ophthalmology
BBP: biophysical profile, GA: gestational age, CS: caesarian section, NST: non-stress test, GBS: group
B Streptococcus
‫ اروى محمد‬: ‫جتميع وتنس يق‬
Blueprint for Comprehensive OSCE
Index:
NO.
Title
Page No.
Pediatrics:
NO.
Title
Page No.
Psychiatrics :
1.
Nutrition
5
1.
Social phobia
93
2.
Normal Development
7
2.
Dementia
94
3.
Normal growth
9
3.
Bipolar affective Disorder
96
4.
Immunization
11
4.
Major Depressive Disorder
99
5.
Asthma
14
5.
Anxiety Disorder
100
6.
Bronchiolitis
18
6.
Schizophrenia
104
7.
Respiratory Distress
22
7.
Obsessive compulsive Disorder
108
8.
Skin Rash
25
8.
Suicide and self-injuries
109
9.
Down Syndrome
29
9.
110
10.
Acute Diarrhea
32
Psychiatric disorder in
pregnancy
Derma
11.
Chronic Diarrhea
35
12.
Fluid management
39
13.
Hypovolemic shock
42
14.
Renal Disease
47
15.
DM
51
16.
Rheumatic Heart Disease
54
1.
Pre-exciting DM in pregnancy
57
2.
Ectopic Pregnancy
60
3.
Cardiotocograph ( CTG )
62
4.
Uterine Fibroids
65
5.
IUGR
67
6.
PROM
68
7.
Pre-term Labor
70
8.
Post-partum Hemorrhage
72
9.
Partogram and abnormal labor
75
10.
Pap Smear
82
OB :
ENT :
1. Hearing Loss And vertigo
85
2.
90
Neck Mass Evaluation
3. Obstructive Sleep apnea
91
1.
Bacterial Skin Infection
112
2.
Syphilis
114
3.
Cutaneous sarcoidosis
116
4.
Urticarial and angioedema
118
Ophtha:
1. Cataract
122
2. Corneal Ulcer
124
3. Diabetic Retinopathy
126
4. Eye trauma
128
5. Glaucoma
134
6. Strabismus
136
7. Uveitis and autoimmune
Disease
137
) ‫ حتى أبلغ‬.. ‫( ال أبرح‬
"‫سأص ًم ًم على بلوغ هدفي حتى لو كان الثمن أن "أمضي ُحقُبا‬
..‫وكل حقبة ( أربعين عاما ) فإن اجتمعت كانت أمدا طويال‬
) ‫( ال أبرح‬
" ‫ ولو كانت بعيدة ُبعد " مجمع البحرين‬, ‫حتى أبلغ غايتي‬
ُ ‫ ولربما أخطأت ف ُع‬, " ‫ولربما لقيت من سعيي هذا " نصبا‬
‫دت‬
" ‫على آثاري " قصصا‬
! ) ‫لكني ( ال أبرح‬
Done by:
Asmaa Salem
yara subahi
Neveen Ali
Dalia almatrafi
Lujain Gari
Amal Alsaadi
Abeer Melebari
Alaa malki
Waffaa Al-malki
Jawaher Alzahrani
Esraa kaheel
Khawla Kalantan
‫"تم التعديل على بعض ملخصات‬
" ‫الشورتي بيديا و نقلها الى هذا الملف‬
Reviewed By :
Amal Alsaadi
Arwa Alahmadi
reference :
Nelson's book
Illustrated book
Alhawasi book
our lecture nots
Toronto notes
Dr. Royal notes
Forms of proper nutrition : Macronutrients ( carbohydrates, fat, protein
& fluid ) Micronutrients ( vitamins, trace elements & minerals )
Factors affecting growth : familial , environmental & socioeconomic
Conditions that increase nutritional requirements : infection, truma &
burns, Inflammatory conditions, Inborn error of metabolism, Chronic
illness & Malignancy
Advantages of Breast Feeding : No preparation, Natural temperature,
Free of microorganism, Easy digestion and absorption of nutrients,
Increased mother-infant bonding, Improves cognition, Anti-infective
property & Protect against chronic illnesses .
Colostrum contents & benefits : High protein/low fat lactose product,
Small amount, Minimal nutritional value, High immune property, High
growth value, Facilitate passage of meconium.
Infants who breast feeding should have supplements of vitamin K at
birth, iron at 4-6 months & vitamin D .
Contraindication of breast feeding : mothers who have TB, HIV, Typhoid,
herpes, Syphilis, psychosis & who's on certain medications like lithium .
Breast milk can be used up to 4 hours at room temp, 5 days after
refrigeration & 3 months after freezing .
Sometimes the baby will have oral thrush infection ( fungal infection )
we should treat both the child & the mother together .
3 main formulas of milk : cow's milk, soy based milk & special formulas
like lactose free formula .
Breast milk contain 62 calories & has Ig A immunoglobulin while the
cows milk contain 65 calories
Weaning : introduction of solids while the baby is breast feed between
the age 4-6 months, should give pureed diet first like cerelac, fruits &
vegetables, give lumpy food if the baby is able to chew BUT avoid sugar,
salt & scratchy food ( until the age of 4 because they can chock on it )
Marasmus :
- The commonest type of PEM, The baby's weight is below 60% of
ideal weight, Have caloric deficiency, Comes with cystic fibrosis, HIV,
TB & celiac disease, The baby will have dry skin, thin hair, apathetic
state, decreased heart rate & temp, atrophy of papillae of the
tongue, oral thrush & chronic diarrhea
Kwashiorkor :
- Inadequate protein intake ( low protein diet ), The baby's weight is
60-80% of ideal weight, In chronic illness like IBD
- The baby will come with fair subcutaneous fat, pitting edema,
muscular wasting, the hair is sparse ( easily pulled with brown, red or
yellow color ), hyper pigmented & hyperkeratotic skin that
desquamated on pressure, macular rash on trunk and extremities,
angular stomatitis, oral thrush, distended abdomen and decreased
bowel sounds with basal lung rales .
(( The difference between marasmus & kwashiorkor is the edema ))
PEM therapy :
- Proper nutrition, Slow nutritional rehabilitation ( because there will
be electrolyte ,mineral and vitamin disturbance with rapid feeding )
& avoid cardiac and renal overload
- The baby will be at risk of nutritional recovery syndromes (
Diaphoresis ,hepatic glycogenesis ,eosinophilia )
- TPN may be required
Nutritional assessment:
1-dietary assessment: record the food the child eats during several day.
2-anthropometry: weight, height, mid-arm circumference, skin fold thickness.
3-laboratory investigation: low plasma protein, low concentration of specific
minerals & vitamins.
Consequences of malnutrition:
Multisystem disorder. When severe immunity is impaired, wound healing is
delayed & operative morbidity & mortality increased.
birth
50 cm
Height
Boy
girl
1 yr
75 cm
Peak Ht
11.5 yr
13.5 yr
3 yr
90 cm
Stop growth
14 yr
17 yr
4 yr (double birth)
100 cm
Puberty growth
9 yr
11 yr
Weight gain
1st 4months 30 g/day, rest 1st year 15-20 g/day,
between 1 and 2 yr = 2 kg
1st days
Decrease 5-10%
7 – 10 days
Return BW
6 months
Double BW
12 months
Triple BW
24 months
Quadruple BW
(2 years)
HC
1st year
2nd year
3 year
adult
At birth 35 cm
47 cm
49 cm
50 cm
56 cm
HC
1st 3 months
2nd 3 months
Last 6 months
Rest of life
At birth 35 cm
2 cm/month
1 cm/month
0.5 cm/month
10 cm
Growth chart
Objective continuous assessment for comparison, follow up, detection of
deviation or disappropriate growth and based on the population size for each
age group and differ between Male and Female.
Done each vaccination visit, normal between 3rd and 97th %ile and used to
measure 3 parameters:
-
-
-
-
Weight; to detect FFT, overweight > 110 % BMI, obese > 120% BMI.
Head circumference, should be 3 measures, occipitofrontal; to detect
micro/macrocephaly.
Height; to detect tall and short statures which is due to (Genetic cause
most common and bone age = chronologic age. Constitutional cause
which the bone age less than chronologic age ,due to use of steroid,
hypothyroidism, growth hormone deficiency)
What is bone Age? measure somatic maturity of hand and wrist by X ray
and copared to standard.
Mid parental height : with 5 cm more or less
o For boy: (Mother + father heights + 13 ) / 2
o For girl: (Mother + father heights - 13 ) / 2
U:L “Upper Length : top of head to top of pubic, Lower length: top of pubic to
feet bottom”
Upper to Lower segment ratio : At birth = 1.7:1 then at 10 yr = 1:1
-
-
Increase ratio: when increase Upper length , D.D is : ( Keep HanDs Going
Up)
o Klinfelter, Gonadal dysgenesis, Hypothyrodisim, Dysplasias
Decrease ratio: more in Lower length in (Marfan syndrome, spinal
scoliosis and radiation)
Hx:
Check the immunization card for routine vaccine
See if it follow the MOH schedule or not & If not ask why ?
Last vaccine ?
Complication ?
Extra vaccine ? number of doses ?
Active immunization: is the process of inducing immunity by vaccination
Passive immunization : administration of antibody eirher as immunoglobulin
or monoclonal antibody .
The preferred sites for administration are the anterolateral aspect of the
thigh in infants and the deltoid region in children and adults .
Type of vaccine :
Live attenuated
BCG
MMR
OPV
vericella
Rota virus
Killed vaccine
PCV
DTP
IPV
Hepatitis B
Hepatitis A
General Contraindication to immunization:
1) fever with moderate or sever illness
2) Hypersensitivity to the vaccine or its constituents
Contraindication to live attenuated vaccines:
1) immunocompromised states like :
(Pregnant Female, Congenital immunodeficiency ,HIV infection ,Leukemia , lymphoma,
immunosuppressive medication “cancer therapy” , Prolonged course of high-dose
corticosteroids) except measles “ MMR vaccine “ in HIV patient
2) within 3 weeks of another live vaccine
3) recent administration of immunoglobulin
4) pt with TB should not receive measles vaccine unless on full treatment for TB
special contraindication :
1) anaphylactic like reaction to egg >>influenza & yellow fever vaccine +MMR
2) CNS disorder >> pertussis
3) Hx of Guillain barre syndrome >> conjugate meningococcal vaccine
4) ITP within 6 week >> MMR
For premature infant:
1) Should be vaccinated at the same chronological age.
2) HBV vaccine for infants weighing <2000 g and the mother is hepatitis B virus surface
antigen (HBsAg)-negative should begin a 1 month instead of at birth .
asplenic children :
1) PCV ,HIB & meningococcal vaccine should be given in addition to routine
vaccination.
2) When elective splenectomy is performed give vaccines 2 weeks before the
operation .
Basic vaccination schedule in KSA 2014 “see alhowasi page 39”
Extra vaccines: :
1) MCV 2) PCV
3) Influenza: for pt. with SCA+ immunocompromised patient.
4) Rabies: if there is contact with animals Note: if the patient hasn’t received any rabies
vaccine before give him Rabies-Ig “immediate short term protection”
Site of injection :
intradermal
IM
SC
oral
Intranasal
BCG
HBV
MMR
OPV
Influenza “ live
attenuated “
DTP
Varicella
rota
Hib
MCV ”polysaccharide “
IPV
PCV” polysaccharide”
PCV “conjugated”
MCV “ conjugated “
Influenza “inactive
virus “
At birth >> BCG & HBV
1) HBV :
*Vaccine induced protection should result in antibody level of 10 mIU/ml or
higher
*Infant of HBsAg positive mother should receive hepatitis B immunoglobulin
shortly after birth + immunized with HBV within 12 hours of age.
2) DTaP :
*pertussis vaccine side effect (serious allergic reaction , encephylopathy , temp
of 105 F or higher , collapse or shock like state , perisistant crying >3h
,convulsion within 3 day )
a persone who developed one of theses adverse effect after pediatric DTaP
vaccine may receive Td as an adult
3)Hib :
infant at 2,4,6 m , asplenia , immunodeficiency , cancer therapy , HIV
4) polio:>> 2 type ( OPV , IPV )
* OPV is better at stopping the spread of the virus to others " give immunization
against this virus to the others ", in contrast it can affect immunocompromised
pt in the family because it can easily spread .
5) MMR :
side effect >> fever , rash , joint pain , thrombocytopenia
6) varicella :
contraindication >> anaphylaxis to vaccine , children with T cell
immunodeficiency
7) rota-virus vaccine : the maximum age for first dose is 14 weeks , and the
maximum dose for second dose is 8months , otherwise it will cause gut
intusseption .
immunization schedule should be memorize
Ddx of wheeze > vascular ring , hypocalcaemia , CP,GERD ,pneumonia,
bronchiolities, trachiomalacia , foreign body, double aortic arch.
Asthma is a chronic inflammatory disorder caused by airway hyper
responsiveness & recurrent wheeze &reversible airway obstruction. So
there're Bronchoconstriction + mucos hypersecretion + inflammation(
inflammatory cells & mediators).the main cells are eisinophil & mast cells , and
the main mediators are histamine & lukotriens.
Diagnosis of asthma? It's diagnosed mainly by hx + P.E . we have to know that
the presence of wheeze NOT express the severity of asthma as we can find pt
silent chest so he's in severe asthma ./w
There's skin prick test & peak expiratory volume can help us to diagnose
asthma or in small children we sometimes give a treatment to diagnose
asthma .
·
Asthma control & monitoring : by giving questioner to the relevant of a pt , or
peak expiratory flow , environmental control, food control in case of atopic
asthma .
Types of asthma treatment :
> this is for acute asthma exacerbations . ‫ انقاذية‬Reliefer ( rescue )/1
After we check for ABC and dehydration , we put him on o2 & then start with
SABA (Short Acting B2 Agonist e.g salbutamol (ventolin)) and we add
anticholenergic (e.g atropine) as well as normal saline < all of these on
nebulizer , we repeat them 3 times and if he didn't improve we give systemic
corticosteroid and if he again not improved we can give mg sulfate ,lastly if
there's no response at all , admit him in ICU .
maintenance ( control) > inhaled corticosteroid , anti leukotrien ( e.g /2
montelukast) .
N.B inhaled corticosteroid isn't effective in acute asthma .
* there's step wise therapy which is important and is better to read it from
illustrated book or nelson .
Chief complain
1 – SOB .
2 – Wheezing .
3 – Tachypnea .
4 – Tachycardia .
5 – Cyanosis .
6 – Fatigue & drowsiness .
Examination :
1 – Decrease level of consciousness .
2 – Cyanosis .
3 – Exhaustion .
4 – Use of accessory muscle & chest recession .
5 – Pulsus paradoxus .
6 – Decrease arterial oxygen saturation .
7 – Decrease peak flow .
Investigations :
1 – Chest X-ray only if there is :
- Unuseal featurs .
- Sever dyspnea .
2 – ABG → only indicated in life threatening or refractory cases .
Assessment and management of acute asthma illustrated textbook page 292
( important )
SOB
DD of asthma :
cardio
GI
1- CHF
1- DKA
1-Asthma
2- anemia
2-pneumonia
3- valvular
heart
disease
2-anaphylactic
shock
Resp
3-Bronchilitis
4-TB
5-foreign body
6-Cystic
fibrosis
Hx asthma :
Personal data
Chief complaint + duration
HPI (onset, character, w/sputum, progression, duration, timing, frequency,
relieving and exacerbating factor, severity)
1. Rapid & shallow = pneumonia
2. Rapid & deep = Kussmaul's breathing
Associated symptoms :3. Steatorrhea (fatty stool) + recurrent URTI or LRTI = Cystic
fibrosis (CF)
4. Sudden SOB + chest pain + cyanosis = pneumothorax
5. Tachypnea +tachycardia + Chest tightness + recurrent wheeze
+ dry cough at night = Asthma
6. Fever + peluritic chest pain + abd pain + SOB + tachycardia +
dry cough = pneumonia.
7. Fatigue + pallor + dizziness + palpitation + sleep more than
usual = anemia
8. Fever + dry cough + SOB + tachycardia = bronchitis
9. Abd pain + acetate smell (fruity) + vomiting = DKA
10. Fever + wt loss + FTT + loss of appetite + night sweating +
hemoptysis = TB
11.Sweating + poor feeding + sweating & cyanosis during feeding
+ SOB + tachycardia = Congestive Heart failure
Risk factors:
preceded by URTI (sore throat, sneezing)
Asthma / bronchitis.
Allergens, cold weather, URTI, cigarette smoke, fumes, B- blockers,
aspirin, emotional stress = Asthma risk factors.
Hx of swallowed nuts or playing = foregin body
Contacy w/ TB patient.
Chest trauma
Chronic DM = IDDM, missed dose
Past medical Hx + drugs Hx + Hospitalization Hx + allergy Hx (anaphylactic
shock)
Antenatal Hx
Developmental Hx
School Hx
Nutritional Hx
Immunization hx
Family hx (consanguinity, eczema, allergic rhinitis, asthma, CF)
Social hx (2nd hand smoking )
It’s the commonest serious respiratory viral infection of infants 1-9 months (rare > 1 year),
most severe in age 1-2 months. that result in inflammation and constriction of bronchioles .
Causes :
- RSV in 80% of cases , the remainder by human metapneumovirus , parainflunza virus ,
rhinovirus , adenovirus , influenza virus and mycoplasma pneumonia .
Pathophysiology :
the virus infects the respiratory epithelial cells of the small airways, leading to necrosis,
inflammation, oedema, and mucus secretion. The combination of cellular destruction and
inflammation leads to obstruction of the small airways ( bilateral ) , ait-trapping and
overinflation .
Risk factors :
-
Prematurity ( bronchopulmonary dysplasia )
Congenital heart disease .
Underlying lung disease ( cystic fibrosis )
Immunodeficiency .
Clinical manifestation In history :
-
Proceeded by URTI ( coryzal symptoms ),(often from household contact) .
Low grade Fever
Dry cough.
Feeding difficulty .
Dyspnea.
In examination :
-
Inspection :
Signs of respiratory distress :
- Tachypnea .
- Tachycardia .
- flaring of ala nazi .
- Using of accessory muscle.
-Subcostal and intercostal recession.
- Cyanosis or pallor in severe cases .
-
-
Palpation :
Hyperinflation of the chest .
- Prominent sternum
- Liver displaced downward .
Percussion : hyperressonance
Auscultation :
Fine end-inspiratory crackles.
Prolonged expiratory phase .
High pitched wheezes .
Investigation :
-
Pulse oximetry to monitor arterial oxygen saturation " continuously "
Blood gas analysis ( in severe cases to identify hypercarbia ).
PCR analysis of nasopharyngeal secretions .
CXR " hyperinflation of the lung and focal atelectasis ".
Management : ( see guideline management )
-
Supportive
Humidified oxygen by nasal cannula.
Fluid by nasogastric tube or IV
Good hand hygiene " RSV is highly infectious "
No steroids
Complication :
-
Recurrent apnea is serious complication .
The illness may result in permanent damage to the airways ( bronchiolitis obliterans
"
Bacterial superinfection
Prevention :
A monoclonal antibody to RSV " palivizumab " given IM monthly , given to infants with high
risk only , it will decrease the need for hospitalization and limit severity of the illness .
Guideline for management of bronchiolitis :
Definition: severe difficulty in achieving adequate oxygenation in spite of significant efforts to breathe. It is
usually associated with increased breathing rate and the use of accessory muscles in the chest wall.
Patho-physiology: Respiratory distress can occur in a great many conditions, including those arising in the
lungs, bronchi, bronchioles, heart, muscles, nerves, or brain. .
Causes:
Infant
Respiratory distress syndrome (Preterm infant)
Pulmonary hypoplasia
Bacterial sepsis (GBS)/ Viral infection (e.g. herpes simplex, Cytomegalovirus)
Spontaneous pneumothorax
Congenital anomalies (e.g. diaphragmatic hernia)
Congenital heart disease
Inborn metabolic error
Children:
Lower respiratory tract causes: Asthma (very common), Pneumonia (common), bronchiolitis and
bronchitis.
