1) Skin exam :
History :
A history of passage of clots in urine? In Extraglomerular cause
Hematuria due to glomerular causes is painless history .
A history of fever, abdominal pain, dysuria, frequency, and recent enuresis ? UTI
A history of recent trauma to the abdomen ? In Hydronephrosis
A history of a recent throat or skin infection ? In postinfectious glomerulonephritis
A history of joint pains, skin rashes ? In HSP and SLE
Physical :
skin examination ? Purpura
abdominal examination ? palpable kidneys
Genitalia
ophthalmological evaluation
Discuss the methods of detection of
hematuria
history and urine examination
Urinalysis : Dip strip analysis or dipstick test : dip
the strip in the urine, tap off excess urine, and read
the strip at the recommended time (usually 1 min). A
freshly voided urine should be used.
Urine culture: A midstream or clean-catch specimen
of urine : whenever a urinary tract infection is
suspected.
BUN/serum creatinine: Elevated levels suggest
significant renal disease as the cause of hematuria.
CBC counts and, platelet counts : bleeding disorder
Urine calcium: calcium-creatinine ratio can be
helpful in establishing hypercalciuria as a cause of
hematuria.
Phase-contrast microscopy : for the presence of a
significant number of dysmorphic RBCs
features between
glomerular and non-
glomerular causes of
hematuria based on
urine analysis
Formulate an appropriate management plan to
evaluate an infant with hematuria.
? ?? ? ? !!
Additional : DISEASES PRESENTING PRIMARILY WITH
HEMATURIA
Alport Syndrome :
glomerulonephritis, end-stage kidney disease, and hearing loss.
Hereditary nephritis (X-linked dominant)
1–2 days after upper respiratory infection
Asymptomatic hematuria
Hearing deficits
Ocular abnormalities
renal biopsy shows foam cells
Hemolytic Uremic Syndrome (HUS) :
Most common cause of acute renal failure in young children
• Prognosis—more than 90% survive acute stage; small number develop ESRD (end-stage renal
disease)
− Most common <4 years old
Most from E. coli O157:H7 (shiga toxin–producing) : from undercooked meat or unpasteurized
milk . Also from Shigella, Salmonella, Campylobacter.
characterized by triad of : micro-angiopathic hemolytic anemia, thrombocytopenia, and renal
injury ( uremia )
• Pathophysiology : mesangial deposits of granular, amorphous material—vascular occlusion,
glomerular sclerosis, cortical necrosis → localized clotting → damage to RBCs as they pass
through vessels → Intrarenal platelet adhesion and damage
(abnormal RBCs and platelets then removed by liver and spleen)
helmet cells, burr cells, fragmented cells, platelets usually 20,000–100,000/mm3, low-
grade microscopic hematuria and proteinuria
• Clinical presentation :
− Bloody diarrhea
− 5–10 days after infection, sudden pallor, irritability, weakness, oliguria occur; mild
renal insufficiency to acute renal failure (ARF)
• Treatment : fluids and electrolytes , dialysis , Plasmapheresis if no diarrhea or CNS problem .
− No antibiotics if E. coli O157:H7 is suspected—treatment increases risk of
developing HUS
URINARY TRACT INFECTION (UTI)
UTI more common in boys than in girls until after second year
• Etiology—colonic bacteria (mostly E. coli, then Klebsiella and Proteus;
some S. saprophyticus)
Types :
• positive urine culture
• dysuria, urgency, • abdominal or flank pain,
without signs or
frequency, suprapubic fever, malaise, nausea,
symptoms; can
pain, incontinence, no vomiting, diarrhea;
• become symptomatic if
fever (unless very • nonspecific in newborns
untreated; almost
young) and infants
exclusive to girls
UTI in childhood is important because:
• up to half of patients have a structural abnormality of their urinary tract
• pyelonephritis may damage the growing kidney by forming a scar,
predisposing to hypertension and to chronic renal failure if the scarring is
bilateral.
dehydration
cystic fibrosis
PANCREATIC DISEASE
CF is a chronic progressive disease that can present with protein and fat
malabsorption
The cause of inadequate pancreatic digestive function in 95% of cases is
cystic fibrosis
CFTR mutations : The gene for CF, located on the long arm of chromosome
7, encodes for a polypeptide, the cystic fibrosis transmembrane
regulator (CFTR),
autosomal recessive disorder .
The secretory and absorptive characteristics of epithelial cells are affected
by abnormal CFTR, resulting in the clinical manifestations of CF.