Upper respiratory tract causes: epiglottitis, croup, retropharyngeal abscess
Foreign body ingestion.
Cystic fibrosis
Lung abscess
Pleural effusion/empyema
Psychologic disturbance (e.g. hysteria, anxiety, pain, fear)
Clinical manifestation: there are 11 main signs of respiratory distress:
1- Tachypnoea + flaring of the nostril
2- Tachycardia
3- Rescissions (Usage of accessory Ms. Of respiration: subcostal, intercostal, supraclavicular and
suprasternal)
4- Inability to speak
5- Irritability
6- Sweating
7- Pallor
8- Cyanosis
9- Reduced air entry on auscultation
10- Pulses paradoxus
11- Symptoms and signs of CO2 retention:
a) Confusion, drowsiness, and later coma
b) Warm and sweaty hands (peripheral vasodilatation)
c) Bounding pulse
d) Coarse flapping tremors of the outstretched hands
e) Papilledema (cerebral edema) in chronic CO2 retention
Investigation: initial laboratory evaluation of respiratory distress include:
Test
Arterial blood gas
Rationale
To determine severity of respiratory compromise, hypoxemia, hypercapnia and
type of acidosis.
Complete blood count Check for Hgb/hematocrit (anemia, polycythemia), WBC count (neutropenia,
sepsis), platelet count and smear (DIC)
Blood culture
To recover potential pathogen
Blood glucose
To determine the presence of hypoglycemia, which may produce/occur
simultaneously with respiratory distress, or to determine stress hyper glycaemia.
Chest radiograph
A chest radiograph is useful in determining the site and nature of the lesion.
It helps to recognize foreign bodies, identify opacifications in lung
parenchyma or bronchial tree, identify pleural effusions or pneumothorax,
recognize pulmonary tuberculosis, and identify cystic, nodular or reticular
changes suggestive of lymphoid interstitial pneumonitis
To determine reticular granular pattern of RDS, cardiomegaly, or
life-threatening congenital anomalies.
Echocardiogram, ECG In the presence of a murmur, cardiomegaly, or refractory hypoxia to determine
structural heart disease or PPHN.
Further specific investigations are needed to identify the underlying cause of the respiratory distress.
Management: Rapid assessment is aimed to ascertain adequacy of airway patency, breathing, and circulation:
(a) restoration of airway patency- by positioning (head tilt -chin lift), cleaning the oropharynx, and/or
insertion of oropharyngeal airway.
(b) Supporting breathing- with high flow oxygen and assisted ventilation (with bag and mask or endotracheal
intubation and ventilation).
(c) Restoration of circulation- using fluid boluses and inotropes.
*if necessary. Immediate specific management may require endotracheal intubation/tracheostomy for upper
airway obstruction; needle thoracotomy and drainage of pneumothorax; and first dose of antibiotic for febrile
children.
» Thereafter meticulous history, focused physical examination, and specific laboratory/radiological
investigations are undertaken to identify the underlying cause to initiate specific treatment.
» Further respiratory support by Continuous Positive Airways Pressure (CPAP) and mechanical ventilation
may be required in some cases.
» All children with respiratory distress must be monitored for early detection of worsening/ complications,
assessment of response to therapy and rapid documentation of clinical state.
Complication: Respiratory arrest » cardiac arrest
A) History:
◙ Personal data: ◙ Age: bronchiolitis is a common cause of respiratory distress in babies, particularly those
under 6 months of age. (because the lungs and immune system aren't yet fully developed).
◙ chief complain: ◙ expiratory wheezing, chest tightness, shortness of breath and dry cough – symptoms
occur/worsen especially at night or early in the morning/after contact with triggering allergen » asthma.
◙ high grade fever, coughing often with sputum, pleuritic Chest pain or tightness, shortness of breath,
wheezing/stridor, chills and tiredness » pneumonia
◙ mild fever and a runny nose for a couple of days. Then he will develop cough and difficulty in breathing,
wheezing, poor feeding (Feeding takes energy and when babies are struggling to breathe they have no energy
left for feeding) » bronchiolitis
◙ History of presenting illness: ask about: onset & duration, frequency, severity and factors that worsen the
child's symptoms.
*Onset and duration: ◙ Hours (hyper-acute) » foreign body aspiration, ◙ Days (acute) » infective lung
disease e.g. pneumonia, bronchiolitis, empyema etc. ◙ Month/since birth (chronic) » cardiac or less
commonly chronic lung disease, ◙ Episodic (with symptoms-free periods) » Bronchial asthma.
*precipitating factors: ◙ viral infection, exposure to: (smoke, strong odors, fumes), exercise, emotions, and
change in weather/humidity » asthma.
◙ Winter season: (bronchiolitis are commonly caused by the respiratory syncytial virus infection. Seasonal
outbreaks of RSV infection occur every winter) » bronchiolitis
◙ associated symptoms & Systemic review:
◙ Rhinorrhea, red eye, cough, hoarseness, skin rashes (evidence of other atopic disease such as
eczema/allergic rhinitis) » asthma.
◙ hemoptysis » pneumonia
◙ Past medical history: ◙ hx of previous asthmatic attack, recent flu or common cold that trigger the attack,
hx of atopic dermatitis (eczema) and allergic rhinitis » asthma
◙ Hx of recent lower respiratory tract infection, neurologic diseases/impairment (↑ risk of aspiration),
immunocompromised status, hx of diagnosis of anatomic abnormalities of the respiratory tract
» Risk factors for pneumonia. Hx of recent hospitalizations especially in an ICU/mechanical ventilation »
Nosocomial Pneumonia.
◙ hx of an underlying heart or lung condition, a depressed immune system » bronchiolitis
◙ Pregnancy and neonatal history: hx of premature birth » bronchiolitis
◙ Nutritional history: Never having been breast-fed » bronchiolitis (breast-fed babies receive immune
benefits from the mother)
◙ Medication & allergies history: Beta-Blockers / NSAIDS (cause bronchoconstriction » Drugs-induced
asthma), Hx of Symptomatic improvement with bronchodilator/inhaler » asthma.
◙ Immunizations Hx: immunization deficient » Streptococcus Pneumoniae, HaemophilusInfluenzae,
Pertussis » pneumonia
◙ Family and social history: ◙ Family history of asthma and allergies including atopic dermatitis (eczema)
and allergic rhinitis (‘hay fever). Home environment (exposure to smoke, pets…) » asthma ◙ Recent history
of traveling/ contact with ill patient » pneumonia
◙ Exposure to tobacco smoke, Contact with multiple children, such as in a child care setting, Living in a
crowded environment with low socioeconomic status » bronchiolitis
B) Physical examination:
o General observations: the most important thing during the general PE is to recognize the signs of
respiratory distress (the previously mentioned 11sings)
o Respiratory system: Assess chest expansion, percussion and auscultation: beware of the silent chest
(this means that very little air is going in and out).
Disorder
Percussion note
Breath sounds
Added sounds
Pneumonia
Dull
Bronchial
Crackles
Bronchial asthma
Normal/decreased
Expiratory wheezes
Bronchiolitis
Resonance
Vesicular (Normal)/silent
chest (in advanced BA).
Reduced breath sounds
o Other systems - Cardiac system – CNS (Agitation ± drowsines
Fine inspiratory crackles/
End expiratory wheezes
Exanthem definition:
Eruptions of the skin accompanied by inflammation
Primary lesions of exanthema:
1-Macule : Small flat area of altered color blanch on pressure
Red macule is known as erythema
2- solid elevation of skin blanch on pressure
Nodule:
Papule:
if less than"0.5cm"
if more than"0.5cm"
3-elevation of skin contains clear fluid
Vesicle:
if small size
Bullae:
If large size
4-red spot that doesn't blanch on pressure
Petechie:
if less than 2mm
Purpura:
if more than 2mm
5- Pustule : Visible accumulation of pus in the skin
6- Desquamation; dry and flaky loss of surface of epidermis
•
Types of exanthematous lesions:
Petechial purpuric rash
Infections
Thrombocytopenia due to
infection,
ECHO and Coxsackie
Bacterial endocarditis
Others: ITP, leukemia
Drugs
Vesiculopustular rash
Infections
Herpes
simplex
Varicella
{chicken pox, varicella
zoster}
Coxsackie's
and ECHO viruses
Scalded skin syndrome
Toxic shock syndrome
Drug eruption
Maculopapular rash
Infections
Measles
Rubella
Erythema infectiosum
Enteroviruses eg ECHO, Coxackie
Epstein-Barr virus
Scarlet fever { Bacterial }
Drugs
Maculopapular rash
1- Measles:(Measles virus { RNA paramyxovirus })
Clinical features:
- Prodrome stage(Cough, Coryza, Conjunctivitis
and fever-KOPLIK spots"white dots in the buccal
mucosa opposite lower3rd molar,12-24 hs before
the rash") - Rash stage(Temperature rise as rash
appears up to 40-40.5C- It begin to fade in the same
sequence disappears within 7-10days)
- Convalescent phase(Rash disappears
and leaves behind brownish post-measles staining)
-Prophylaxis: Active
Complications:
common early: otitis media immunization
- Vitamin A
Rare and late : SSPE :
supplementation
Sub-acute sclerosing panencephilitis
3-Erythema infectiosum(Human parvovirus
B19): 5th disease
Clinical presentation:
Age: school –age children
Asymptomatic, Slapped cheek with typical
•
rash, Aplastic crises or Arthritis
In pregnant women cause (hydrops
fetalis)
2-Rubella(Rubella is a RNA virus
•
Clinical features:
Prodrome– mild catarrhal symptoms
Rash : usually small begins on the face and
clears by 3rd day
*RETROAURICULAR/POST.CERVICAL POST.
OCCIPITAL LYMPHADENOPATHY
complication: Cong. Rubella
syndrome(Growth retardation, cardiac
anomaly {PDA}, cataract, glaucoma,
deafness) in the 1st 3 months of pregnancy
high risk. Diagnosis : serology and virus
isolation
Prevention: Vaccination with MMR during
childhood
4-Infectious Mononucleosis(Epstein-Barr virus)
Clinical features:
Prolonged fever, Pharyngitis, tonsillitis,
Lymphadenopathy,Spleenomegaly,
hepatomegaly. Rash may appear after use of
ampicillin or amoxicillin
•
Lab findings:Blood: Leucopenia, Anti-EBV
antibody, monospot test.
complications: Spleenic rupture, CNS
TREATMENT: Bed rest, symptomatic Tt
Vesiculopustular rash
1-Exanthem subitum(human herpes virus 6): 6th
disease
clinical feature:
High fever that subsides when rash appears
2-Enteroviruses(Coxackie, ECHO viruses)
manifestations: Respiratory tract illnesses,
pleurodynia, Acute onset of fever and post.
Pharyngeal ulcers, Hand, foot, mouth disease
3-Chicken pox(Varicella zoster, Highly contagious disease):
Presentation: centripetal distribution
Pleomorphic Rash(Papule – vesicle – pustule on erythematous base)
improves within 10 days
Complication: Bacterial superinfection, Cerebellitis
( acute cerebellar ataxia), DIC in immunocompromised pt
Treatment with Human
varicella zoster IG only
recommended for high risk
Immunocompromised pt
History of rash
Patient ID ( name , age , gender )
History of presenting complain:
Onset ( sudden – gradual ) .
duration .
progressive changes: macule > papule > ..etc .
site of onset , pattern of spread and distribution .
describe the rash ( color _ flat / raised _ contents ) .
Come & go or persistent :
Itchy or not .
Any precipitating factors( drugs _sunlight _food _detergents _insect bite .. etc )
Aggravating or relieving factors ? ( drugs _ creams .. )
Previous history of the same complain .
Associated symptoms :
If Meningitis :
fever, headache, photophobia, neck stiffness, irritability & poor feeding .
If Measles:
Prodromal stage (cough , coryza , conjunctivitis ( ,
Fever and when its started ? (with \ after rash ) (high \ low grade), is ther a whitish spot in the
buccal mucosa .
If Rubella :
Prodromal stage , neck swelling ( for cervical lymphadenopathy ).
If Kwasaki’s disease :
red & edematous palms and soles \ peeling of fingers & toes .
conjunctival injection .
neck swelling ( lymphadenopathy ).
If GI infection ( gastritis , IBD ) ;
Abdominal pain , diarrhea ( bloody ) , Vamiting .
IF SLE :
Hematuria , Arthritis .
If Bleeding disorder :
easily bruise , epistaxis or other mucous membrane bleeding , bleeding from other orifices .
If H-S purpura :
Arthritis , abdominal pain , hematuria , edema .
Past medical history :
Previous infection or other illness >> SLE , RA , IBD .
Drugs ( immunosuppressant ) , Abx .
Blood transfusion .
Hx of atopic disease .
Hx of trauma .
Antenatal and perinatal history :
Congenital infection (TORCH) .
Illness or drug used by mother during pregnancy .
Allergy history :
Allergy to any food or medications .
Vaccination :
MMR vaccine .
Family history :
Present of family member with history of atopic disease _ psoriasis _ SLE _ RA _ IBD .
Present of the same illness in family .
Contact with affected family member .
Social history :
Child abuse .
Recent history of travel .
Contact with affected person .
Definition
Down syndrome "DS" (trisomy 21)
The most common trisomy chromosomal abnormalities
1 in 650 in incidence
Clinical manifestation
In general examination:
(( for dysmorphic features ))
Head :
Fine silky hair.
Large anterior fontanel.
Brachiocephaly “flat occipit”.
Face:
Round face
Eye:
oblique eye fissures
thick epicanthic fold
Pale conjunctiva.
Brushfield spots in iris
Decrease red light reflex due to cataract.
Accommodation problem.
Hypertolorism “widely spaced eyes”.
Nose:
flat nasal bridge
ears:
Small ears.
Low sit ears.
Hearing impairment.
Mouth:
Small mouth & protruding tongue.
Pallor in the mouth.
Neck:
Short neck. ((webbing))
At risk of atlanto-axial instability
Thyroid examination “risk of hypothyroidism”.
Cervical lymphadenopathy “Risk of leukemia”.
Congestive neck vein due to heart failure.
Hand :
Wide hand.
Single palmar creases.
Brachydactyly “shortness of the fingers”
Clinodactly “incurved 5th finger”
Foot :
sandal gap a wide gap between the big & 2nd toe
In Chest examination :
Signs of pneumonia due to recurrent respiratory infections.
In Cardiac examination:
Signs of “congenital heart defect”.
In GIT examination:
Abdominal distention due to“duodenal atresia”.
Umbilical hernia.
Hepatomegaly “due to heart failure”
Splenomegaly “due to recurrent infection or leukemia”
At risk of Subluxation in pelvic bone.
In Skin examination :
for peripheral eruption “due to leukemia”.
In CNS examination:
Short stature.
Hypotonia.
Causes
Extra chromosome 21 result from one of these three:
1-Meitotic non disjunction (94% of the cases) ((common in old lady))
what happened that at the meiosis phase the chromosome will not separate and then we have a
gamets contain two chromosomes then fertilized with the (maternal or paternal) gamets to end with
offspring contain 3 chromosomes called trisomy DS
2-Translocation (5% of the cases) ((common in young lady))
part of ch 21 joint to ch 14
If a parent carries the rare 21:21 translocation all the offspring will have down syndrome 100% ‫القسم‬
‫يجيب المعلومة دي كل سنة والناس تخربط ركزوا في السوال مزبوط‬
if the mother is carrier the risk to have DS is 10-15%
if the father is carrier the risk to have DS is 3%
3-Mosaicim (1%) normal cells and trisomy cells the milder form of DS
Risk factor
1 in 200-300 after having 1st DS baby
mother age related:
o all ages 1 in 650
o 20 Y/O 1 in 1530
o 30 Y/O 1 in 900.
o 35 Y/O 1 in 385.
o 37 Y/O 1 in 240.
o
o
Investigation
40 Y/O 1 in 110.
44 Y/O 1 in 37.
For screening
biochemical marker(free Bhcg, unconjugated estrol, inhbin, fetorotles )
nuchal thicking US+
for diagnosis
Chromosomal analysis
Complication
Moderate to Sever learning difficulty.
Delayed motor milestone.
Increase susceptibility to infection.
Hearing impairment due to secretory otitis media.
Visual impairment due to cataract, myopia and squints.
Epilepsy.
Alzheimer disease.
Congenital heart disease most common CHD in DS is VSD
The most common associated syndrome with AV canal is DS
Duodenal atresia = vomiting and dibble bubble on x-ray
Hirschprung disease result in absent stool
Increase risk of:
o Atlanto axial instability.
o Leukemia and solid tumor.
o Hypothyroidism.
o Coeliac disease.
D.D of acute and Chronic Diarrhea :
diarrhea
Acute
gastroenteritis
bacteraia
E.coli,
salmonella
.shigella
,clostridium
deffecil
viral rota virus
protozoa
cryptosporidi
um , giardia
lamblia, E.
histolytica
traveller
diarrhea
chronic
others
(OM,
pneum
onia)
inflammatory
cron's disease
congenita
l chronic
disease
toddler
diarrhe
a
METABOL
IC
DISEASE
lactose
intoleranc
e,
glucosegalactose
metabolic
malabsorpa
tion celiac
diseae,CF
Personal data : name, age, gender , nationality , admission & when
Chief complain & duration :
Chief complain >> (increase in frequency, decrease in consistency, Loose
stool , watery stool) For <2 week
Hx of presenting illness :
Onset , frequency , consistency , amount , odor , color , progression
content of undigested food , blood ( in cause of HUS caused by Ecoli ,
Entamoeba Histolytica) , or pus
aggravating or relieving factor
Relation to specific food
Hx of outside food intake >> gastroenteritis , hepatitis
Dehydration symptom
Impact of symptoms on life
Associated symptom:
( nausea , vomiting , abdominal pain , anorexia , jaundice “hepatitis A,E “
abd.distention , flatulence )
convulsions >> shigella
Blood in the urine , acute renal failure , purpura >> HUS
Abdominal pain , Vomiting, Acute diarrhea gastroenteritis
bloody diarrhea E.coli(EHEC) , E. histolytica
watery diarrhea virus ,cholera
Any infection in another site (otitis media ) fever ,vertigo ,vomitting ,ear pain)
(tachypnea ,fever ,cough ,chest pain Pneumonia
Constitutional symptom :
Fever( more with bacteria +- virus) , loss of appetite or weight , fatigability
& rash
Risk factors PMHx past hx of same disease ,family hx of same disease
Eating uncooked food or contaminated food gastroenteritis
Traveling hx traveler diarrhea
Past medical surgical hx : hx of chronic bowel disease or chronic illness ,
hx of recent gastric surgery
Antenatal and perinatal history:
Developmental history:
Nutritional history:
Current diet
Breast or formula
If formula ( who prepare , how prepare , water hygiene , bottle hygiene ,
type of milk)
Time of weaning
"Describe to me what he eats since he/she wake up till sleep"
Immunization history: rota virus vaccine
Family hx: same complain , milk intolerance , coeliac disease
Drug allegy hx : laxatives , antibiotics , food allergy
Social hx: recent travel , contact with infected person or animals
D.D Chronic Diarrheal
Disease :
Chronic Non specific diarrhea
Toddlers Diarrhea
Cause is unknown. Juice sugars ?.
Between 6 months 3years
Diarrhea is the only
symptom
Undigested vegetable in
stool
growth & activity not
affected
Dx history
R+ juices ( if applicable)
reassure parents
Celiac Disease
Glutine sensitive entropathy
Caused by Glutine: Wheat ,Oat
,Barley &Rye
Glutine sensitive entropathy
Vellus atrophy + Crypts
Hyperplasia
Chronic diarrhea (Steatorrhea)
Starts at introduction of
cereals (< 2years)
Irritable child and FTT
Typical appearance
(wasted, protuding abd &
wasted buttocks)
W' IDDM or Down
Syndrom
Diagnosed by jejunal biopsy& tissue
transgutamase antibody
Rx: Gluten free diet for life
Lactose intolerance.
Congenital or post
infectious( post
gastroenteritis).
Diarrhea , bloating,
cramps , flatus &
excoriation at diaper area.
Dx Stool reducing
substance
Lactose free formula
R+ lactose free diet
Cow's Milk Protein allergy
Immune mediated in
about 1-7%
50% allergic to soy
protein
Over diagnosed
Diarrhea (bloody), failure
to thrive,
urticaria&wheeze
R+ Replace cows milk
Glucose-Galactose
Malabsorption
Inherited disease
Diarrhea starts at birth
Diarrhea with feeding
Stopping feeding stops
diarrhea
ttt: Glucose & Galactose free
formula
Galaktamine 19
Congenital Chloride Diarrhea
Autosomal recessive
Impaired chloride
transport in ileum +
colon
Polyhydamnios
Chloride more than 90
mmol in the stool
Low serum cl, Na, K and
Alkalosis
Sever watery diarrhea
and FTT
Replace and monitor
electrolytes
Omeprazole
Intractable diarrhea of infancy
Affects infants around 3-6 months.
Secretary diarrhea
(explosive& watery)
May start with fever &
vomiting
Babe will be cachectic &
marasmic with abdominal
distention
Stopping feeding dose not
stops diarrhea
No etiology defined
mortality
Cystic fibrosis
Autosomal recessive
Lung disease
Hx of meconium plug or
rectal prolepses
Pancreatic enzyme def.
Steatorrhea
Fecal fat (qualitative &
quantitative)
Dx sweat chloride
R+ Antibiotic & enzymes
replacement
Protein losing interopathy
Intestinal loss of
protein & diarrhea.
Etiology
- intestinal permeability
e.g. post infection
- lymphangectasia
* Primary
* Secondary
-Allergic
Dx -History
-Stool Protein (Fecal alpha
1-antitrypsin)
-Serum Protein (albumin &
TP)
Isotope scan
R+ as per etiology
Hx of Chronic Diarrhea :
Presenting complaint (any of these)
Loose stool
Watery stool
Increase frequency
Increase amount
History of presenting complaint
Onset.
Duration.
Frequency.
Aggravating & Relieving factors.
Consistency ( watery, formed, oily )
Amount.
Odor (foul odor\ not)
color
Presence of blood or pus.
Proceeded by fever, headache, cough, constipation às in case of ( typhoid fever).
Relation to specific food orstop \ continue after cessation of food (lactose
intolerance)
History of outside food intake.
Associated symptom:
o Fever
o Anorexia
o Nausea.
o Vomiting
o Heart burn.
o
o
o
o
o
Past medical history
Jaundice.
Abdominal distention.
Abdominal pain or cramps
Flatulence
Tenesmus (painful urge to defecate) or rash.
Hx of admission due to same problem
Hx of any chronic bowel disease or any chronic illness.
Hx of recent gastric surgery.
Magnesium-containing antacids, laxatives, antibiotics.
Immunization history
Rotavirus immunization
Family history
Hx of same problem in the family.
milk intolerance, coeliac disease.
Social History
Water supply, meal preparation, sanitation, pet or animal exposure.
Risk factors: ( must mention it in history also)
o Season (rotavirus occurs in the winter(.
o Hx of recent traveling.
o Family member involvement
Complications: “due to dehydration” ( must mention it in history also) Oliguria.
Hypotention and shock.
o
o
o
o
o
Headache.
Muscle cramp
Dizziness.
Tachypnea.
Tachycardia .
FTT.
Examination:
Signs of dehydration and shock:
Dry, sticky mouth
Dry skin (lacks elasticity and doesn't "bounce back" when pinched into a fold)
Sunken eyes
sunken fontanels (the soft spots on the top of a baby's head)
Sleepiness or tiredness — children are likely to be less active than usual
Thirst
Decreased urine output (oliguria - anuria)
No wet diapers for three hours for infants
no tears when crying
Headache
Constipation
Dizziness or lightheadedness
Low blood pressure (hypotension)
Rapid heartbeat (tachycardia)
Rapid breathing
Topical picture of ciliac.d:
Wasted body + protruding abdomen + wasted buttocks
Invistigation:
General:
CBC + esoinophils,
Hgb for Cow's Milk Protein allergy
serum protein + challenge test (Protein serum) for Cow's Milk Protein allergy
Fluid and electrolyte for dehydration
ABG For acid base imbalance
Specific:
enzyme assessment for ( lactose intolerance)
Serology (tissue transgutamase a.b ,anti-endomysial a.b) for (celiac)
Intestinal biopsy (lactose intolerance,celiac disease, Glucose-Galactose Malabsorption)
Management:
ABC
Fluid and electrolytes replacement to manage dehydration.
Treat the underling Couse.
Definition
Diarrhea: is increase in the frequency or decrease in the consistency.
chronic diarrhea is : diarrhea more than 2 weeks.
Total Body Water and Compartments:
The total body water is divided into
1- Extracellular (ECF) made up:
2- Intracellular (ICF)
- Blood volume - Interstitial fluid
Trans-cellular fluid
The maintenance of the body fluid is depend on the osmolarity
Water balance; in critically ill children achieved by administration of:
Maintenance fluid
Replacement of ongoing loss Replacement of deficit
Most losses arise from insensible water losses (respiratory and skin) and sensible water losses
(mainly urine)
1) maintenance fluid :
Maintenance fluid are designed to prevent dehydration or volume depletion from occurring (
replacement of daily body loss of fluids )
There two ways used for estimating maintenance fluid requirement in ill child
- Body surface area method
- Caloric expenditure method (most common used: (how to use it )
Energy expenditure (kcal) or Maintenance water (ml) need based on weight (Kg):
Kg
Kcal or ml
0 – 10
100/kg/day = 1000/day
10 – 20 50/kg/day (for each kg > 10)=
1000+500=1500/day
20 >
20/kg/day (for each kg > 20)
Ex : pt wt was 25Kg .to calculate maintenance water need =
first : divide the we to be easy to calculate : 10+10+5
1 = 10×100= 1000
2 = 10×50 = 500
3 = 5×20 = 100
maintenance water need is = 1600 ml/day , then it divide by 24h/day= 67ml/h.
then this equation Simplified “4-2-1 rule” for calculating hourly maintenance fluid rate:
Kg
Hourly maintenance fluid rate
0 – 10
4 ml/kg/h =40 ml/h
10 – 20 2 ml/kg/h (for each kg > 10)=20ml/h
20 >
1 ml/kg/h (for each kg > 20)
If we calcualate it according previous example :
40+20+5 =65 ml/h .
Daily maintenance electrolyte based on Energy expenditure (kcal):
Electrolyte Maintenance need
Sodium
3 mEq/100 kcal/day
Chloride
2 mEq/100 kcal/day
potassium
2 mEq/100 kcal/day
Maintenance prescriptions usually also provide a daily amount of Na, Cl, K ,the basic
electrolyte lost in normal urinary excretion .
2) Water loss ( replacement of deficient )
Estimated water loss in special cases
Condition Urine output Insensible
ml/100 cal 45 - 55
35 – 45
Condition Oliguria
Polyuria
ml/100 cal - deficit
+ excess
Fever
10 ml/degree > 37.2
Anuria
Only 25 ml/100 cal
tachyapnea
30% of maintenance
Degree of dehydration:
Extremities Warm
Cpill. Refill time
HR
RR
Pulse Weak/absent
Mucus
BP
Sunken Eye/fontanel
Urine
PH
BUN
5% mild
hand & feet
1–3s
N
N
N
Dry
N
N
Low
7.40 – 7.30
N
10% moderate
To elbow/knee
3–5s
Increase
N
distal
Very dry
N
depressed
Very low
7.30 – 7.10
high
15% severe
Cool
> 5s
Very
increase
proxinal
cracked
Low
Sunken
Anuric
<7.10
Very high
Dehydration management
In severe dehydration, (shock) restoration of the intravascular volume is a priority
How to calculate the deficit? The total deficit =multiplying the estimated dehydration percentage by
total body wt of the child multiplying by 10 , E.g. 5% deficit in child's wt : 10kg
total deficit = 5×10×10=500ml/kg
In severe dehydration we start manage the pt with phase 1 , while in mild to moderate
dehydration we start manage the pt with phase 2 because the pt is already vitally staple .
Isotonic dehydration :
The Na level within normal range = 135-145
The type of fluid solution recommended to be given is isotonic crystalloid ( NS , ringer's
lactate ) .
is the most common type of dehydration.
Hypotonic dehydration :
the Na level below the normal range = less than 135 .
is the most severe type of dehydration .
mainly caused by : poly-excessive salt loss or excessive water intake .
in significant hyponatremia is present ( serum Na less than 120 ) it is frequently associated
with seizure and can lead to cerebral edema , we trat such pt with rapid correction of Na by
given hypertonic saline ( 3% Nacl ) within 3-4 hours ( should not exceed 2 Meq/h ) until
serum Na reach 125 meq/L ( this is called safe Na level ) . then by slow correction of
hyponatremia give isotonic solution ( 0,9% NaCl )
fast and aggressive correction of severe hyponatremia has major side effects and can lead to
severe and irreversible neurologic disorder called osmotic demylination. Therefore
correction should not exceed 10-12 meq/L in the first 24 h .
hypotonic dehydration :
the Na level exceed the normal range = more than 145 .
correct with slow rehydration over 48 h , allowing a gradual decrease in Na serum level 1012 meq/day .
associated with high intake of salt.
rapid correction of the hypernatremia should be avoided since this may result in seizure and
cerebral edema .
3) fluid replacement :
blood replacement indicated when blood loss exceed 30-40% or ( 20-30 ml/kg)
Q/ this child come to ER complain from diarrhea you fear from what ?
- Dehydration
Q/ What you want to ask in Hx ?
-
Underlying disease \recent infection or illness\trauma\surgery , travelling Hx , if
other member of the family affected by the same disease .
- Sign of shock :
- Recent wt change
- Decrease urine out put
- Pale child
- Cold extremities
- SOB
Q/ what is the definition of shock ?
-
Is a condition of a sustained and progressive circulatory dysfunction that results in
tissue hypo perfusion and inadequate delivery of oxygen and substrates to meet
tissue metabolic demands
Q/ What it is the clinical sign ( how you know this pt in shock or not ) ?
Early (compensated) reversible
Tachycardia 1st sign Most sensitive
Tachypnoea
decreased skin turgor
delayed capillary refill more than 2 s
sunken eyes and fontanelle
mottled, pale colored skin
decreased urinary output
Late (decompensated) irreversible
Hypotension Most specific
Acidotic (kussmaul) breathing
bradycardia
Cyanosis
absent urine output
confusion\depressed cerebral state,coma
N:B : urine output only for moniter the pt
Q / what is the type of shock ?
Hypovolemic shock. ( most common in child )
Cardiogenic shock.
Distributive shock
Causes Hypovolemic shock :
Blood loss: trauma, fracture, GI bleeding , surgery
Water loss: vomiting, diarrhea ( most common ), diabetes insipidus, adrenal
insufficiency, D.K.
Plasma loss: burns, capillary leak(sepsis,anaphylaxis),third spacing , nephrotic
syndrome , ascitis , intestinal obstruction
Cardiogenic shock : ( common in adult )
-
Causes:
Cardiomyopathy
Dysrhythmia: bradycard,AV block,SVT,VT
Congenital heart disease: aortic stenosis, coarctation , severe pulmonary stenosis,
left heart hypoplasia.
- Pneumothorax.
- Tamponade + pulmonary embolism
- Cardinal signs :
- Respiratory distress.
- Gallop rhythm.
- Hepatomegaly.
- Chest X-ray : cardiomegly, pulmonary venous congestion
Distributive shock:
normal peripheral vascular tone becomes inappropriately relaxed. distributive shock is a
decrease in preload that results from inadequate effective intravascular volume as a result
of massive vasodilation.
Common causes of distributive shock include the following:
Anaphylaxis
o Medications (eg, antibiotics, vaccines, other drugs)
o Blood products
o Foods
Neurologic causes
o Head injury
Sepsis.
Intoxication ( barbiturate )
Q/ How you can diffrentiat b/w them ?
assessment
Hx
Capillary refill
Gallop rhythm
CX-ray
hypovolemia
Diarrhea , vomiting ,
trauma
prolonged
no
Heart size small ,
lung clear
cardiogenic
Congental heart D ,
cardic surgery
prolonged
yes
Heart size large , lung
wet
Septic
Fever , lethargy ,
irritable
Normal early
No
Heart size small ,
lung clear early
Q/ how assess the hydration state of the pt ( sign of shock , sign of dehydration )
-
By physical examination
pale
Cold extremities
pulse
RR
BL.P
Volume
Capillary refill
Skin tourg
Mucosal
membrane
Mental state
Sunken eye
fontanel
Urine output
mild
5-10%
(<5%)
N
N/increase
N
N
N
Sever = shock
More than 15 %
( > 10 % )
Gray
All body b/c VC
Very increase
Very increase
Decrease
Decrease in center
and absent in the
peripheral
1- 3 sec
N
N
Moderate
10-15%
( 5-10 % )
yes
Till elbow / knee
increase
increase
N
Decrease volume
in the peripheral
and normal in
center
3-5 sec
Decrease
dry
N
N
flat
decrease
lethargy
yes
depressed
decrease
Decrease / coma
Yes
sunken
anuric
Q/ how u manage this child in ER ?
More than 5 sec
Decrease
‫متشققة‬
the colloid like dextrose is
contraindication
- See diagram at the end
- N:B = if the HR = very low may this heart block so give atropine and norepinephren
- If no I.V line ( vein collapsed what u can do ?)
- < 6 y = interossous b/c also centeral line difficult and bone marrow active
- > 6 y = centeral line , if u can’t made surgical cut down in foot
Q/ calculate the deficit , maintenance ?
- See the diagram at end
Q/ which investigation u need ?
Investigation
CBC + WBC DIFF
Serum electrolyte + glucose
Urea + CR
Liver enzyme
ABG
Why
Infection = septic shock
b/c usually with shock there is
electrolyte disturbance
Rena function
Acid – base state
( metabolic acidosis )
Coagulation panel
Blood + urine culture
Chest X - ray
Abdominal + pelvic X-ray
CT
ECG
CSF
ECHO
b/c bleeding = hypovelomic
shock
Infection = septic shock
Cardiogenic shock
Trauma
Trauma ( when stable pt.)
Cardiogenic shock
Infection
Cardiogenic shock
I will follow the protocol , call for help , ABC , connect pt to moniter
( N:B = O2 = 100% )
PHASE 1 : TREAT SHOCK
20ml/kg bolus ( NS = 0.9%saline , RL )
3 time back to back withen 0.5 hr for 20ml/kg bolus
( you should measure vital sign to see the responce of the pt and put folly
catheter )
insert centerl line to measure the CVP (RA)
> 8 or 10 = cardiogenic shock , < 5mmHg or1 ccm of water = hypovolemic
cardiogenic shock = ionotrope + stop fluid
anaphlactic shock = epinephrein , antihistamine , then steroid
sepsis = give ABx , cuture + / - steroid
PHASE 2 : REHYDRATION
if improve from shock = low or N plasma Na = 0.45% NS / 2.5% dextrose over 24 hr
= high plasma Na = 0.45% NS / 2.5% dextrose over 48 hr
maintenance :
1st 10 kg = 100 ml / 24 hr
DON'T FORGET :
2nd 10 kg = 50 ml / 24 hr
Na = 3-4 meq / 100 ml of fluid
subsequant kg = 20 ml / 24 hr
K = 2 meq / 100 ml of fluid
then calculate deficit :
- calculate how much child loss from his wt e.g : 2 kg loss = give 2 L
OR
- asses % of dehydration ( ml ) = % dehydration x 10 x wt(kg)
ongoing loss :
fever , hyperventilation , vomiting and diarrhea , polling of fluid in gut ,capillary lack
General
Ask about: polyuria, oliguria, frequency, dysuria, nocturia, itching, fever, hematuria, loin
pain, suprapubic pain, Hx of sore throat/URTIs, joint pain/swelling, abdominal pain, GI
bleeding, edema, rash
Investigate:
Urine: Urinalysis, culture, osmolality, microscopy, 24hr urinary protein excretion,
protein creatinine ratio
Blood: CBC, urea, creatinine, electrolytes, albumin, glucose, ASO, complements,
coagulation profile, ANA/Anti-dsDNA – ANCA – lipid profile
Imaging: US – CT/MRI
In special cases: [DMSA, MCUG, MAG3 renogram] (VUR, obstruction), Throat swab
(GAS), Stool culture: E. coli 0157 (HUS), PTH (CRF)
Congenital abnormalities
Vesicoureteric reflux
Potter syndrome (oligohydramnios, characteristic facies, lung hypoplasia, limb
deformities)
Multi-cystic renal dysplasia
Polycystic kidney disease (autosomal dominant, recessive)
UTIs (E. coli)
Urine sample (clean catch, adhesive plastic bag, urethral catheter, suprapubic
aspiration)
<3 years urine microscoped and cultured
<3 months admit + IV antibiotics “cefotaxime”
Bacterial culture > 105 CFU of a single organism 90% infection
Acute kidney injury (AKI)
Pre-renal
o The commonest
o Hypovolemia (gastroenteritis, burns, sepsis, hemorrhage, nephrotic
syndrome)
o Circulatory failure
Renal (blood, protein, casts in urine – salt and water retention)
o Vascular (HUS, vasculitis, renal vein thrombosis)
o Tubular (ATN, ischemic, toxic, obstructive)
o Glomerular (glomerulonephritis)
o Interstitial (Interstitial nephritis, pyelonephritis)
Post-renal
o Urinary obstruction (posterior urethral valve, acquired: blocked urinary
catheter)
Chronic renal failure (stages, causes: congenital, hereditary, glomerulopathies,
multisystem disorders, tumors
Dialysis vs. transplant
Nephrotic syndrome
Heavy proteinuria, Hypoalbuminemia, Edema, Hyperlipidemia
Investigations
Urine:
o Urinalysis: proteinuria more than 3.5 g/day , microscopy: hematuria/casts,
Na+, protein creatinine ratio, hepatitis B and C screen
Blood:
o CBC “Hgb”, serum albumin: <25g/L, urea, electrolytes, creatinine,
complements, lipid profile
Management
Admit
Fluid restriction/diuretics and prevention of hypovolemia
Oral steroid therapy, if relapses use immunosuppressant agents
Prophylaxis against bacterial infection (oral penicillin V) until edema free –
pneumococcal vaccine
Complications: infection, thrombosis, hypovolemia, acute renal failure
Hemolytic uremic syndrome (E. coli 0157. H7 type)
Triad: hemolytic anemia, thrombocytopenia, acute renal failure
History of bloody diarrhea, eating/drinking contaminated food/milk, contact with
farm animals
Investigations
CBC, blood culture, urea and electrolytes, LFTs, E. coli PCR, stools microscopy and
culture
Management
Dialysis may be needed
Supportive treatment, no antibiotics
Monitor fluid and electrolyte balance and nutrition
Blood transfusion
Treat hypertension
Hematuria “>10 RBCs per HPF”
(macroscopic – microscopic), distinguish from
hemoglobinuria and myoglobinuria
Causes: Infectious, hereditary, glomerular, stones, trauma, tumor, vascular,
hematological, drugs
HSP
Rash on the buttocks
Joint pain and swelling
Abdominal pain
Hematuria
Periarticular edema
Proteinuria (> 0.15 g/24hr)
Causes:
o Non-pathological: Transient, fever, exercise, UTI, orthostatic
o Pathological: nephrotic syndrome, glomerulonephritis, CKD, TIN
Definition: a chronic disease, which is characterized by hyperglycemia and glycosuria.
Diabetes is due to one of two mechanisms: 1) Inadequate production of insulin, or 2) Inadequate
sensitivity of cells to the action of insulin. The two main types of diabetes correspond to these two
mechanisms, and are called insulin dependent (type 1) and non-insulin dependent (type 2) diabetes.