The altered chloride ion conductance in the sweat gland results in
excessively high sweat sodium and chloride levels. This is the basis of the
sweat chloride test,
elevated sweat chloride > 60 mEq/L in 99% of patients with CF .
(failure to thrive, hypoalbuminemia, steatorrhea),
liver disease (cholestatic jaundice),
chronic respiratory infection
Ninety percent of patients with CF are born with exocrine pancreatic
insufficiency This leads to malabsorption of proteins, sugars (to a
lesser extent), and especially fat.
Fat malabsorption manifests clinically as steatorrhea (large foul-
smelling stools), deficiencies of fat-soluble vitamins (A, D, E, and K),
and failure to thrive.
Protein malabsorption can present early in infancy as hypoproteinemia
and peripheral edema .
celiac diseases
Epidemiology
The prevalence of CP at age 8 in the United States is 3.6 per 1000;
prevalence is much higher in premature and twin births.
Prematurity and low birth weight infants (leading to perinatal asphyxia),
congenital malformations, and kernicterus are causes of CP noted at
birth.
Ten percent of children with CP have acquired CP, developing at later
ages. Meningitis and head injury (accidental and nonaccidental) are the
most common causes of acquired CP (Table 10-10).
Nearly 50% of children with CP have no identifiable risk factors. As
genomic medicine advances, many of these causes of idiopathic CP may
Risk factors
Most children with CP, except in its mildest forms, are
diagnosed in the first 18 months of life when they fail to
attain motor milestones or show abnormalities such as
asymmetric gross motor function, hypertonia, or
hypotonia.
CP can be characterized further by the affected parts of
the body (Table 10-11) and descriptions of the
predominant type of motor disorder (Table 10-12).
Comorbidities in these children often include epilepsy,
learning difficulties, behavioral challenges, and
sensory impairments.
Many of these children have an isolated motor defect.
Some affected children may be intellectually gifted.
Neurodegenerative disorders and C.P
Neurodegenerative disorders encompass a large
heterogeneous group of diseases that result from
specific genetic and biochemical defects and varied
unknown causes. Neurodegenerative disorders can
present at any age.
neurologic deterioration may be demonstrated as loss
of speech, vision, hearing, and intellectual or motor
abilities—sometimes in concert with seizures, feeding
difficulties, and mental retardation.
Progression may be slow over many years, or may lead
to death in early childhood.
Differential Diagnosis
- Cerebral palsy.
- Congenital myopathy.
- Spinal cord lesion
- Global developmental delay as in many syndromes
or unidentified cause.
- Metabolic Neuropathy
- Traumatic Peripheral Nerve Lesions
- Subdural hematoma
- stroke
Imaging
MRI: it is most useful after 2-3 weeks of life and is the diagnostic
neuroimaging study of choice for older children. Also for
determination of appropriate myelination for a given age.
Functions
Structural integrity and metabolism of bone (bone growth and remodeling).
Tooth formation.
Synaptic transmission.
Stimulus – secretion coupling: in nerve terminals; endocrine and exocrine glands (exocytosis).
REGULATION OF
CALCIUM
Three hormones- PTH, calcitonin,
activated vitamin D
The regulatory mechanisms
comprise:
• Intestinal absorption :duodenum
and proximal jejunum
• Renal tubular reabsorption and
excretion
• Exchange of calcium between
plasma and bone
Vitamin D deficiency
usually presents with
bony deformity and the
classical picture of
rickets.
Rickets signifies a
failure in mineralisation
of the growing bone.
Failure of mature bone
to mineralise is
osteomalacia.
Craniotabes is softening or
thinning of the skull in infants
and children
The costo chondral
junctions may be palpable
(rachitic rosary)
,wrists (especially in
crawling infants)
and ankles (especially in
walking infants) may be
widened
and there may be a
horizontal depression on
the lower chest
corresponding to
attachment of the softened
ribs and with the
diaphragm (Harrison
sulcus) .
The legs may become
bowed
List the laboratory and radiological findings and
explain the management of different types of rickets.
https://
emedicine.medscape.com/article
/412862-overview#a2
management
NUTRITIONAL VIT D DEFICIENCY:
Vitamin D + Calcium + Phosphorus
2 strategies for vitamin D administration :
1 - Stoss therapy: 300,000-600,000 IU of vitamin D oral or IM as 2-4 doses
over 1 day.
2 - Alternative: Daily, high-dose vitamin D, with doses ranging from 2,000-
5,000 IU/day over 4-6 wk.
Wheezes can originate from airways of any size throughout the proximal
conducting airways.
Wheezing requires sufficient airflow to generate airway oscillation and
produce sound in addition to narrowing or compression of the airway.