Pathophysiology
Causes
Risk factor
Clinical
manifestation
Investigation
Management
Complication
Type 1 DM
T1DM is the most common type occurring in
childhood, which is caused by autoimmune
destruction of the insulin-producing B- cell
(islet) of the pancreas leading to permanent
insulin deficiency.
Genetic, Environmental, Autoimmune factors,
Idiopathic.
Type 2 DM
Results from peripheral insulin
resistance and compensatory
hyperinsulinemia, followed by
failure of the pancreas to maintain
adequate insulin secretion.
Develops when the body becomes
resistant to insulin or when the
pancreas stops producing enough
insulin. Exactly why this happens
is unknown, although excess
weight, inactivity and genetic
factors seem to be important.
The autoimmune process tough to be triggered
by: cow's milk feeding at an early age, viral
infectious agents (Coxsackie virus,
Cytomegalovirus, mumps, rubella), vitamin D
deficiency and perinatal factors. In addition to
the presence of a + family history of diabetes or
diabetes susceptibility genes.
Polyuria, polydipsia, polyphagia, easy
Fatigability and weight loss.
Genetic, Obesity, Physical
inactivity & Childhood obesity,
High/low birth weight,
Gestational diabetes mellitus
(GDM), Poor placental growth,
the metabolic syndrome, ethnicity,
and a family history of DM2.
Polyuria, polydipsia and
polyphagia.
A diagnosis of DM is made based on 4 Glucose abnormalities that may need to be
confirmed by repeat testing: 1) Random serum glucose concentration ≥ 200 ml/dl 2)
Fasting serum blood glucose concentration ≥ 126 mg/dl 3) Oral glucose tolerance test
with a 2-hr postprandial serum glucose concentration ≥ 200 mg/dl 4) HgbA1c ≥ 6.5 %
Insulin therapy: there are many types of insulin,
*Asymptomatic patient with
which can be used in various combination. The
mildly elevated glucose » life
most commonly used regimen is that of multiple style modification.
injections of fast-acting insulin given with meals *New onset uncomplicated T2DM
in combination with long-acting basal insulin
» metformin + life style
given at bedtime.
modification.
*Sometimes insulin injections are
needed.
In addition to: life style modification (dietary adjustment + exercise), SelfMonitoring of Blood Glucose. A child with DM for more than 3-5 y should receive
annually: ophthalmic examination, urine collection for assessment of
microalbuminuria, cholesterol measurement and periodic assessment of BP.
◙ Diabetic coma or ketoacidosis (more commonly in DM1, but it also can occur with
DM2) ◙ Renal dysfunction and Nephropathy ◙ Neuropathy ◙ Retinopathy
◙ High blood pressure and hypercholesteremia » ↑ risk of coronary disease and
stroke.
◙ Failure to thrive ◙ Hypoglycemia: more commonly with DM1, results from a
relative excess of insulin in relation to serum blood glucose.
A) History: ◙ Personal data: Ethnicity: some ethnic group consider as risk factor for T2DM: black, Hispanic,
Native American, Asian-American or Pacific Islander
◙ Chief complain: usually it could be one or more of the following symp: polyuria, polydipsia, polyphagia,
weight loss/failure to thrive, nocturnal enuresis, abd. pain, fever and nonspecific malaise.
◙ History of presenting illness: onset: T1DM » acute onset, T2DM » insidious onset, duration, progression,
severity and precipitating factors.
◙ Systemic review: ask specifically about: ◙ other symp. of DM if not mentioned by the patient himself ◙
Symptoms of ketoacidosis include: Abdominal pain, Vomiting, Drowsiness and coma.
◙ symptoms of slow-healing sores or frequent infections: fever, SOB, cough, ↑ frequency of urination …
(hyperglycemia impairs immunity and renders a child more susceptible to recurrent infection, particularly of
the urinary tract, skin, and respiratory tract.
◙ Past medical history: ◙ hx of recent respiratory tract infection / urinary tract infection.
◙ hx of other medical condition e.g. thyroid diseases, metabolic syndrome.
◙ Pregnancy and neonatal history: Hx of Gestational diabetes mellitus (GDM), Poor placental growth,
High/low birth weight » risk factors for T2DM.
◙ Nutritional history: cow's milk feeding at an early age/early introduction of cereal into a baby's diet » risk
factor for T1DM.
◙ Developmental history: Has growth and development progressed normally? » failure to thrive one of
complication of T1DM.
◙ Family and social history: family hx of DM
B) Physical examination:
◙ General examination and vital signs: Signs of Severe dehydration (tachycardia, hypotension, loose skin, a
dry mouth, or sunken eyeballs …) Smell of ketones, Acidotic breathing (ie, Kussmaul respiration),
masquerading as respiratory distress + Abdominal pain, Vomiting, Drowsiness » diabetic ketoacidosis
(emergency case).
.* Hypertension may occur in children with type 2 diabetes
◙ Growth parameter: Measure the child height and weight. Compare it to standards that are normal for his
age groups. (a Lean child more suggestive for T1DM, while obesity - body mass index (BMI) above the 85th
percentile- more suggestive for T2DM).
◙ Systemic Examination: check specifically for
-
Check the skin for signs of insulin resistance: ◙ skin-acanthosis (suggestive for T2DM ) a dermatological
manifestation of hyperinsulinism and insulin resistance, presents as hyperkeratotic pigmentation in the
nape of the neck and in flexures area ◙ sign of candida infections
- Feel the neck to evaluate the thyroid gland. (Thyroid problems sometimes develop in people who have
diabetes).
- Check the eyes for eye-hemorrhages, exudates, neovascularization (may occur as complication with
diabetic child for more than 3 – 5 year).
*Differentiating T1DM from T2DM in children on only clinical grounds can be challenging. The possibility
of T2DM should be considered in patients who are obese, have a strong hx of T2DM, have other
characteristic of metabolic syndrome, or have absent of antibodies to beta cell antigens at the time of the
diagnosis of di
Emergency case: Diabetic ketoacidosis (DKA)
Diagnosis:
Hyperglycemia (serum glucose concentration
ranging from 200 – ≥ 1000 mg/dl)
Arterial PH is below 7.30
Serum bicarbonate concentration is less than 15
mEq/L
Urine serum ketones are (+)ve
Management: confirm the dx and admit to the
hospital/ICU.
◙ Replace fluids: A) If in shock (↓ BP): resuscitate
with any fluid (preferably NS) at 10 – 20 ml/kg as
quickly as possible. Once corrected proceed with
rehydration as per the degree of dehydration and
electrolytes imbalance. B) If not in shock (normal
BP): rehydrate the patient with 0.9% NS or 0.45% NS
(as per the degree of dehydration & electrolytes
imbalance).
*Degree of dehydration is 3, 6 and 9 for mild, moderate
and severe for children > 2 years of age, and 5, 10 and
15 for children < 2 years of age.
◙ Insulin: 0.1 unit/kg/hr by continuous infusion,
continue insulin dosage at that rate till acidosis is
corrected (pH > 7.3and/ or bicarbonate > 15 mmol/L)
◙ Electrolytes: A) sodium: 0.9% or 0.45% NS, once the
blood glucose is less than 250 mg/dl continue with
D5W 0.45 (preferred) or D5W 0.2 NS.
B) Potassium: 4-6 meq/kg/24 hr is needed. Rate should
not generally exceed 0.5 meq/kg/hr. continuous
monitoring is needed (ECG).
C) Bicarbonate: this is rarely needed, fluid and insulin
in most cases is enough to correct acidosis.
Complication: cerebral edema (most common 1% -5%
of cases of DKA), intracranial thrombosis /infraction,
acute tubular necrosis with acute renal failure (severe
dehydration), arrhythmia (electrolytes imbalance),
pulmonary edema and bowel ischemia.
Skin infection by GAS can cause post-streptococcal glomerulonephritis but not RF
GAS Infection immune-mediated 97% resolve, 2-3% JONES Criteria,
glomerulonephritis, scarlet fever
Risk of rheumatic heart disease with rheumatic fever 3% after first attack, 20%
after second attack
History
URTI, JONES Criteria (major, minor), socioeconomic status
Physical examination
Vital signs (most important heart rate, temperature)
Inspection: rash erythema marginatum, subcutaneous nodules, chorea, joints,
SOB
Palpation: cardio thrill, JVD, pulsus paradoxus – joints warm, swollen, red,
restriction of movement
Auscultation: friction rub, decreased heart sounds
Investigations
↑ESR, CRP, ASO
Leukocytosis
ECG PR interval prolongation
JONES Criteria
Major:
Joint inflammation (polyarthritis)
O looks like heart^^ (pancarditis)
Nodules (subcutaneous)
Erythema marginatum
Sydenham's chorea
Minor:
Fever
Arthralgia
Abnormal ECG: prolonged PR interval
Elevated ESR/CRP
Evidence of previous group A streptococcal infection; raised ASO titers
History of previous rheumatic fever
Diagnosis: Two major or one major and two minors
Management
Bed rest
Aspirin
Corticosteroids (2-3 weeks)
Diuretics/ACE inhibitors in heart failure
Antibiotics (penicillin V for 10 days)
Prevention of further attacks
Antibiotic prophylaxis (daily oral penicillin or monthly IM penicillin G)
Chronic rheumatic heart disease
Scaring and fibrosis of heart valves (most commonly mitral)
‫ " لو أنكم تتوكلون على هللا حق توكله لرزقكم‬: ‫قال صلى هللا عليه وسلم‬
‫ رواه الترمذي‬," ‫ تغدو خماصا وتروح بطانا‬, ‫كما يرزق الطير‬
‫ التذلل هلل‬: ‫ " و إذا استعنت فاستعن باهلل " واالستعانة هي‬: ‫وقال‬
ً
) ‫ ( ابن عثيمين‬. ‫وثقة بكفايته‬
‫بتفويض االمر له اعتمادًا عليه‬
Done by:
Jehad Alzahrani
Mohammed Basuony
Asim Al Ali
Abdulbari Bahha
Naif Mohammad
Moath abdullah
Majdi Al Zahrani
Saeed Balubaid
Abdullah Alharbi
Mohammad SHaheen
Moad Basfar
Reviewed By :
Mohammed Alshareef
Arwa Alahmadi
Samah Alqurashi
Elham Ahmad
Salmah Aljahdli
Eman Sulaiman
Reference :
Toronto Notes 2015 (Chy
Yong)
The Johns Hopkins
Manual of Gynecology
and Obstetrics .
Hacker's Book
Lecture Notes
Pre-existing DM in pregnancy
Complication:
Maternal
Increase insulin requirement
Hypoglycaemia
DKA
Infections ( vaginal candidiasis , UTI .. )
Retinopathy, neuropathy, nephropathy
Preeclampsia
Polyhydramnios
Increase caesarean section rate
PPH
Fetal
Abortion
Congenital abnormality( sacral agenesis ,
congenital heart disease " ASD , VSD " ,
NTD , renal agenesis )
IUFD
IUGR
Macrosomia > Shoulder dystocia
RDS
Jaundice
Neonatal hypoglycaemia
Polycythaemia
Notes:
Most common congenital abnormality is congenital heart disease, and most specific
is sacral agenesis .
Pathophysiology of Macrosomia: maternal hyperglycaemia leads to fetal
hyperglycaemia and hyperinsulinemia, and insulin has an anabolic effect.
Pathophysiology of RDS: insulin antagonises the effect of cortisol in the lung and that
will lead to delay in the lung maturity, so avoid delivery before 39 weeks in absences
of maternal and fetal indications unless amniocentesis indicates lung maturity.
One extra test that done only in chronic DM is : Fetal Echocardiography at ( 22-24w)
Investigations:
for mother :
For fetus :
Kick chart
Urine
Urine
Biophysical
FBG H1C Fundoscopy ECG ur/cr
BP AFP/US/Fetal
CTG
analysis culture
profile
echocardiogram
Management :
o
o
o
o
o
o
Diet ( 50% CHO , 20% protein , 20% fat , fiber ) & Exercise.
Tight control of blood glucose( FBG<90,1-hour PP<140 , 2-hour PP<120).
Shift from oral hypoglycaemic to insulin in case of type 2 DM.
Referral to the endocrinologist/ ophthalmologist/ nephrologist.
Regular follow up
Time and mode of delivery individualised.
o If the Blood suger can't be controlled and a complication happened > immediate
admission .
o If the pt has : (chronic DM) deliver her at 38 w . while in( GDM that controlled by
insulin ) deliver here at 39 w , in ( GDM that controlled by diet ) deliver here at 40 w .
o C/S is indicated only if the fetal estimated wt more than 90th percentile .
History :
Personal data ( name, age, gravity and parity)
Present complain( onset, duration, progression, aggravating/reliving factors,
severity, associated symptoms, constitutional symptoms) .
Current obstetric history :
LMP: sure? , pregnancy test: when?
Antenatal care: booked? With regular follow up?
Frist U/S: when? Corresponding to with GA?
Any abnormality in the U/S or in the other investigation?
( e.g.: abnormal weight, morphology, presentation, twins, amniotic fluid volume,
placental localization elevated enzymes…e.t.c)
Any complication during pregnancy?
Use supplement and medications?
Ask about complication of DM( vaginal discharge, vaginal bleeding, vaginal itching,
decrease fetal movement, dizziness, loss of consciousness, headache, abdominal
pain, nausea, vomiting, decrease of vision)
Past obstetric history( time, place, GA, mode of delivery, complication, weight, sex,
health of the baby) for each pregnancy.
Menstrual and gynaecological history( menarche, regularity, length, volume,
associated symptom).
Contraceptive history.
Past Medical/Surgical history.
Family history( HTN, DM, Congenital disorder, multiple pregnancy,
thromboembolism)
Medications and allergy
General Examination:
WEPPER/ABCDE
Vital sign
Examine the eye looking for( cataract, glaucoma, macular edema, diabetic
retinopathy).
Look for Acanthosis nigricans in the neck and the axilla.
Examine the foot for ulcer and peripheral neuropathy.
Obstetric examination:
1. Inspection( distension, linea nigra, striae , prominent vines, fetal movement ,
scares)
2. Palpation:
Uterus: ( size, consistency, tenderness, regularity)
Fetus: ( lie, presentation, engagement , back)
Liquor: ( volume, size of the uterus)
How to calculate (calorie requirement ) for pregnant lady complain with DM :
calorie requirement = 35 Kcal/ Kg/ day
then divide the result : 50% CHO , 20% protein , 20% fat .
To calculate the starting dose of insulin :
.) ‫ حيسأل عنها‬%
‫ لو جاء في االختبار‬, ‫( هذي المعادالت والحسابات دكتور تيمور ركز عليها‬
Ectopic pregnancy
Definition :
Embryo implants outside of the endometrial cavity.
# Methotrexate
Pathology:
-Fertilized ovum borrows through the epithelium
Zygote reaches the muscular wall
-Trophoblastic cells at zygote periphery proliferate, invade,
and erode adjacent muscularis
-Maternal blood vessels disrupted leading to hemorrhage
Outcome: tubal abortion or rupture with hemorrhage
Absolute contraindication :
Etiology :
-50% due to damage of fallopian tube cilia following PID.
-intrinsic abnormality of the fertilized ovum.
-conception late in cycle.
-transmigration of fertilized ovum to contralateral tube.
1- breast feeding
2- overt or lab. Evidence of
immunodeficiency.
3- Alcoholism, alcoholic liver disease or
other chronic liver disease .
4- Preexisting blood dyscrasia ( bone
marrow hypoplasia,
leukopenia,thrombocytopenia,
significant anemia.
5- Peptic ulcer disease
6- Renal dysfunction .
Clinical Features of Ectopic Pregnancy :
4Ts and 1S
Relative contraindication :
Temperature >100.4 F.
Tenderness: abdominal +/- rebound.
1- Gestational sac > 3.5 cm
Tenderness on bimanual examination, cervical motion tenderness.
2- Embryonic cardiac motion .
Tissue: palpable adnexal mass.
Signs of pregnancy (e.g. Chadwick’s sign, Hegar’s sign)
Side Effects:
If Ectopic Pregnancy Ruptures :
- Elevated liver transaminase , mild
• Acute abdomen with increasing pain.
stomatitis, GI upset ( most common )
• Abdominal distention.
- Neutropenia , reversible alopacia ( rare)
• Shock.
Sites of EP implantation :
Ampullary (70%) >> isthmus (12%) > fimbrial (11%) > ovarian (3%) >
interstitial (2%) > abdominal (1%)
Risk Factors :
•previous ectopic pregnancy.
• gynecologic :
ƒ- IUD use – increased risk of ectopic if pregnancy occurs
ƒ- history of PID (especially infection with C. trachomatis), salpingitis.
ƒ- infertility .
ƒ- clomiphene citrate (for induction of ovulation)
•previous procedures :
ƒ- any surgery on fallopian tube .
- abdominal surgery for ruptured appendix, etc.
ƒ- IVF pregnancies following ovulation induction .
• smoking .
• structural :
ƒ - uterine leiomyomas .
ƒ- adhesions .
ƒ - abnormal uterine anatomy (e.g. T-shaped uterus )
Box( 1-1 )
Investigations
• Quantitative β-hCG levels : normal doubling time with intrauterine pregnancy is 1.6-2.4 d
in early pregnancy
ƒ -rise of <20% of β-hCG is 100% predictive of a non-viable pregnancy
ƒ - prolonged doubling time, plateau, or decreasing levels before 8 wk implies nonviable
gestation but does not provide information on location of implantation.
ƒ -85% of ectopic pregnancies demonstrate abnormal β-hCG doubling.
# slow rising of B-hCG In 48hr (increase <50% in 48hr or in plateau level or decreasing level
>> EP
• ultrasound :
ƒ U/S is only definitive if fetal cardiac activity is detected in the tube or uterus.
specific finding on transvaginal U/S is a tubal ring.
# US finding that suggest EP :
1- Empty uterus + BhCG level above the discriminatory zone .
2- Adenexal mass.
3- Echogenic fluid (Hemoperitoneum) or blood clots in the cul-de-sac .
# Discriminatory criteria of BhCG :
1500 -2000 mlU/ml + presence of IU pregnancy by Transvaginal US.
6000 – 6500 mlU/ml + presence of IU pregnancy by abdominal US .
This is Normal discriminatory zone in IU pregnancy.
But If the pregnancy is absent ( empty uterus ) by US + BhCG above discriminatory
zone >> Ectopic Pregnancy .
• laparoscopy (for definitive diagnosis).
Treatment :
• goals of treatment: conservative (preserve tube if possible), maintain hemodynamic stability .
• surgical (laparoscopy) :
- linear salpingostomy if tube salvageable
- salpingectomy if tube damaged or ectopic is ipsilateral recurrence.
-15% risk of persistent trophoblast; must monitor β-hCG titres weekly until they reach non-detectable
levels.
-consider Rhogam if Rh negative.
- may require laparotomy if patient is unstable, extensive abdominal surgical history, etc.
• medical = methotrexate See box (1-1 )
‫يفضل تعرفوا االنديكيشن و الكونترا االنديكيشن و السايد افكت لتحصيل أفضل‬
* Follow the B-hcg level every 48h, for 3 measurements to confirm that it continue to
decline . and then follow it weekly until β-hCG is non-detectable .
- plateau or rising levels suggest persisting trophoblastic tissue (requires further treatment).
Prognosis :
• 9% of maternal deaths during pregnancy.
• 40-60% of patients will become pregnant again after surgery.
• 10-20% will have subsequent ectopic pregnancy.
Important notes :
• fourth leading cause of maternal mortality, leading cause of death in first trimester.
• increase in incidence over the last 3 decades.
• three commonest locations for ectopic pregnancy: ampullary (70%), isthmic (12%), fimbrial(11%) .
CTG
1- Contractions :
Record the number of contractions present in a 10 minute period . Each big square is equal to 1
minute, so look at how many contractions occurred within 10 squares. assess contractions for the
following: Duration - Intensity
2-
Baseline heat rate : Normal rate 120 – 160 bpm
o Fetal tachycardia
1. Fetal hypoxia
2. Chorioamnionitis – if maternal fever also present
3. Hyperthyroidism
4. Fetal or maternal anemia
5. Fetal tachyarrhythmia
6. intrauterine infection
7. excessive oxytocic augmentation of labor
8. atropine , β-adrenergic agonists
o Fetal bradycardia :
Post-date gestation
- Occiput posterior or transverse presentations
compression - Cord prolapse - Epidural & spinal anesthesia
Prolonged cord
Maternal seizures
-
Rapid fetal descent
- local A, β-adrenergic blockers
3- Baseline Variability :
o
o
o
Most important sign of fetal wellbeing
Short-term or beat-to-beat variability. control by parasympathetic . Normal short-term
variability fluctuates between 5 and 25 beats/minute.
Long-term variability. control by sympathetic . The normal long-term variability is 3 to 10
cycles per minute.
o Reduced variability :
Fetal sleeping – this should last no longer than 40 minutes – most common cause
acidosis (due to hypoxia) – more likely if late decelerations are also present
Drugs – opiates / benzodiazepines / methyldopa / magnesium sulphate
variability is reduced at earlier gestation (<28 weeks)
abnormalities
o Increase variability :
o
Early hypoxemia - Fetal movement -
Fetal arrhythmia
Fetal
Fetal tachycardia
Prematurity –
Congenital heart
4- Periodic changes; - Changes in FHR in relation to contraction
Accelerations :
are transient increases in FHR of 15bpm or more above the baseline and lasting 15 seconds. This is a
normal response always reassuring , conducted by Sympathetic >>> due to fetal movement or
stimulation
Decelerations :
are transient episodes of decrease of FHR below the baseline of more than 15 bpm lasting at least 15
seconds.
EARLY DECELERATION (HEAD COMPRESSION) :
start when uterine contraction begins and recover when uterine contraction stops. Due to The pressure
on the fetal head leads to increased intracranial pressure that elicits a vagal response (Parasympathetic
), not important clinically .
LATE DECELERATION (UTEROPLACENTAL INSUFFICIENCY) :
This pattern are shifted to the right in relation to the contraction. usually indicate fetal metabolic
acidosis (Myocardial depression ), Fetal hypoxia due to UTEROPLACENTAL INSUFFICIENCY
(Parasympathetic ; vagal )
Reduced utero-placental blood flow can be caused by:
Maternal hypotension
Pre-eclampsia
- Uterine hyper-stimulation
VARIABLE DECELERATION (CORD COMPRESSION) :
Variable decelerations are caused by umbilical cord compression(Parasympathetic ). causes a sudden
increase in blood pressure in the central circulation of the fetus.
o Mild to moderate>>> not significant
o Severe >>> drop 60 beat for 60 s. >>>or 60 below the baseline
o Prolonged repetitive or deep are not reassuring
The presence of persistent variable decelerations indicates the need for close monitoring. Variable
decelerations without the shoulders is more worrying as it suggests the fetus is hypoxic.
Sings of well-fetal being :
.Normal baseline, Normal variability ,No late deceleration and No sever variable deceleration .
For more detail : http://www.mediafire.com/download/2uery27f339c221/CTG.docx
Uterine Fibroids
Uterine fibroids (leiomyomas) are benign tumors derived from the smooth muscle cells of the
myometrium. They are the most common neoplasm of the uterus. Their malignant potential is
minimal.
Causes and Pathogenesis: not known, but research and clinical experience point to these factors:
genetic changes and ovarian sex steroids (estrogen and progesterone) which appear to promote the
growth of fibroids. Leiomyomas rarely develop before menarche and seldom develop or enlarge
after menopause due to decrease in hormone production, unless stimulated by exogenous
hormones; on the other hand, it can also enlarge dramatically during pregnancy. However, many
fibroids that have been present during pregnancy shrink or disappear after pregnancy, as the uterus
goes back to a normal size.
Risk factors: There are few known risk factors for uterine fibroids: increasing age during the
reproductive years, family history, nulliparity, higher body mass index, onset of menstruation at an
early age, race (black women are more likely to have fibroids than women of other racial groups).
Characteristics of Leiomyomas: Leiomyomas are usually spherical, white, well-circumscribed, firm
lesions. Leiomyomas always arise within the myometrium (intramural), but some migrate toward the
serosal surface (subserosal) or toward the endometrium (submucosal). Rarely, pedunculated
subserosal myomas attach to the blood supply of the omentum or bowel mesentery and lose their
uterine connections to become parasitic leiomyomas.
Symptoms: Most uterine leiomyomas cause no symptoms. The symptoms depend on fibroid
location, size and number. Symptomatic patient may complain of:
Abnormal uterine bleeding (intermenstrual bleeding or menorrhagia) usually due to submucosal or
intramural fibroids, pelvic pressure (if the fibroid protrudes above the pelvis), pelvic pain (fibroids
are not generally painful, but severe pain may be associated with red degeneration (acute infarction)
within a fibroid, which occurs most commonly during pregnancy but in the most common observed
degenerative change is that of hyaline acellularity), frequent urination (if the fibroid presses on the
bladder) usually occur with subserosal fibroids, dyspareunia (common with incarceration of myomas
within the pelvis) and infertility (submucosal leiomyomas may be associated with an increased
incidence of infertility because of placentation challenges).
Differential Diagnosis: The most common differential diagnoses are an ovarian neoplasm, a tuboovarian inflammatory mass, a pelvic kidney, a diverticular or inflammatory bowel mass, or cancer of
the colon. Ultrasonography may visualize the fibroids and identify normal ovaries apart from the
leiomyomas.
Investigation and Diagnosis: The diagnosis of uterine fibroid is based on the history, clinical
presentation, and the results of bimanual pelvic exam. So further investigation may be needed to
confirm presence of uterine fibroids, which are:
Lab tests (to investigate potential causes. These might include CBC to determine if there anemia
because of chronic blood loss and other blood tests to rule out bleeding disorders or thyroid
problems), Ultrasound (is modality of choice in the detection and evaluation of uterine fibroids, US
has a sensitivity of 60%, a specificity of 99%, and an accuracy of 87%.), Pelvic MRI (show the size and
location of fibroids, identify different types of tumors and help determine appropriate treatment
options, also assessing disease in patients in whom US findings are confusing, it has a sensitivity of
86-92%, a specificity of 100%, and an accuracy of 97%), Hysterosonography (is used to get images of
the uterine cavity and endometrium. This test may be useful if there heavy menstrual bleeding
despite normal results from traditional ultrasound), Hysterosalpingography (used if infertility is a
concern, also determine if the fallopian tubes are open), Hysteroscopy (can detect uterine fibroids
projecting into the uterus, but cannot see any part of a fibroid in the uterus wall or outside the
uterus) and Uterine biopsy (if cancer is suspected).
Management: In general, if the fibroids are small, asymptomatic or cause only mildly annoying signs
and symptoms that the patient can live with, watchful waiting could be the best option. Unless the
fibroid is excessively large (>12-week gestational size) or is implicated as a cause of infertility in a
woman seeking pregnancy, the first line of treatment is targeted to her symptoms.
Medical Management: To help prevent more growth of the fibroid, stop taking birth control pills or
hormone replacement therapy maybe recommended. However, in some cases, oral contraceptives
are prescribed to help control the bleeding and anemia from fibroids.
NSAID: Antiprostaglandine (ibuprogen) to relive pain.
GnRH Agonists: Is prescribed to shrink fibroids. These drugs are expensive and shouldn't be taken for
more than six months due to the risk of developing osteoporosis. A low-dose of progestin may be
given with GnRH agonists to avoid osteoporosis and menopausal symptoms. Once women stop
taking the drug, the fibroids regrow. Therefore, this treatment is usually given primarily to shrink the
size of the fibroids or to improve anemia in preparation for surgery.
Selective antiprogesterone receptor antagonist: used to reduce the size of uterine myomas without
producing the changes in bone density noted with GnRH agonists and without untoward
glucocorticoid effects.
Progestin-releasing Intrauterine Device: It doesn't shrink the fibroids, it can control the associated
bleeding and cramping.
Generally, failed medical therapy or large uterus (>12-14 weeks gestational size) need surgical
intervention.
Surgical Management: Myomectomy or uterine artery embolization: are used if the fertility is
desired. Both procedures are usually used for a limited number of leiomyomas. If the endometrial
cavity is entered during myomectomy, future delivery must be by cesarean birth. If an inadequate
amount of uterine tissue remains, a hysterectomy may be needed. After UAE is performed,
pregnancy is still possible but is higher risk.
Endometrial ablation: used if desired uterine preservation or poor surgical risk.
Hysterectomy: is definitive therapy, if there no desired fertility or uterine preservation. If the uterus
is large or bulky, laparotomy is generally the preferred approach. GnRH Agonists is used if vaginal
hysterectomy will be done.
IUGR
When the birth weight of a newborn infant is below the 10th percentile for given gestational age. It’s
two type (symmetrical & Asymmetrical)
Causes:
Maternal : poor nutritional intake , smoking , drug abuse , alcoholic ,cyanotic heart disease ,
pulmonary insufficiency and antiphospholipid syndrome.
Placenta : any condition that affect the transfer this will lead to placenta insufficiency ( HTN, chronic
renal disease and pregnancy induce HTN)
Fetal : intrauterine infection ( torch ) , congenital anomalies and chromosol abnormality .
In Hx:
-
Fetal assessment if IUGR remote from
term :
reassure dating
Same problem before.
Genetic disorder in the family
Chronic illness & is it control well?
Smoking , alcohol , drug abuse
Daily kick count
Serial fetal growth ultra sound q 3-4 wk
BBP or NST once/ twice weekly
Umbilical artery Doppler velocimetry
PE:
- uterine size to GA
- may oligohydramnios.
Dx: fundal height and sonographic parameter.
BPD
Symmetrical
( mostly due to fetal
cause)
Decrease
HC
Decrease
AC
Decrease
FL
Decrease
Head to
abdomen
circumference
normal
Asymmetrical (mostly
due to placenta
&maternal cause)
Decrease
Increase
TTT:
Pre- pregnancy : improve nutrition , stop smoking , control chronic illness if we can.
Antepartum : avoid complication,,, , so, in 34 week and above if US suggest IUGR delivery is
indicated ( don’t forget lung maturity ) .
Labor and delivery : monitor for high risk group to detact fetal distress ( hypoglycemia, RDS
((acidosis)).
PROM
PROM or amniorrhexis: rupture of
membranes prior to labour at any GA
PPROM: rupture of membranes before 37 wk
AND prior to onset of labour
History
History of fluid gush or continued leakage
Presence of RF ( etiology ) : infection
(bacterial vaginosis , cervicitis, vaginitis,
STI, UTI), multiparty, cervical
incompetence, uterine anomalies ,
trauma , polyhydramnios , prior or family
history of PROM, low socioeconomic
class/poor nutrition, antepartum vaginal
bleeding ,
Maternal risk
Chorioamnionitis & endometritis
↑rate of CS
Failed induction
PPH
Placental abruption
Fetal Risk
Premature delivery
infection
Pulmonary hypoplasia <22WK
Oligohydramnios & it’s consequences
Malpresentation
Cord prolapse
Investigation
Sterile speculum exam (avoid introduction
of infection)
Pooling of fluid in the posterior fornix
, MAY observe fluid leaking out of cervix on
cough/Valsalva
Cultures (cervix for GC, lower vagina for
GBS)
Assess fetal lung maturity by L/S ratio of
amniotic fluid
Amniotic fluid should also be examined
with Gram stain and culture.
Monitor vitals and watch for sign of
chorioamnionitis ( Deliver urgently if
evidence of fetal distress , placental
abruption or chorioamnionitis )
Prophylactic AB ( IV ampicillin +
erythromycin for 48 ,then oral
amoxicillin + erythromycin q8h for 5
days )
Steroid
(Dexamethasone 6 mg I.M 12 hrly for 48
hrs Betamethasone 12.5 mg 12 hrly for
24hrs )
Nitrazine (amniotic fluid turns nitrazine
paper blue)
Ferning (high salt in amniotic fluid
evaporates, looks like ferns under
microscope)
Suspect chorioamnionitis if
↑maternal temperature
fetal tachycardia tender uterus
uterine irritability on NST
Management
Acquire the following data and manage
accordingly:
Daily BBP
U/S for GA
IF >36 WK :
Awaiting the onset of labor for 12-24h
Termination after 24 h
If <36wk
BBP: biophysical profile, GA: gestational age, CS: caesarian section, NST: non-stress test, GBS: group
B Streptococcus
68
( History of PROM )
Personal Data:
1) Name.
2) Age.
3) Marital status.
4) )Gravity & parity.
5) Weeks of gestation.
C.C:
Gush of fluid
HPI:
Analyze the symptom
Onset ,amount, color, odor, continues or
Intermittent & associated with blood clots,
pain, fever, history of trauma, urinary
incontinence, vaginal infection, previous PROM or PTL & smoking.
Present OB History:
Polyhydramnios , Multiple gestation
Past OB History:
Previous PROM ,Previous PTL
Past Gynecological history:
Past medical & surgical History:
HTN, DM, cardiac & hematological disease.
Family History:
HTN, DM, cardiac & hematological disease.
Social History:
PTL
Definition: Regular uterine contractions (4 per 20 minutes or 8 per 60 minutes) and / or cervical effacement of
80% or cervical dilatation of 2cm or more) after 24 weeks of gestation and before completed 37 weeks
gestation.
Early symptom : menstrual like cramp – new low back pain – pelvic pressure – change in vaginal discharge
Pathogenesis:
Activation of Fetal Hypothalamic Pituitary Adrenal axis (ass with maternal depression, stress)
Inflammation
Decidual hemorrhage
Pathological uterine distention
Pathological cervical change
RISK FACTORS FOR SPONTANEOUS PRE-TERM LABOUR
•Previous preterm delivery
•Multiple gestation
•Maternal history of one or more
spontaneous second-trimester
miscarriages (PP and AP ).
OBSTETRIC
DEMOGRAPHIC
UTERINE
INFECTIONS
Clinical Diagnosis
(predication )
Preterm Labour
Persistent uterine
contractions
4/ 20 min or 8/ 60 min
Cervical change
• Low socioeconomic status
• Non-white race
• Maternal age <18 years or >40 years
•Fibroids
•Uterine septum
•Bicornuaateuterus
•cirvical incompetance
•Chorioamnionitis
•Bacterial vaginosis
•UTI
Management of
Preterm Labour
Bed rest,
hydration and
sedation
80% effacement or> 2cm dil.
tocolysis
Complication of preterm labor ( morbidity ) :
cerebral palsy
retinopathy of prematurity
respiratory distress syndrome
necrotizing enterocolitis
bronchopulmonary dysplasia
intraventricular haemorrhage
PREVENTION
Smoking cessation.
Good prenatal care
Transvaginal ultrasound of
cervical length is
recommended only for highrisk pregnancies
Vaginal
fibronectin
transportation
for rule out
for steriod
Reduction of multiple
gestation
Steroids.
Cerclage
Cervical U/S
for cervical
lenght
bet 24-34 WK
History of PTL
Personal Data:
1) Name.
2) Age.
3) Marital status.
4)
Gravity & parity.
5) Weeks of gestation.
C.C:
Lower abdominal or back Pain & duration
HPI:
Analyze the symptom :
Site, onset, duration, frequency, progression, nature, aggravating or reliving factor, radiation,
shifting
Associated symptoms (bleeding, discharge, fever, GI symptoms or urinary symptoms).
Present OB History:
PROM
DM
HTN
polyhydramnios
multiple gestation
Infections.
Past OB History:
previous PTL
Past Gynecological history :
Past medical & surgical History: HTN, DM, cardiac & hematological disease.
Family Hx : HTN, DM, cardiac & hematological disease
Social History:
Post Partum Heamorrage
Primary( early) postpartum hemorrhage: is the loss of < 500 ml of blood following vaginal delivery,
or < 1000 ml ofblood following cesarean section or 1500 ml of blood following C/S hysterectomy
within 24 hours and If
less than 500ml and causing hypovolemic shock. Can occur before, during, or after placenta delivery.
Secondary( late) postpartum hemorrhage: It is a blood loss of a volume greater than expected after 24 hours
Within the first 6 weeks of delivery [mainly due to trauma].
- Secondary PPH is more likely due to infection and retained placental tissue.
- Hemorrhage is still one of the leading causes of maternal mortality all over the world.
- Incidence of primary PPH is 10% of all delivery.
Causes & Risk factors of PPH :
-
Other Causes & Risk factors of PPH:
Prevention of PPH by :
1-Active management of third stage of labor(AMSL) for all women : i.e
*Syntometrine 10IU (IM) at delivery of anterior shoulder
*cord traction
*uterine massage after delivery of placenta
2-Correcting anemia prior to delivery
3-Episiotomies only if necessary
Examination
*examine genital
Tract .
*inspect placenta
* observe clotting
and manual
exploration
of the uterus to
rule out birth
canal injury
and retained
placenta & if birth
canal injury
present Suturing
under anesthesia
ex : FFP , platlets
transfusion
Notes :
12345-
IV oxytocin 20-40 IU in 1000-1500 ml/hr is acceptable alternative for AMTSL
Carbetocin IV instead of oxytocin in elective c/s
Utrine atony most common cause of PPH
Thrombin=coagulopathy like : DIC, hemophilia , aspirin use , vWD (most common )
Ergometrine can be used as 2nd choice to oxytocin & it contraindication in pt with HTN .
5- Prostaglandins can be used as (PGF 1 alpha) and it is contraindication in CVS, resp, renal
and hepatic dysfunction
6- Tranexamic acid (antifibrinolytic ) can be used
7- DDx of secondary pph :
*retained placenta
*infections
*endometriosis
*sub-involution of the uterus
Partogram & Abnormal labour
A partogram is used to monitor the progress of labor once the labor is establish
ed.
The onset of labor is defined as regular, painful uterine contractions resulting in
progrssive cervical effacement and dilatation.
Identification data
o Name.
o Age.
o Parity (number of times that she has given
birth of a fetus with gestational age of 24 or
more regardless was born alive or stillborn)
o Weeks by date or scan.
Fetal Heart Rate FHR
o Normal: 120 – 160 beats/min.
<120 bradycardia
>160 tachycardia
In the 1st stage of labour,
we assess the heart rate
every 15 mins.
In the 2nd stage of labour, we assess it every 5 mins, so a continuous
fetal heart monitor.
When membranes rupture, we should record if the heart rate is
present or not, as well as the character.
Amniotic fluid (liquor)
o When the membrane are intact, mark
“I“
o When the membrane is ruptured:
If the liquor is Clear, mark “ C “
If the liquor is stained Meconium, mark “ M “
Meconium: is the fetal feces (GI secretion of fetus).
If the liquor is stained with Blood, mark “ B “.
If the liquor is Absent, mark “A “.
o If she comes with ruptured membrane: write the duration in the
beginning;
e.g., she had ruptured membrane 5 hours ago.
o Color of liquor:
Normally, the liquor is Clear (watery, or slightly yellowish or
whitish).
Dark greenish: If stained with meconium.
In case of hypoxia, or asphyxia of the fetus during delivery,
this meconium is released staining the amniotic fluid.
Blood: with abnormal placental separation.
Purulent: indicates infection.
Molding
Molding is the overlapping of skull bones when the fetal head passes through
the birth canal. It is normal to have some degree of molding during labor but
excessive molding might indicate
cephalo-pelvic disproportion and
Caesarean section is then required.
Degree of molding
1. The bones are separated normally (suture is still felt).
2. The bones are touching each other “approximation”
3. The bones are overlapping but can be easily separated with digital
pressure.
4. The bones are over lapping and cannot be separated by digital
pressure (sign of cephalo-pelvic disproportion)
Mild moldings (2 or 3) are part of the normal labour as they help to facilitate
the passage of the baby since it decreases the transverse dimeter of the fetal
head. However, the severe molding (4) is harmful as it may lead to
interacranial hemorrhage.
Cervical Dilatation
The dimeter of the internal os of
the cervix is measured in
centimeters by vaginal
examination from 0cm to 10cm,
with 10cm corresponding to
complete cervical dilatation.