Thus, the absence of wheezing in a patient who presents with acute
asthma may be an ominous finding, suggesting impending respiratory
failure.
PHYSIOLOGICAL CONSIDERATION OF THE
CHILDS AIRWAY THAT PREDISPOSE TO
WHEEZING
The child’s respiratory system, including airways, continues
to mature until at least eight years of age, therefore the
pediatric airway is described and managed differently from
the adult’s.
Structural and mechanical differences predispose infants and
young children to respiratory compromise.
The newborn’s larynx is just one-third of the diameter of the
adult larynx. Narrow nasal passages, in combination with
being obligatory nose-breathers up to 5–6 months of age,
means that infants may experience respiratory distress if
nasal passages become oedematous or contain secretions
such as mucus or blood.
With the airway of an infant measuring around 6 mm in
The pediatric airway is characterized and differentiated
from an adult airway by the following features:
short maxilla and mandible
large tongue
floppy epiglottis
shorter trachea
more acute angle of airway, particularly notable
when attempting to visualize with a laryngoscope
a more cephalad larynx that moves distally as the
neck grows
the cricoid ring is the narrowest portion of the
airway
Cont.
smaller lower airways, less developed with fewer
alveoli
true alveoli not present until 2 months, with full
complement developed by around eight years of age
little smooth muscle present in airways
little collateral ventilation in airways.
CLINICAL HISTORY
Two important aspects of the medical history include the patient's
age at the onset of wheezing and the course of onset (acute versus
gradual)
Acute onset of wheezing raises the possibility of foreign body
aspiration, particularly if there is a history of choking.
In addition, it is helpful to distinguish between intermittent and
persistent wheezing.
Persistent wheezing presenting very early in life suggests a
congenital or structural abnormality.
In contrast, paroxysmal or intermittent wheezing is a characteristic
finding in patients with asthma.
Persistent wheezing with sudden onset is consistent with foreign
body aspiration, whereas the slowly progressive onset of wheezing
may be a sign of extraluminal bronchial compression by a growing
mass or lymph node.
Cont.
Cough is a symptom commonly associated with wheezing
The nature of the associated cough (wet versus dry) may be
helpful in determining the underlying etiology.
Wet cough typically results from excessive mucus
production, mostly due to infection or inflammation (eg,
bronchiectasis, cystic fibrosis, asthma, and chronic
aspiration).
In contrast, pure bronchoconstriction or structural causes for
airway narrowing (eg, asthma, or compression, foreign body,
vascular ring) are usually associated with a dry cough.
However, the underlying etiology of a dry cough can be
complicated by a secondary process, making this distinction
difficult (eg, mechanical obstruction can lead to impaired
mucus clearance resulting in infection and a wet cough).
Features in the history that favor the
diagnosis of asthma include:
Intermittent episodes of wheezing that usually are the
result of a common trigger (ie, upper respiratory
infections, weather changes, exercise, or allergens)
Seasonal variation
Family history of asthma and/or atopy
Good response to asthma medications
Positive asthma predictive index
features that suggest a diagnosis other
than asthma include the following
History
Onset of symptoms in early infancy
Neonatal respiratory distress +/- ventilatory support
Neonatal neurologic dysfunction
Intractable wheezing unresponsive to bronchodilators
Wheezing associated with feeding or vomiting
Difficulty swallowing +/- recurrent vomiting
Diarrhea
Poor weight gain
Stridor
Oxygen requirement >1 week after acute attack
PHYSICAL EXAMINATION
Acute Wheezing
Chronic or Recurrent Wheezing
Management
– Distribution pattern:
Atopic Dermatitis (Eczema) :
° Infancy: face, scalp, extensor surfaces of extremities
° Older, longstanding disease: flexural aspects
• Complications
– Recurrent viral skin infections—Kaposi varicelliform
eruption (eczema herpeticum) most common
Management
Cutaneous hydration
° Dry skin, especially in winter (xerosis) , Avoiding soap, frequently using
emollients? , Avoiding nylon and wool clothes?
Is there a need to give or change medications:
Topical corticosteroids
Seven classes—the higher potency classes are not to be used on face or
intertriginous
areas and only for short periods
° Goal—emollients and low-potency steroids for maintenance
• Treatment
– Most respond to avoidance of trigger and oral antihistamine
– Severe—epinephrine, short-burst corticosteroids
– If H1 antagonist alone does not work, H1 plus H2 antagonists are
effective; consider
steroids
– For chronic refractory angioedema/urticaria → IVIg or plasmapheresis
drug rash
Chapter 85 u Adverse Reactions to Drugs 297
– In vitro:
° Peripheral eosinophilia
° Eosinophils in nasal and bronchial secretions; more sensitive than blood
eosinophils
Treatment :
—environmental control plus
removal of allergen is most
effective method
- house dust mite, cat, cockroach
– No smoking
– No wood-burning
stoves/fireplaces
• Pharmacologic control
– Antihistamines (first-line
therapy):
– Intranasal corticosteroids —
most effective medication, but
not first-line:
management of an anaphylactic episode
Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.