The rate of cervical dilatation during the active phase is usually around 1 –
1.2cm/h in primipara and around 1.5cm/h in multipara.
o Further examinations are made at least every 4 hours, preferably every 2
hours in active stage of labour until full dilatation.
o The WHO put 2 lines:
Alert line.
Action line.
o The cervix should be fully
dilated and the head
engaged before reaching the alert line.
o If the dilatation is prolonged and touches the alert line, this alerts the
doctor to reassess the patient to see where the problem is.
o If it is prolonged till it touches the action line, the doctor should take an
action:
If there are no sign of obstruction or fetal distress
Oxytocin infusion.
Ventouse or forceps are used if needed.
If there are sign of obstruction or fetal distress
Cesarean section.
o The problem can be in:
Power, or
Passage, or
Passenger.
Power (Uterine Contraction):
o The uterine contraction should be effective.
o At least 3 contractions every 3 minutes.
o Each contraction lasts for 40 – 60 mins.
o In the first stage, only the power of contraction is needed whereas
in the second stage bearing down of the mother is also needed.
Passage (pelvic):
o She may have a narrow pelvis.
o Assessed by pelvimetry to see the AP diameter.
Passenger (fetus):
o The fetus may be big.
o Malpresentation.
o Malposition.
Descent of the head
o The descend of the head is assessed by abdominal examination following
the rule of fifth.
o Assess also, the station of the head of the head by vaginal examination:
. Station 0: at the level of ischial spine.
. Station +1: 1cm above the ischial spine.
. Station +2: 2cm above the ischial spine,…etc.
. Station -1: 1cm below the ischial spine.
. Station -2: 2cm below the ischial spine,…etc.
Uterine contraction
o There are vertical columns of 5 squares in the partogram.
o Each square represent one contraction.
∙ Assess the number of contractions in 10 mins period.
∙ A
s
s
A
s
sess the duration of each contraction.
- Measure in seconds from the time when the contraction is
first felt abdominally until the contraction phases off.
o Normally, there should be at least 3 contractions on every 10 mins, and
each contraction lasts at least for 40 mins.
o If the contractions are less → called hypotonic uterine action
o CTG can use to confirm the utrain contractions
o It help to assess the amplitude , duration and number of contraction
o It also , measure the fetal heart rate
Oxytocino
o Syntocinon is a synthetic form of oxytocin indicated for the induction and
o
o
o
o
augmentation of labour.
It should not be given in as a large bolus because it can cause a marked
transient fall in maternal blood pressure.
The contraction is recorded on the upper line and the rate of infusion
(drops/min) is recorded in the bottom line.
They are noted from the time the IV drip is started.
It is quite important to monitor oxytocin infusion because over dose may
lead to uterine rupture. So that it has a separate part in the partogram.
Drugs given and IV fluids
o All given drugs and fluids during the labour should be recorded with their
dosage, and routes of administration.
BP, pulse & Temperature of the Mother
o The blood pressure is recorded every 2 hours.
o The pulse is recorded every 30 mins.
o The maternal temperature is also recorded in the bottom line.
Urine
o The amount of the urine is noted.
o A urine sample is obtained and checked for the presence of ketones and
proteins.
o Proteinuria and hypertension are seen with preeclampsia.
o Ketones (acetones): with DKA.
Advantages of partogram
All the necessary information is on a single sheet of paper
which is easier than making detailed notes
It is a straight forward . both nursing and medical staffs can
understand the progress of labor by looking to it and this will
facilitate to them distribute their duties
It has good value to estimate the expected time of delivery in
case of normal progress
It serves as an early warning in case of impending problems
so that a paper action is considered
Pap Smear
Definition: It is a medical procedure in which a sample of cells of a woman
cervix to be spread on microscopic slide and examined under the
microscope for pre-malignant or malignant changes.
Indications: Screening for malignant and premalignant conditions of the
cervix.
Candidates for pap smear:
Screening should start by the age of 21 regardless of sexual activity.
Repeated every 3 years between the ages of 21-65.
More frequent pap smear is recommended for women having these risk
factors:
Positive sample of cancerous or precancerous cells.
HIV infection.
Immunocompromised women.
Note to remember: pregnancy is NOT a contraindication for Pap smear.
Women underwent subtotal hysterectomy should continue screening
according the guidelines mentioned above.
General rules:
Introduce yourself and take consent.
Check privacy and explain the procedure to the patient.
Have chaperone with you.
Take history:
LMP.
History of abnormal Pap smear.
Vulvar or vaginal symptoms.
Contraceptive history.
Sexual history.
Wash your hands and wear gloves.
Position the patient in lithotomy position with ONLY the genital area
exposed.
Examine the genital area.
It should not be done during menstruating period.
Patient should avoid sexual intercourse prior the test.
equipments:
Good light.
Gloves.
Speculum.
Lubricant.
Spatula.
Brush.
Rovers brush.
Slide (with name of the patient written on it).
Fixative.
Types of Pap smear:
Conventional type: prepared by scrubbing the spatula or the brush directly
on the slide.
Liquid-based Pap smear: (SurePath) done by breaking the rovers brush
into a solution after taking the sample of the cervix and send it to
cytology.
Procedure:
Warm the blades of speculum with warm water and apply lubricant
(ensure the lubricant is not placed at the end of speculum as this may
alter the results).
Inform the patient that you are starting the procedure and use
nonedominant hand to separate the labia minora and insert the speculum
with your dominant hand with the screw facing sideways.
After inserting the speculum turn it, so the screw face upwards.
Open the speculum.
Inspect for any gross pathology (lesions, masses, discharge) and identify
the transitional zone.
o Conventional pap smear method:
Insert the cervical brush into cervical opining and rotate it 3 times then
take it out with making sure it does not touch anything then swap it
immediately on it proper position in the slide (endocervical sample).
Then place the ayre's of spatula on cervix and rotate it three times and
take it out, swap it on its proper position on the slide (ectocervical
sample).
Spray fixative on the slide and send it for cytology.
o Liquid based pap smear method:
Insert the rovers brush in the cervical opining and rotate it five times (it
will take endo and ectocervical sample) then take it out and make sure it
does not touch anything and break it into the solution cup and send it to
cytology.
Tips:
Explain to the patient that the result will be available within 3 to 4 weeks.
You should know the risk factors for cervical cancer.
You should know about high risk for HPV and vaccination indications and
doses.
Causes of ASCUS.
OB Pic : file:///C:/Users/t/Downloads/Blank%2024.pdf
‫ت في رِْزقي عَلَى اللَِّه خَالقي‬
‫تَوك ْل ُ‬
‫ليس يفوتني‬
‫وما ُ‬
‫يك من رزقي ف َ‬
‫به اهلل العظيم بفضلهِ‬
‫سيأتي ِ‬
‫ُ‬
‫ُ‬
‫ففي أي ٍ‬
‫النفس حسرة‬
‫تذهب‬
‫شيء‬
‫ُ‬
‫ُ‬
‫شك رازقي‬
‫وأيقنت َّ‬
‫أن اهللَ ال ٌ‬
‫ُ‬
‫الغوامِ ِق‬
‫ان في قَاع البَ َحارِ َ‬
‫َولَو كَ َ‬
‫ِ‬
‫بناطق‬
‫اللسان‬
‫ولو لم يكن مني‬
‫ُ‬
‫‪Done by:‬‬
‫‪Noura Abdulazeez‬‬
‫‪Sundos Anis‬‬
‫‪Zeyad Qadi‬‬
‫‪Reviewed By :‬‬
‫‪Reference :‬‬
‫‪Toronto Notes‬‬
‫‪Lecture Notes‬‬
‫‪PubMed‬‬
‫ن رِْز َق الْخَالَئِ ِق‬
‫َوقَ ْد قَ َسمَ َّ‬
‫الر ْحمَ ُ‬
Anatomy :
-Normal audible frequency: (20 – 20000 Hz).
-Range of speech: (500 – 2000 Hz)
-In noise induced HL HL is seen at 4000 Hz.
--audiometry test range (250 – 8000 Hz
1-to collect sound
waves.
2-aid in sound
Resonance
localizationchamper
for frequency region
(2000-5500 Hz)
What is the (impedance mismach)?
it is a normal loss waves=30 db,why?
cause the waves travel from air filled
(middle ear)to fluid filled(cochlea)
ossicles
1) functional
-hysterica
-malingerer
2) organic:
1-conductive HL:
So the compensation going to be by:
1-TM –footplate= 17.1 X
2-lever action of ossicles= 1.3 X
transforming ratio=17 x 1.3 =22.1
finally the overall magnification=27 dB
!!‫بحسابات معقدة طلعت كدة‬
Cochlea :
has basilar membrane, tectorial membrane and hair cells
work together for the movement of sound waves.
:‫المكان المخصص لكل نبرةصوت‬Tonotopic arrangement
1-basel end of basilar membrane for: high frequency
voices.
2- Apical end of the membrane for: low frequency voices.
Hx: chronic HL without problems in speech
Ex findings: -air bone gap
- N speech discrimination.
-tympanometry
type B mostly.
-absent ipsi and contralateral stapedias reflex
It's 2 types:
1-congenital
eg. Atresia .
2-acquaired
Cerumen impact(wax)(most common)
Otitis external
Forging body.
stapedius ‫يقيس قدرة عضلة ال‬
‫على االنقباض لحماية االذن من‬
‫االصوات العالية‬
Ext. ear
Otosclerosis (2nd common )
ET dysfunction
COM, OME
Ossicular fixation
Trauma(drum perforation)
middle ear
2-Sensorinural HL(SNHL)
Hx: c.o HL .
Ex: - no air bone gap
-decrease speech discrimination.
-Normal tympanometry.
-good ipsi and contralateral stapedial reflex if <60db HL.
SNHL types : 1-congenital
2-acquaired
prenatal, genetic, rubella.
prenatal hypoxia, jaundice.
trauma: temporal bone fracture ,noise ,iatrogenic.
presbyacusis (bilateral HL, old age, most common).
inflame. : viral(measles &mumps),COM, TB.
ototoxic: aminoglycoside ,salicylate .
acoustic neuroma (unilateral HL ,old)
Menier's dis (vertigo ,HL, tinnitus).
3- Mix HL: Both air and bone will be below 20 in audiogram
There is air- bone gap
4- Neurogenic (retrochochlear ):
-No air bone gap.
-decrease speech discrimination. (roll-over phenomena)
- normal tympanogram.
-decrease or No ipsi and contra lateral stapedial reflex.
Diagnostic tests for HL :
Tuning fork(512
Hz) test
A)Rinne test/
Comparing bt air
and bone
conducting.
AC> BC
+ve(normal)
AC < BC -ve (it's
the diseased
ear)(ConductiveHL)
AC >BC +ve but
both reduced
(SNHL)
*in Conductive HL
,vibrations
lateralize to
diseased ear.
* in SNHL
,vibrations
lateralize to the
normal ear.
B) weber test:
Put the fork in the
center of the
forehead and
detect if it was
centrally or
lateralize .
lateralization:
Ipsilateral
conductive HL ,
and contralateral
SNHL .
Tympanometry
Audiometry
The tympanogram
)‫(التخطيط اللي حيطلع‬
-measure the pressure of external acoustic
canal which ( the compliance of TM and
middle ear against the pressure)
Normal range/
(-100 to +50)
-it's 3 types :
A(s and d)
As)Normal pressure + low amplitude
otosclerosis (fixed ossicles)
w/
Ad)N pressure + high amplitude w\ossicular
chain discontinuity or TM scaring.
B)no pressure
poor TM movement w/ OME
or perforated TM.
C) –ve pressure w/ Eustacian tube
dysfunction or early stage otitis media without
effusion.
The pure tone
audiometry
measures:
1- hearing
threshold (2508000 Hz)
2- speech
discrimination.
I already
mentioned the
audiometry
patterns in
deferent HL
and their
audiograms
previously ~
It's a sensation of rotational movement of the environment ,can be peripheral
(inner ear) or central .
Vertigo characteristics
Head move exacerbated.
Episodic
Ataxia
Vertigo
Emesis
If all present, likely vestibular disorder or migraine associated vertigo.
Causes of vertigo: central(neurologic cause) or( peripheral (inner ear or otologic ) represent 50%)
Vertigo DDx:
1} BPPV (benign paroxysmal positional vertigo):
most common cause of vertigo.
1- vertigo last seconds<1min and recurrent .
2- No HL
3-No tinnitus
4-vertigo increase with position changing .
5- nausea without vomiting .
#diagnosed by {Dix-Halpike maneuver}.
# ttt by repositioning maneuver (Epley by MD & Brandt by Pt) or spontaneously
2}Menieres: (b.c of endolymphatic hydrops over accumulation )
1- vertigo last min
hr <24hr and recurrent.
2-uni\bilateral HL (SNHL)
3- (+ve) tinnitus.
4- Aural fullness like pressure.
5- nausea and vomiting.
#ttt \ restrict salt intake , stop smoking.
diuretics and betahistine .
Intratympanic Garamycine injection.
Surgical (rare) vestibular neurectomy or labrynthectomy.
3}Labrynthitis(inner ear inflamation):
1- acute infection cause vertigo lasting days.
2- sudden SNHL (uni).
.‫مع وجود فقدان السمع‬vestibular neuritis ‫زي أعراض ال‬
4} vestibular neuritis (cause is idiopathic or viral).
1- acute sudden debilitation vertigo lasting hr to days.
2- ataxia .
3- nausea and vomiting .
4- Nystagmus beating towards unaffected ear.
5- investigations AUDIO: normal
ENG: reduced vestibular activity.
#ttt\ labyrinthine sedatives and antiemitics, rehabilitation.
5} Migraine.
periphral ‫ بينما جميع االمراض السابقة سببها‬central ‫الوحيد ال‬
1- similar to Meniere but without HL.
2- Triggers :
family Hx.
motion intolerance
menopause ,menses, stress , allergy.
photo/phonophobia .
Dietary triggers (chocolate ,blue cheese , nuts).
summary
General Considerations:
1- Age of the patient
Pediatric age group 15> most likely to be congenital or inflammatory.
Young adult 16-40 y same as pediatric
Late adult >40 most likely to be neoplastic and 80% of it would be malignant.
2- Duration of the mass
-Congenital: since birth.
-Inflammatory: days to weeks.
-Neoplastic: months even years.
3- Rate of growth
-Slow growth rate suggest benign cause .
-Rapid growth rate suggest malignant cause.
DDX:
1- Congenital
-Midline (thyroglossal cyst, Dermoid cyst, Laryngocele )
-Lateral (Branchial cyst, Venolymhpatic malformation)
2- Inflammatory
-Lymphadenopathy (bacterial, viral),
3- Neoplastic
-Metastatic head and neck carcinoma, Thyroid masses, Salivary gland neoplasm,
Lipoma, Lymphoma .
Examination:
-Inspection :
-Obvious masses, surgical scar, ask patient to swallow then stick tongue out
(thyroglossal cyst moves on tongue protrusion )
-Palpation :
-Site, shape, surface, consistency, color, temperature, tenderness
-Regional lymph node (hard:Malignancy, rubbery:lymphoma)
-Percussion :
- Retrosternal goiter
-Auscultation :
- Carotid bruit, Thyroid bruit.
Investigation:
-FNA( most important initial diagnostic procedure )
-CT ( distinguish cystic from solid mass, detection of metastasis
-MRI ( similar as CT but better for upper neck and skull base )
-CXR ( for retrosternal goiter )
-U/S (non invasive can be used in pediatric )
Definition & Pathophysiology :
Adenotonsillar disease (adenoiditis and recurrent tonsillitis) is a prevalent
otolaryngologic disorder aetiologically based on chronic inflammation
triggered by a persistent bacterial infection , persist predominantly intracellular
and within mucosal biofilms. The recurrent or chronic inflammation of the
adenoids and faucial tonsils leads to chronic activation of the cell-mediated
and humoral immune response, resulting in hypertrophy of the lymphoid
tonsillar tissue.
- size peaks at age 5 and resolves by age 12
Clinical features. : Hx. , P/E
- Nasal Obstruction :
Adenoid face ( open mouth , high arched palate , narrow midface ,
malocclusion )
Hyper nasal voice
Long term mouth breathing
Recurrent pharyngeal infection
Recurrent chest infection
Snoring and disturbed sleep , episodic sleep apnea in sever cases
- choanal obstruction:
Chronic rhinosinusitis /rhinitis
Obstructive sleep apnea
- chronic inflammation:
Nasal discharge, post-nasal drip, and cough
Cervical lymphadenopathy
- Eustachian tube :
Recurrent OM
Secretory OME
CSOM
- sleep apnea for adenoiditis or sore throat, dysphagia and halitosis for
recurrent tonsillitis
Diagnosis :
Enlarged adenoids on nasopharyngeal exam (usually with flexible
nasopharyngoscope)
Enlarged adenoid shadow on lateral soft tissue x-ray
Treatment :
Adenoidectomy (indications , contraindications and complications
.Toronto Notes2014 OT40)
Complications :
Eustachian tube obstruction leading to serous otitis media
Interference with nasal breathing, necessitating mouth-breathing
Sleep apnea/respiratory disturbance
Orofacial developmental abnormalities
Done by:
Jawaher Alzahrani
Mohammed Alahmadi
Shahd Hafiz
Zeyad Almatrfi
Rami Fawzi
Musaab Ahmed
Shoroug Almasoudi
Rawaa Almagrabi
Reviewed By :
Basmah Allogmani
Asmaa Salem
Reference :
lectures & royal notes
Medscape & Toronto
notes
Psychiatry made
redicioulsly
simple.Lecture
SOCIAL PHOBIA
Definition: marked and persistent fear of social
occasions in which one is exposed to unfamiliar people or
to criticism; patient feels that he/she will act in
humiliating or embarrassing way (e.g. public speaking,
eating in public) beyond voluntary control.
Prevalence:
13-16% life time prevalence and more in Females.
Onset usually after puberty.
More in young adults.
Hx:
Ask the patient if there is any provoking factor ?
As Exposure to stimulus almost always causes
immediate anxiety symptoms and may causes a
panic attack.
Exclude other disorders: Panic disorder (panic attack
w/o stimulus & unpredictable), GAD ( anxiety
symptoms w/o social stimulus), substance abuse,
alcohol.
Patient recognizes fear as unreasonable and avoids
stimulus (e.g. presenting a case, work interview, etc…).
if there significant interference with life(social, work,
personal life, etc…)
Duration of the social phobia is at least 6 months.
Anxiety symptoms in
Social phobia
Tachycardia
Sweating
Restlessness
Muscle tension
Mental block
Phobia= marked and
persistent fear that is
excessive or unreasonable,
cued by presence or
anticipation of a specific
object or situation
Management: indicated when there is disturbance of
Psychological/Behavior
al Therapy is better in
social phobia.
function:
Reassurance.
Psychological/ behavioral therapy: start cognitive
behavioral therapy by desensitization or flooding.
counseling
medical ttt: beta blockers ”control of performance
anxiety ” or low dose benzodiazepine for acute panic
attack + antidepressants “SSRI” when needed.
Prognosis:
chronic disease and may persist for years
Desensitization =
exposure to the stimulus
gradually and virtually to
control symptoms and
improve performance.
Flooding= confrontation
with the stimulus
suddenly until the patient
develops immunity.
1-Definition
Dementia is a mental disorder resulted from structural disturbance of brain that is
severe enough to interfere with normal activities of daily living, lasting for months and
years
2-Clinical manifestation :
-
-
The 1st symptom to appear is short memory disturbance.
The most important thing there is no impairment of consciousness but there is
generalize impairment of intellect, personality, and memory.
Behavior : reduction of interest, irritability, short tempered, but there is a
sudden explosion of anger or other emotion.
Mood : depression, lability mood.
Thought : slow, delusion, concrete thinking.
Disturbance: in orientation of :
1- Time
2- Place
3- Person
Impaired attention, concentration and memory.
Insight is impaired .
3-Causes :
1- Degenerative cause :
-Alzheimer : most common cause of dementia ,worsening with time
-Vascular ( multi infract ) : deterioration is stepwise ( this one has a worse
diagnosis because the strokes)
2345-
Metabolic causes
Endocrine causes
Intracranial tumor
Vitamin b12 and folic acid def.
4-Assessment of dementia:
ABCDEFGH-
Recent and remote memory
Language abilities (aphasia):
Apraxia
Agnosia
Executive function
Visuospatial skills
Calculating abilities
Look for frequently associated symptoms:
5-management :
A) if in aggression or anger explosion
1- give a tranquilizer such as halopridol to calm down the pt
6-RISK FACTOR:
— -Age
— -Family history: 4 fold
increase in first degree
relatives
— -Apolipoprotein E4
— -Female gender
— -Head trauma
— -Low education
-Down’s syndrome
( overproduction of amyloid
precursor protein
2- admit the pt
3-investigate to find the cause :
-CBC
-level of vit B12 and folate
-electrolyte imbalance and glucose
-renal function test
-liver function test
-thyroid function test
-CT scan of head
4-establish treatment:
-treat the underlying treatable causes (vit B12 and folate deficiency ...etc )
-pharmacological treatment (cholenistrase inhibitor "Rivastagmine
,donepezil ,galantamine "to prevent further degradation of acetyl choline to
improve cognitive function ---> effective in mild to moderate dementia that is
associated with cholinergic deficiency as Alzheimer disease
*dementia reassessment after 4-6 weeks after treatment to detect cognitive
improvement *
-non pharmacological:
— Pleasant activity with or with out social activity
Exercise
Hand massage
Art work
Purposeful activity ( volunteer activity, access to outdoor,..ect)
B) if not in aggression:
same as previous without step 1
Definition:
Recurrent episodes of altered mood and activity involving up & down
swings “mania & depression”
Types:
1. Mania.
2. Depression.
The episodes are usually weeks in duration.
*Euthymic: when the mood neither high nor low (between episodes).
First: Mania
At least 1 wk of mood disturbance characterized by elation, irritability,
expansiveness.
3 or more of the following sym. Must also be present:
Clinical features
Euphoria
extremely over active
disinhibited
Excessive talking & pressured speech
Racing of thoughts or Flight of ideas
grandiose delusion.
Patient sleeps very little.
Sexually over active.
Insight is impaired.
Aetiology:
genetic
1 parent – 25% chance in child
2 parent – 50-75% chance in child
MZ Twin- 40- 70% chance
DZ Twin- 20% chance
Treatment
Counseling
chemistry
Increased noradrenaline, serotonin
and dopamine activity
always the 1st step.
Acute management:
1. Antipsychotic drugs; maybe used alone or in combination
with other meds e.g. lithium or valproate or other mood
stabilizers in severe forms of mania.
Electro-convulsive therapy (ECT) one of the best, safest
treatment modalities, performed under ultra-short general anesthesia
Disadvantages of ECT: has poor compliance from the pt & it is
expensive.
Psychological & social treatments.
Prognosis
Generally poor especially with the absence of counseling.
Suicide rate of 10% in the depressive stage.
90% mania or depression recurrence” Average 4 episodes/10
years”.
minority develop rapid cycle w/ 4 or more episodes/ 1 year.
Mania
Sever
Psychotic symptoms
Grandiose delusions
Function is impaired
Hypomania
Less sever
No psychotic symptoms
Grandiose ideas
No impairment of function
When to admit to hospital??
DDx. Of mania:
Risk to harm himself or others.
Extreme over activity and disturbed behavior.
1. Substance abuse.
2. Schizophrenia.
Poor compliance.
3. High dose steroid
Absent family support.
Second: Depression
What is the different between depressive illness and depressive
symptoms?
Depressive symptoms: normal, associated with social, mental &
physical disturbance. They need social & behavior therapy and no
need for antidepressant.
5 or more of the clinical feature of depressive illness should be
present over period of at least 2 weeks Including:
Low mood and Loss of interest
Change in appetite 90% loose weight & 10% gain it.
Decreased energy and poor concentration
Loss of confidence or self esteem
Sleep disturbance of any type 90% sleep & 10% sleep.
Feels guilty and have suicidal ideas
Psychotic symptoms in severe depression.
Almost all depressed people wish to die, about 60% of them have
suicide thought and about 10-15% of them commit suicide.
Types of depressive illness; The difference between them “in severity
& duration of the symptoms”:
1. Mild
2. Moderate
3. Severe.
Etiology
Decreased noradrenaline, serotonin and dopamine activity in
depression.
Chronic illness or use of some mediation e.g. b-blocker, digoxin,
digitalis, OCP.
Genetics: if 1 parent have depression- 10% risk in child, MZ:DZ
twin 54:20%.
Management
Counseling
Assess suicidal risk
Antidepressant; chose new generation or old generations
Electro-convulsive therapy (ECT)
Psychological and social treatment.
When to admit to hospital??
Absent family support.
High suicidal risk.
Prognosis:
Mostly self limited, usually lasts for 6-8 months
60% of patient have recurrence
20% depression for 2 years or more.
DDx.:
normal sadness e.g. exams, hypothyroidism.
alcohol & drug abuse.
personality disorders.
anxiety
If the patient is not responding, why? What to do?
Resistant cases
Is the patient taking his medication regularly (compliance)
Is he taking the right drug!
Did he take the drug for enough period?
Is the dose enough!
Check the family and other factors.
Reviewing the diagnosis.
Initially about 30% do not respond, try changing the
antidepressant.
May add folic acid, lithium, carbamazepine
Note: please read about antipsychotics and antidepressant and their side
effect.
It's about 2-5% of general population .
Etiology :
Genetic (e.g monozygotic twin) .
Environmental ( unemployed , separated relationship, low
education, homeless, having medical diseases. Childhood trauma).
Neurotransmitter : low NE ,serotonin ,dopamine .
DSM5 Criteria : 5 or more of these symp present for 2 weeks including
core symptoms >> Low mood (core symp) , loss of interests (core sym),
sleep disturbance, guilt feelings, change appetite, agitation, suicidal
attempts , decreased energy/fatigue , impairment function .
Classification : mild / moderate / severe > (delusions ,2nd person
hallucination, catatonia, cotard's syndrome) .
DDX of depression : bipolar depression – anexity disorders-psychotic
disorders- dementia- substance abuse- pre menstrual syndrome .
Investigation: to roll out organic disease >TSH , CBC, folate & vit 12 .
Rx : SSRIs ( best choice ) , NASA , SNRI, TCA , MAOI .
Bipolar disorders
Manic episode
At least 1 w of 3 or more
hypomanic
Duration of mood
>(grandiosity, little sleep ,Excessive disturbance at least 4
days without affect
talking , racing Though or flight
function
ideas ,Distractibility, increase
Activity at work or home).
mixed episode
Meet criteria of manic
episodes & criteria of
depression for 1 week only .
Etiology: genetic (MZ twin , both parents) / neurotransmitter( high
serotonin ,dopamine & NE) .
Treatment : bood stabilizer (best choice) – antipschotic drugs –
nenzodiazepine – ECT 4 times twice weekly .
Anxiety is common normal response to a perceived threat, it is important to clinician
to be able to distinguish normal from pathological anxiety.
When anxiety is pathological :
1- it is inappropriate
2- there is either no real source of fear or the source is not sufficient to account for
the severity of the symptoms
3- symptoms interfere with function and personal relationships
Often have an early onset- teens or early twenties
Woman have higher prevalence for all AD( 3-2:1) exception for OCD & SAD( 1:1)
Panic
Disorder
Have a waxing and waning course over lifetime
GAD
such as diabetes in functional impairment and decreased quality of life
Anxiety disorders Etiology
Combination ( genetic, environmental, biological ) factors..
Post-Traumatic
Stress Disorder
Specific
Phobia
Similar to major depression and chronic diseases
Social
Anxiety
Disorder
OCD
Neurochemical changes:
Decrease of serotonin and GABA
Increased activity of norepinephrine.
Panic attacks are discrete periods of intense anxiety
that occur to pt. With panic disorder/ other mental disorders
It peak in several min. And subside within 25 min.
They rarely last > 1 hour
Attack can be either unexpected or come about
due to specifics trigger
DSM IV criteria
—
Recurrent unexpected panic attacks.
(no obvious precipitant)
At least one of attacks are followed by 1 month by 1>=
a. Continuous concern of having additional attacks.
b. Worry about implication of attack
Treatment: Acute initial
treatment with
benzodiazepine ( only for
short period up to 5 weeks).
SSRI : it is drug of choice for
panic disorder
SSRI takes 2 to 4 weeks to
be effective
Treatment should be For 1
year
Panic disorder co
—
morbidity agoraphobia ,
major depression and
substance dependence
c. Behavior will change due to attacks.
Prognosis:Good with treatment.
Course is variable, but often chronic,Relapse are common
Social anxiety disorder: A. A marked fear of one or more social or performance
situations in which the person is exposed to unfamiliar people.
The individual fears that he or she will act in a way (or show anxiety
symptoms) that will be humiliating or embarrassing.
B. Exposure provokes anxiety /panic attack.
C. The person recognizes that the fear is excessive or unreasonable.
D. situations are avoided or else are endured with intense anxiety or
distress.
Prognosis: Chronic disorder
Can disturb patient academic achievement, job& social development.
Treatment SSRI ,Beta blocked ( control symptoms of performance anxiety)
,Cognitive behavior therapy.
Specific Phobia :Marked or persistent fear that is excessive or unreasonable cued
by the presence or anticipation of a specific object or situation
The person recognizes the fear is excessive or unreasonable
It interferes significantly with the persons routine or function
Treatment : systemic desensitization
Gradual exposure to feared object / situation while teaching relaxation and breathing
techniques.
Obsessive-Compulsive Disorder
Obsessions as defined
(1) recurrent, persistent and intrusive thoughts, impulses, or images that
cause marked anxiety
(2) They are not simply excessive worries about real-life problems ( senseless
(3) the person attempts to ignore them or to neutralize them with some other
thought or action (4) the person realizes thoughts are a product of his or her
own mind
Compulsions as defined :
(1) Repetitive behaviors or mental act that the person feels driven to
perform in response to an obsession.
(2) the behaviors or mental acts are aimed at preventing or reducing anxiety
Etiology :Neurochemical: Abnormal regulation of serotonin
—
Genetic Rate are higher in first –degree relatives monozygotic twins than in
general population
Psychosocial:OCD is triggered by stressful life event
Treatment : SSRI :
first drug of choice
Higher than normal doses may be needed
It require 1 to 2 months to have an effect
Clomipramine a TCA with high serotonergic properties
Antipsychotic: adjunct therapy with serotonergic agent_ Risperidal ,
Aripiprazole
Behavioral treatment:
Exposure and relapse prevention
Prolong exposure to the obsesstional idea and prevention of the relieving
compulsion
Relaxation training
Generalized Anxiety Disorder ( GAD :Criteria DSM V)
Excessive anxiety and worry about daily events and activities for at least 6
months
B. It Is Difficult to control the worry.
C. The anxiety associated with 3>= of the following (1) restlessness
(2) fatigued .
(3) difficulty concentrating
(4) irritability
(5) muscle tension
(6) sleep disturbance (difficulty falling or staying asleep, or unsatisfying
sleep)
Treatment:
Pharmacological:
SSRI ,Effexore XR , Adjunct treatment with Benzodiazepine ( Clonazepam,
Diazepam )
Others:
Psychotherapy ,Relaxation
Prognosis:Chronic illness, with low probability of achieving recovery
Panic Disorder
Attacks of intense fear, No trigger,
duration 10-30 min.
Social phobia
Fear of embarrassment-panic attacks
in social situations
GAD
Worry++++++,about daily activities
PTSD
Nightmares, flash backs after major
trauma
OCD
obsessions and compulsions
Specific phobia
Irrational fear of specific object
/situation
Definition:
No satisfactory one.
It is a mental disorder defined in terms of abnormal clinical features of
behavior, affect, thinking and perceptions, in absence of organic disease.
Epidemiology: Prevalence 1%
Pathophysiology :
genetic theories
biochemical theories
Family studies Relationship to schizophrenia
Prevalence:
Second degree relative:5%.
Siblings:10%.
Child of one schizophrenic parent:14%.
Child of two schizophrenic parents:46%.
Twin studies: MZ:DZ Twin:42%:10 %.
Age of onset:
Disturbance of neurotransmitter function
Dopamine hypothesis: dopamine over activity in the
mesolimbic pathways, suggested by:
Amphetamines increase DA release, can
induce a psychotic symptom.
Antipsychotics block DA receptors.
Any age, but usually between 15-35.
Clinical Features:
Positive symptoms” Acute schizophrenia”: Psychotic symptoms, such as
hallucinations, which are usually auditory”2nd/ 3rd person hallucination”;
delusions” persecutory, primary, secondary, grandiose”; and disorganized
speech and behavior, thought “insertion, withdrawal, broadcasting”, lack
of insight” most common feature”.
Negative symptoms “chronic schizophrenia”: A decrease in emotional
range, apathy, poverty of thoughts, and loss of interests; the person with
schizophrenia has tremendous inertia, social withdrawal.
Cognitive symptoms: Neurocognitive deficits (e.g. abstract thinking,
neologism, tangentaility ) patients also find it difficult to understand
nuances and subtleties of interpersonal cues and relationships.
Mood symptoms: Patients often seem cheerful or sad in a way that is
difficult to understand; they often are depressed.
Types of Schizophrenia:
Acute: Positive symptoms.
Chronic: Negative symptoms.
Diagnostic criteria:
A. 2 or more of the following during I month:
1. delusions
2. hallucinations
3. disorganized speech.
4. Disorganized behavior.
5. Negative symptoms.
B. Signs of disturbance persist for at least 6months including “1 month of criteria
A Symptoms”
C. Significant Impairment of function.
D. Exclusion of substance abuse or general medical condition.
Aetiological theories:
Prognosis: the following are factors indicate either good prognosis\ poor
prognosis:
factors indicate good prognosis
Acute onset with obvious
precipitating factors.
2) Good premorbid
personality.
3) Mood symptom: depression.
4) Paranoid subtype.
5) Negative family Hx.
1)
factors indicate poor prognosis
Insidious onset with no
precipitating factors.
2) Earlier age of onset.
3) Family history of
schizophrenia.
4) Hebephrenic & simple
schizophrenia.
5) No compliance.
6)
Neuro-cognitive deficit.
1)
Prognosis:
Complete recovery:15%
Relapsing illness:70%
Poor outcome:10%
Suicide:5%
Management
1)
2)
3)
4)
Counseling.
Physical: Psychopharmacology “Antipsychotic, pt. may need antidepressant” & Electro-convulsive Therapy (E.C.T).
Psychological: support from family and staff.
When to hospitalize ?
Social treatment.
Resistant cases:
If a patient is not responding, consider the followings:
1. Acute psychotic
episode w/
impairment of
function.
2. Homicidal, suicidal.
3. Catatonia refusal of
food
4. Refusal of treatment.
Is the patient taking his medication regularly?
Is he taking the right drug!
Did he take the drug for enough period?
Is the dose enough!
Reviewing the diagnosis ? Drug abuse
initially about 30% do not respond, try changing the drug, try
clozapine.
Hx of schizophrenia
During a medical history for schizophrenia, the health professional will ask
some general questions, such as:
How are you feeling?
Have you recently noticed changes in the amount of energy you have
or in your appetite or sleep?
Have you recently had changes in daily habits, such as changing from
the day shift to the night shift? Does your work require that you travel
frequently?
Have you had unusually high stress lately (for example, due to events
such as the death of a loved one, a change in job, getting married or
divorced, or having a baby)?
Have you had any recent exposure to irritating chemicals or toxins?
Have you recently changed the amount of medicine you take or started
a new medicine?
Have you had any periods of time when you have lost track of time,
such as you "woke up" and didn't know what had happened? Have you
had any times when you were in a stupor?
The health professional will ask some questions specifically about unusual
experiences, such as:
Do you ever hear voices (or see things) that other people do not hear
(or see)?
Do you ever think that you are being given a special message, are
supposed to do a special project, or have been selected to be someone
special?
Are you having confusing thoughts that are hard for you to understand
or follow?
Do you get frustrated easily?
Do you think that you are in danger?
Do you think about hurting yourself or someone else?
Do you think that you are being followed, that someone is controlling
your thoughts, or that someone else knows what you are about to do or
say?
Ask other questions to see whether a person has symptoms of other
conditions, such as depression, anxiety, or heavy alcohol or illegal drug
use.
Ask about the use of illegal drugs known to cause the same symptoms
as schizophrenia, especially phencyclidine hydrochloride
(PCP), methamphetamine, and cocaine.
Also ask questions about family history, including any history of
schizophrenia or other mental illnesses.
The health professional may also ask to interview one or more family
members. During these interviews, ask the family member(s) to
describe the actions and behaviors of the person who has symptoms
that may be caused by schizophrenia.
1. Obsessions as defined as a recurrent, persistent and intrusive thoughts, impulses, or
images that cause marked anxiety
2.
Compulsions as defined as Repetitive behaviors or mental act that the person feels driven
to perform in response to an obsession.
The obsessions or compulsions cause marked distress, take > 1 hour/day or interfere
with the person’s normal routine or function
3. Common pattern of OCD:
Obsession about contamination ------excessive hand washing/ aviodance of feard
contamination
Obsession of doubt------ repeated checking
Obsession of symmetry-------slow performance at task
Common obsessions unpleasant thoughts of sex, violence, contamination, numbers and
doubt.
4. Etiology of OCD
Neurochemical: Abnormal regulation of serotonin
Genetic: Rate are higher in first –degree relatives monozygotic twins than in general
population
Psychosocial: OCD is triggered by stressful life event
Clomipramine a TCA with
high serotonergic properties
5. Treatment of OCD
Pharmacological:
o SSRI : first drug of choice
Higher than normal doses may be needed (Fluxetine 60-80 Mg\day ,
Paroxetine 40-60 Mg\day)
It require 1 to 2 months to have an effect
o Antipsychotic: adjunct therapy with serotonergic agent (Risperidal , Aripiprazole)
Behavioral treatment:
o Exposure and relapse prevention
o Prolong exposure to the obsesstional idea and prevention of the relieving
compulsion
o Relaxation training
6. Prognosis
• There is usually a fluctuating course.
• Relapses under stress & may occur in children.
• At one year 25% are recovered, 50% are better 25% are unchanged or wore.
Suicide: Self Injurious act with at least some wish to die.
Self-harm: injury to the self but with NO wish to die. ( but it will increase the risk of suicide
by 100x)
1 M ppl kill themselves Yearly !
15% of severely depressed patients commit suicide.
Etiology
Affective disorder 50%
Drug and Alcohol 25%
Schizophrenia 10%
Others
Risk Assessment in History (Remember SUICIDAL)
S
Men more in commit suicide than women “ if he
Sex
decided to kill himself he will do it unless you saved him
Significant others (important
“
and beloved ones)
Women suicidal attempt and self-harm are more than
male “female by genetics have tendency to love life
more than male
Divorced > Separated > Single > Married in Suicide
U
What was the method he used?
Unsuccessful previous
Was anyone there? It’s more severe if the patient alone.
attempt
Was there a note ?
I
This action may make suicide more accepted to the
Identification of Family
patient as he have experienced it in his family.
member who previously
Why do u want to die (pain, attention ) Do u have a clear
commit suicide.
Idea of killing yourself? How often do u think of it? How
Ideas of suicide
long does this ides last in your mind? Can u stop thinking
about it? Have u wished u were dead by now? Are there
anything that stop u from suicide? Religion, family..etc
CI
Psychosis, Bipolar disorder, Chronic pain, panic disorder are
Chronic illness
of high risk in committing suicide
D
Depression is one of the leading causes of suicide.
Depression.
Drug Abuse
A
Increase dramatically with onset of adolescent.
Age
Being alone and severely isolated increase the risk
Alcohol
Anniversary of severe trauma
or beloved death
Alone
L
Guns, Hanging, Jumping from high places are the most
Lethality of Suicidal Method
lethal. Greater consideration must be provided to those.