Anaphylaxis Sudden release of active mediators with cutaneous, respiratory,
cardiovascular, gastrointestinal symptoms
• Presentation —reactions from ingested allergens are delayed (minutes to 2 hours);
with injected allergen, reaction is immediate (more gastrointestinal symptoms)
• Most common reasons
– In hospital—latex, antibiotics, IVIg (intravenous immunoglobulin), radiocontrast agents
– Out of hospital—food (most common is peanuts), insect sting, oral medications,
idiopathic
most responsive to treatment in its early phases
• Treatment
– What the patient should do immediately:
° Injectable epinephrine
° Oral liquid diphenhydramine
° Transport to ER
– Medical:
° Oxygen and airway management
° Epinephrine IM (IV for severe hypotension);
intravenous fluid expansion; H1 antagonist;
corticosteroids; nebulized, shortacting beta2 agonist
(with respiratory symptoms); H2 antagonist (if oral
allergen)
Approach to child with Hemolytic
Anemia (Pallor and Jaundice)
Pallor is the paleness of skin and mucous membranes, due to the reduced
amount of oxyhemoglobin or decreased peripheral perfusion.
Sites to look for pallor :
Lower palpebral conjunctiva
Tip and dorsum of the tongue
Soft palate
Nail beds
Palmar or plantar creases
General body skin
Define the causes of pallor and the definition of anemia.
Causes of pallor :
1 - Anemia
2 - Pallor without anemia : Physiologic (“fair skinned”) , Shock ,
Hypoglycemia and other metabolic derangements , Respiratory distress
, Skin edema , Pheochromocytoma .
X-linked
Within 24–48 hours after ingestion of an oxidant
(acetylsalicylic acid, sulfa drugs,
antimalarials, fava beans) or infection and
severe illness → rapid drop in Hb,
hemoglobinuria and jaundice (if severe) .
Acute drop in Hb, saturated haptoglobin → free
Hb and hemoglobinuria, Heinz bodies,
increased reticulocytes
Diagnosis—direct measurement of G6PD
activity .
Treatment—prevention (avoid oxidants);
supportive for anemia .
Approach to a child
with abdominal pain
Chronic and Recurrent abdominal pain.
Identify organic abdominal pain.
Define constipation & list its differential diagnosis according to the age:
Neonatal
Infancy
Childhood
PRESENTATION
CBC
LFT
Amylase and Lipase
Urinalysis
Pregnancy test
Stool hemoccult
Plain radiographs:
demonstrate signs of
obstruction ( distended
bowel) or perforation (such
as free air)
Fluid-filled loops of small
bowel can be seen with
gastroenteritis.
Ultrasonography:
Gallstones.
Genitourinary conditions
(eg, ovarian torsion,
ruptured ovarian cyst, and
testicular torsion).
Intussusception.
Appendicitis.
Computed tomography (CT) with contrast is useful for the
evaluation of patients with acute abdominal pain when a
wide variety of diagnoses are being considered ,such as :
(appendicitis, pancreatitis, intraabdominal abscess, blunt
abdominal trauma, and for the evaluation of an
intraabdominal mass).
Acute abdominal pain
Definition:
Acute abdomen represents:
Rapid onset of severe symptoms.
May indicate potentially life-threatening intra-
abdominal pathology .
Requires urgent surgical intervention, not all acute
abdominal pain needs emergency intervention.
In nearly half of the children admitted to hospital, the
pain resolves undiagnosed.
Acute appendicitis
2. enteroenteral intussusception:
jejunojejunal, jejunoileal, ileoileal which
occurs in older children may be secondary
to other problems.
Cause: Unknown
but there many Risk factors as:
1. Lymphoid hyperplasia
2. Meckels diverticulum
3. Henoch-Schönlein purpura [HSP]
4 cystic fibrosis
5. ascaris lumbricoides
6. juvenile inflammatory polyp
clinical pictures:
1. sudden sever crampy paroxysmal abdominal pain usualy relifed after
vomiting or pass stool
2. vomiting
3. pallor
4. shocked or dehydrated
5. abdominal distention 6. sausage like mass in right upper abdomen
7. PR=passage of red current jelly stool (late sign present in 60% of
cases)
Radiology :
1.xray abdomin:distended small bowel with abscent Of gases in distal
colon and rectum
2.US abdomin: helpful both to confirm The diagnosis and to check
response to treatment
3.barium enema: diagnostic and therabutics Show:
1. claw-sign 2. Coiled-spring
treatment: Correct water and electrolyte imbalance
NGT for decompression
Barium or air enema: 70% success rate\increase % of recurrence
Surgery done in: 1.faliure of reduction by enema 2.signs and symptoms
suggest peritonitis
Chronic and Recurrent abdominal
pain
Defined as pain sufficient to interrupt normal
activities and lasts for at least 3months.
10% of school age children
Hyperbilirubinemia happens
when there is too much bilirubin
in newborn blood .
is a life threatening disorder in
newborns .
the physiological jaundice is the
most prevalent type however in
some regions pathological
jaundice is also common.
Recall the physiological steps in the metabolism of
bilirubin.
https://emedicine.medscape.com/article/974786-clinical
Read from the link
List the key component from the history and physical examination in
patient with jaundice.
Discusses the differential diagnosis of direct hyperbilirubinemia.
Define and enumerate the laboratory findings in cholestatic jaundice.
List the commonest causes of cholestatic jaundice in infancy and
childhood.
Discuss the pathogenesis, clinical presentation and outline the
management of billiary atresia.
Conjugated hyperbilirubinaemia (>25
µmol/L) is suggested by the baby
passing dark urine and unpigmented
pale stools.
Hepatomegaly and poor weight gain
are other clinical signs that may be
present.
Its causes include neonatal hepatitis
syndrome and biliary atresia, with
improved prognosis of biliary atresia
with early diagnosis.
Biliary atresia : also known as extrahepatic ducto-penia , one
or more bile ducts are abnormally narrow, blocked, or absent.
• The reason is that extrahepatic bile ducts are usually present at birth,
but are then destroyed by an idiopathic inflammatory process.
Fr0m :
Illustrated
Textbook of
Paediatrics
Clinical Presentation :
1. • Pyogenic infections
2. • Life-threatening septicemia
3. • Neisseria infections
Normal gait has a stance phase and swing phase; each leg
should have symmetrical timing with each phase.
The stance phase represents 60% of the gait and begins with
foot contact (usually the heel strike) and ends with the toe-off.
During the swing phase (40%), the foot is off the ground. The
gait cycle is the interval between stance phases on the same
limb.
History
Age and Gender
Onset and Duration Red flags
Painful or Painless Fever
Trauma Weight loss
Associated with swelling, weight loss or fever Loss of sensation
Family history Loss of motor function
Past medical history
Remarkable history points in wish to identify
possible cause
Indicate :
Developmental hip dysplasia (DDH) / leg length discrepancy
Posterior displacement in
DDH .
A discomfort is a positive sign, in the absence of pain with passive motion of the hip
joint.
Barlow’s & Ortolani’s Tests
Congential Dislocation of the
hip
Myositis or transient synovitis ,Febrile children without joint effusion and with
normal radiographic and blood studies : followed up
Child with bleeding
disorder
Objectives :
https://opentextbc.ca/anatomyandp
hysiology/chapter/18-5-hemostasis
/
526 Section 20 u Hematology
major causes of
bleeding in children
Microcephaly is classified as either primary (genetic), which is almost always present at birth,
Familial – when it is present from birth and development is often normal
An autosomal recessive condition – when it is associated with developmental
delay
secondary (environmental), which may be present at birth or may develop later
from a postnatal insult .
Myriad syndromes and metabolic disorders are associated with microcephaly
Brain growth is rapid during the perinatal period, and any insult (infectious,
metabolic, toxic, vascular) is likely to impair brain growth and result in
microcephaly e.g. perinatal hypoxia, hypoglycaemia or meningitis, when it is
often accompanied bycerebral palsy and seizures
Rarely, a small head is the result of premature closure of one or more skull
sutures, called craniosynostosis.
Macrocephaly :
macrocrania (increased skull thickness) Diseases of bone metabolism or
hypertrophy of the bone marrow cause macrocrania ( imp could come as
scenario ) .
hydrocephalus (enlargement of the ventricles ) .
megalencephaly (enlargement of the brain) .
Megalencephaly may be the result of a significant disorder of brain
development or an accumulation of abnormal metabolic substances .
If there is a rapid increase in head circumference, raised intracranial pressure
should be excluded.
Clinical approach to infant with large and small head
size.
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