Drug overdose or wrist cutting are less lethal.
Note: That Majority of Suicidal patients have seen a doctor within months before they
commit suicide. They want help but they can’t ask directly! Remember SUICIDAL & u will
save lives!
Management: depends on the patient!
Treat all treatable causes, if he was depressed treat him with antidepressant,
If there was a problem try to remove it or refer him to a specialist who can help him
to cope with, family support.
However some patients may require hospitalization
Maternity blues”baby blues”
Postpartum depression(PPD)
Postpartum psychosis
definition, presentation, causes, treatment
Maternity blues:
1. Occur in about 50-75% of mothers, More frequent among primigravida.
2. It is low grade of depression start at the 3th or 4th day after delivery usually lasts 48
hr and can last up to 10 days, normal physiology and not disease. Pts have often
experienced depressive symptoms in the last trimester of pregnancy.
3. Presentation: mood instability, sadness, anxiety, lack of concentration, episodes of crying.
4. the causes are unknown hormonal changes may be the cause.
5. Treatment: Emotional support.
Postpartum depression(PPD):
1. Affect 10-20% of delivered women.
2. begins after the first two weeks postpartum.
3. Presentation: Excessive worry or anxiety, Irritability, short temper, feeling
overwhelmed by responsibilities, difficulty making decisions, Sad mood, feelings of
guilt, fear, phobias, Hopelessness, Sleep disturbances (insomnia or hyper-somnolence),
fatigue.
4. The causes: previous psychiatric disorder, younger age, early postpartum blues, recent
stressful events, poor marital relationship & absence of social support.
5. treatment: psychological, social and antidepressant agents.
6. Most pts recovers within few months”2-6 months” b\c it’s a self-limiting disorder.
Postpartum psychosis:
1. usually begins within the 1st to 2nd weeks postpartum, and affect 0.1-0.2% of delivered
women. 5% suicide and 4% infanticide rate.
2. Presentation: Visual or auditory hallucinations, Delusional thinking, pt. is very
obviously psychotic, delirium”may occur due to septicemia”.
3. causes: Personal or family Hx. psychosis, bipolar, schizophrenia Previous hx
postpartum psychosis or bipolar episode
4. treatment: according to the status of patient and clinical presentation
in severe cases: hospitalize and close observation is indicated.
Done by:
Lujain Malaka
Hassan albulkhi
Samar Alahdal
Razan Aljawi
Saleh Alzahrani
Reviewed By :
Waffaa Almalki
Referance :
our lecture's notes
Primary pyodermas:
Bacterial Skin Infections
Impetigo; two forms;
Contagious: (honey colored crusted) caused by staph aureus and GBS.
Bulbous: flaccid vesicles & bullae containing turbid to frank purulent
fluid > collaret scale.
- Self limited condition, complications uncommon.
- Treatment; topical Abx for localized.
Systemic Abx ( penicillinase resistant penicillin or 1st
generation cephalosporin.
Ecthyma;
-
Caused by strept. Pyogenicus.
Usually on upper post. Thighs or buttocs.
Vesiculopustule > punched out ulceration covered by thick greenish
yellow crust.
Treatment; topical or oral Abx and optimum wound care.
Soft tissue:
Erysipelas;
-
Acute rapidly spreading erythema with a sharp raised border and
lymphangitis.
Lower legs most common sites followed by the face.
Almost always caused by group A strept, staph, H.influenzae more
common in children.
Tx; depends on whether it is uncomplicated simple erysipelas or
not.
Cellulitis;
- Caused by group A strep. Or Staph. Aureus.
- Red hot swollen, painful and tender erythema with indefinite
borders.
Necrotizing skin and soft tissue: (most lethal and most
dangerous)
Gram positive coccal infection with indirect skin rash due to
toxin production:
Staph Scalded Skin Syndrome (SSSS);
-
Caused by stap. Aureus that produce exfoliatin toxins disseminates
systemically.
With adequate Abx skin heals in 3-5 days with no scaring.
Without therapy death due to fluid & electrolyte loss, sepsis and
hypothermia.
Tx: hospitalization with IV fluid replacement and systemic Abx.
( penicillinase resistant penicillin or 1st generation cephalosporin.)
Scarlet Fever; (scarlatina)
-
Disease of children between the age of 1-10.
Infection transmitted via respiratory secretions.
Caused by strep. Pyogenicus exotoxins type A,B & C.
The primary distinction between strep. Pharyngitis and scarlet fever
is the accompanying exanthema.
1st few days of the illness ( wight strawberry tongue)
By the 4th or 5th day ( red strawberry tongue)
HISTORY: very important
DATA: very important
Syphilis
What’s Syphilis?
It is a sexually transmitted infectious disease caused by Treponema pallidum
and it can affect virtually every organ in the body
how is it spread?
1. Sexual contact with an infectious syphilitic lesion( Chancre, mucous patch,
Conduyloma lata)
2. Congenital infection: In-Utero or perinatal transmission
3. Blood products
Stages of syphilis ?
Primary
Secondary
The hall mark of it is the occurrence of a non-tender
indurated non purulent ulcer a called Chancre at the site of
the inoculation of the spirochete
Untreated it resolves in 4-6 weeks
The infection can then go into latency or secondary stage
Appears 6 to 8 weeks after the healing of the chancre
Fever, sore throat, malaise, anorexia, lymphadenpthy
Skin eruption: Can cause any type of rash in Dermatology but
the Maculopapular and and papulosquamous forms are one
of the most common types seen.
DDx: Drug rash, Pityriasis Rosea, Guttate Psoriasis
Moth eaten
Alopecia of 2nd
stage syphlis
Condylomata Lata
Late (Tertiary)
Syphilis
1/3 of the untreated latent syphilis will develop clinically
apparent tertiary disease.
1/3 of the untreated latent syphilis will develop clinically
apparent tertiary disease.
Laboratory:
Dark field microscopy only from the chancre, serologic
testing: Non-treponemal antigen tests---- RPR, VDRL,
Treponemal antibody tests-----FTA-ABS, TPHA
Be careful of the false positive VDRL in cases of
connective tissue diseases, infectious mononucleosis,
malaria, febrile diseases, infective endocarditis,
Pregnancy, Old age
Treatment:
Benzathine penicillin G, and for penicillin allergic adult non pregnant patients give
Doxycycline.
Cutaneous Sarcoidosis
History :
-sarcoidosis begins with these symptoms:
Fatigue - Fever - swollen lymph node -wight loss
-Lung symptoms :
dry cough - shortness of breath - wheezing chest pain .
-skin symptoms :
A rash of red or reddish-purple bumps, usually located on the shins or
ankles, which may be warm and tender to the touch , Disfiguring sores
(lesions) on the nose, cheeks and ears , Areas of skin that are darker or
lighter in color
Growths under the skin (nodules), particularly around scars or tattoos
-Eye symptoms :
Blurred vision - eye pain - sever redness - photophobia .
Definition :
Sarcoidosis is a granulomatous disease characterized by the presence of
noncaseating granulomas in organs and tissue, such as the skin, lung, lymph
nodes, eyes, joints, brain, kidneys, and heart. Cutaneous lesions may
present with a variety of morphologies, including papules, nodules,
plaques, and infiltrated scars.
: pathophsiolgy
Granulomatous inflammation is characterized primarily by accumulation of
monocytes, macrophages, and activated T-lymphocytes , Sarcoidosis has
paradoxical effects on inflammatory processes; it is characterized by
increased macrophage and CD4 helper T-cell activation .
Also been reported as part of the immune reconstitution syndrome of
HIV, that is, when people receive treatment for HIV their immune
system rebounds and the result is that it starts to attack the antigens of
opportunistic infections .
Causes :
1- Genetic . 2- Infections : mycobacteria, fungi, borrelia, rickettsia and
it may happen with organ transplantation .
3- Autoimmune . 4- idiopathic .
Risk factor :
1- Age and sex: Sarcoidosis often occurs between the ages of 20 and 40,
Women are slightly more likely to develop the disease.
2- Race: African-Americans have a higher incidence of sarcoidosis than
do white Americans. Also, sarcoidosis may be more severe and may be
more likely to recur and cause lung problems in African-Americans.
3- Family history: If someone in your family has had sarcoidosis, you're
more likely to develop the disease.
Investigation :
CXR, Gallium scan, skin bx, lymph node bx, transbronchial lung bx, liver
bx, ACE, serum and urine Ca
Management :
Depends on the extent of involvement : Topical and intralesional Steroids,
HydroxyChloroquine, Systemic steroids, MTX
Complications :
For most people, sarcoidosis resolves on its own with no lasting
consequences. But sometimes it causes long-term problems.
Lungs: Untreated pulmonary sarcoidosis can lead to permanent scarring in
your lungs, making it difficult to breathe.
Eyes: Inflammation can affect almost any part of your eye and can
eventually cause blindness. Rarely, sarcoidosis also can cause cataracts
and glaucoma.
Kidneys: Sarcoidosis can affect how your body handles calcium, which can
lead to kidney failure.
Heart: Granulomas in your heart can cause abnormal heart rhythms and
other heart problems. In rare instances, this may lead to death.
Nervous system: A small number of people with sarcoidosis develop
problems related to the central nervous system when granulomas form in
the brain and spinal cord. Inflammation in the facial nerves, for example,
can cause facial paralysis.
DATA interpretation is very important
Urticarial and Angioedema
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Urticaria is a transient, edematous NON SCALY itchy red wheals eruption. Individual
lesions lasts less than 24 hours
It is a vascular reaction pattern to a stimulus that leads to increased vascular
permeability giving localized edema
Urticaria or hives is divided into acute and chronic forms based on the duration of
the urticaria attack
Acute Urticaria is a pruritic (itchy) common distinctive skin rash reaction pattern
Acute urticaria by definition lasts less than 6 weeks, while chronic urticaria lasts
more than 6 weeks
Mediated mainly by Histamine release by allergens like foods( eggs, fish, shrimps,
nuts), drugs (Antibiotics) Urticarial drug rash, viral infections, pollens, mediated by
IgE Type 1 Hypersensitivity reaction in most cases, some cases are Complement or
immune complex mediated type 3 reaction, or non Immunologic in etiology
The etiology is undetermined in some cases of Acute Urtcaria, but in Chronic
Urticaria most cases are idiopathic one third are due to autoimmune antibodies
again FCR1 on mast cells, others are due to physical urticaria
A dynamic process with new lesions evolving as old ones disappear
Investigations: Usually none is needed if it Is acute urticaria, In chronic urticaria it
may be worth while to do food skin testing, with CBC, thyroid antibodies and Sinus
and panoramic x-rays.
Treatment:
All suspected allergens should be discontinued (Allergen Avoidance)
Antihistamines (Type I receptor antagonists H1 blockers) 2nd or 3rd generation H1
blockers are preferred in cases of Urticaria eg. Loratidine or Cetrizine, Levocetrizine,
Desloratidine for 6 to 8 weeks
Angioedema occurs because of deep increased vascular permeability in the
subcutaneous tissue of the skin and mucosa and submucosal layers of the
respiratory tract and GIT
Urticaria and Angioedema commonly occur together and can have the same
etiology
Angioedema can occur by itself with no evidence of Urticaria
Classification of Angioedema:
•
A-Not Associated with
Urticaria
HAE type I
HAE type II
Acquired C1 INH* deficiency
ACE inhibitor–associated AE
Idiopathic recurrent AE
B-Associated with Urticaria
Chronic idiopathic urticaria/AE syndrome
Allergic (IgE-mediated) AE
Aspirin or nonsteroidal antiinflammatory drug–
induced AE
ACE inhibitor–associated AE
Treatment of angioedema
•
A- Angioedema with Urticaria: Allergen Avoidance if known, systemic (oral or
IV/IM) antihistamines, oral steroids if needed, Intramuscular IM Epinephrine
(0.3 to 0.5mg per dose) is very important if the Angioedema is part of
Anaphylaxis or if Angioedema is causing Stridor/difficulty breathing/dyspnea
and Wheezing
•
B-Angioedema without Urticaria (Hereditary and acquired Angioedema ): For
prophylaxis Danazol, Tranexamic acid. For emergency treatment of
Angioedema C1 INH concentrate, or fresh frozen plasma
Urticaria
Angioedema
NEED history
Mangment in steps and complete the drugs
No need to the tables
‫"ذكر هللا عز وجل يسهل الصعب‪ ،‬وييسر العسير ويخفف المشاق‪ ،‬فما ذكر‬
‫هللا عز وجل على صعب إال هان‪ ،‬وال على عسير إال تيسر‪ ،‬وال مشقة إال‬
‫خفت‪ ،‬وال شدة إال زالت‪ ،‬وال كربة إال انفرجت‪ ،‬فذكر هللا تعالى هو الفرج بعد‬
‫الشدة‪ ،‬واليسر بعد العسر‪ ،‬والفرج بعد الغم والهم‪ ،‬يوضحه أن ذكر هللا عز‬
‫وجل يُذهب عن القلب مخاوفه كلها‪ ،‬وله تأثير عجيب في حصول األمن‪،‬‬
‫فليس للخائف الذي قد اشتد خوفه أنفع من ذكر هللا عز وجل‪ ،‬إذ بحسب‬
‫ذكره يجد األمن ويزول خوفه" ( ابن القيم رحمه هللا )‬
‫‪Done by:‬‬
‫‪Eman Sulaiman‬‬
‫‪Shahad Alshareeef‬‬
‫‪Samah fallatah‬‬
‫‪Muna Alsalmi‬‬
‫‪Arwa Alasmari‬‬
‫‪Ahlam Mohammed‬‬
‫‪Esraa Althubaiti‬‬
‫‪Reviewed By :‬‬
‫‪Eman Sulaiman‬‬
‫‪Enas Alkhotani‬‬
‫‪Reference :‬‬
‫‪Toronto notes‬‬
‫‪our lectures notes‬‬
‫‪Ophtha Book‬‬
Cataract
Definition:
-Lens opacification (not transparent)
-Most common cause of reversible blindness.
Pathphysiology:
Chemical changes in lens protein that affect how lens refract light
and
reduce its clarity by scattering light going to the retina.
Type
Description
1-Nuclear
-Yellow to brown (brunescent)
-Aging
discoloration in the central part of -lens can get bigger, pushes the
the lens.
iris placing patient at increase risk
of angle closure glucoma.
-2nd sight phenomenon: cataract
lens is more powerful (myopic) &
offset coexisting presbyopia.
sclerosis
Asso. with
2-Cortical
-whitish Radial or spoke like
opacification either anterior or
posterior
-aging
-D.M
3-
-deep and more posterior
opacification
(bubble behind the lens)
-Steroids. -Radiation.
-I.O inflammation.
-D.M -Trauma. -aging
Capsular
Phakic: Natural lens
Psudophakic: when cataract
replaced by artificial lens.
Aphakik: cataract removed but isn’t
replaced.
D.D of chronic visual loss: Cataract,
Glaucoma, Age-related macular
degeneration, Refractive errors,
Diabetic retionopathy, Retinitis
pegmintosa.
Causes:
1-Acquired:
-Age-related(90% of all cataract), chemical
include decr. K and incre. Na, Ca, Cl.
-Associated with systemic disease: DM,
Metabolic disorders (wilson's disease,
galactosemia, homocystinuria), Hypocalcima.
-Traumatic (blunt or penetrating injury,
common in young men).
-Intraocular inflammation.
-Toxic (steroids, phynothiazines)
-Radiation.
2-Conginital:
-Idiopathic or inherited
-Must R/O serious causes like Retinoblastoma,
TORCH infection, Galactosemia .
Types and Causes:
Clinical features:
Gradual (over years), painless progressive decrease in V.A. associated with glare, halo
around light at night and monocular diplopia. also patient losses the brightness of colors
(Doesn't cause relative afferent papillary defect).
Diagnosis:
-Visual acuity test: decr. V.A. -Slit lamp: change in the Red reflex. -Fundoscope: impaired
view of the retina.
Management:
Surgical ttt indicated when: visual loss leads to functional impairment, aid management of
other ocular disease (retinal exam or laser ttt), congenital (Urgent surgery to prevent
amblyopia before the age of 2y.) or traumatic cataracts.
Phecoemulsification: most commonly used. topical eye drop (tetracaine) or retrobulbar
bloc injection (block CN3,CN6 movement & V1 of CN5 for sensation) for anesthesia. then cut
through sclera & cornea to lens then using pheco handpeice remove anterior capsule, cortex
and nuclease and keep post capsule (to prevent new lens to fall in retina) then artificial lens
inserted then close up and patient discharged no need for admission but patient must be
seen next day to start antibiotic drops and steroid drop.
Complications:
post-op complications: Retinal detachment, ednophthalmitis, dislocated I.O.L, Macular
edema, glaucoma, post. Capsular opacification (residual epithelial cells are left, & migrate
along the back surface of the implant and opacify. ttt with YAG laser).
Corneal Ulcer
Definition:
Infection and injury cause inflammation of the cornea-a condition called keratitis. And
Tissue loss because of inflammation produces an ulcer, the ulcer can either be centra
lly located, thus greatly affecting vision, or peripherally located.
Etiology
• local necrosis of corneal tissue due to infection which is usually bacterial , rarely
viral (adenoviruses and herpes ), fungal (especially if injury resulted from vegetables), or
protozoan (Acanthamoeba -> contact lens wearer at risk especially if they swim with it.)
• secondary to corneal exposure, abrasion (a Superficial epithelial defects can occur after
trauma, infection, or from exposure.), foreign body, contact lens use (50% of ulcers)
• also associated with conjunctivitis, blepharitis (inflammation of lid margins), keratitis, vitamin
A deficiency.
all corneal ulcers caused by infection until prove otherwise.
Risk factor :
Trauma from a foreign body (including contact lenses)
severe dry eyes
eyelid disease can predispose patients to corneal infections
Clinical Features
• pain, photophobia (The cornea contains more nerve endings per area than anywhere else in
the body, so scratches here are painful, and patients will often have
photophobia), tearing, foreign body sensation, decreased VA (if central ulcer)
• Corneal opacity that necrosis and forms an excavated ulcer with infiltrative base
• Bacterial ulcers may have purulent discharge; viral ulcers may have watery discharge
• may develop corneal edema, conjunctival injection, anterior chamber cells/flare, hypopyon(is
inflammatory cells in the anterior chamber of the eye most common with bacterial ),
corneal hypoesthesia (in viral keratitis)
• Overlying corneal epithelial defect that stains with fluorescein (in investigation)
Investigations:
-Seidel test: fluorescein drop on the cornea under cobalt blue filter is used to detect leaking
Penetrating lesions; any aqueous leaking will change dark orange dye to bright yellow-green at
site of wound.
-Under slit-lamp Dendritic ulcer that stains brightly under fluorescein if HSV is the cause
(after repeated infections).
Treatment:
-Urgent referral to ophthalmology
-Culture prior to treatment
-Topical antibiotics: all ulcers should be treated as bacterial infection until culture result
obtained.
( fortified ABx) : genta ,tobra & vancomycin every 1/2 h,1 for gram +ve,1 for gram-ve around
24h
fungal : give antifungal ( Amphotyricin B )
Acanthameaba: Chlorhexidine or polyhexamethylenebiguanide. (if not response, pain and ulcer
progressive)
Viral: Acyclovir 3% ointment *5 daily (oral if with uveitis/bilateral), trifluorothymidine 1% drop
2-hourly, dendritic debridement, Steroids MUST be avoided and only prescribed only by
ophthalmologist if needed.
-cycloplagia: drops to reduce the pain.
• must treat vigorously to avoid complications
Complications: Decreased vision, corneal perforation, iritis, endophthalmitis
in HX :
To reach the DDX we should think anatomically or acute VS chronic or painful VS
painless .in corneal ulcer it will be :
painful red eye and sub acute (days) in onset
contact lens wear
decrease of VA
Discharge
Recent URTI? to roll out adenovirus infection
hx of trauma
family hx of bacterial or viral infection
in P/E:
look for :
vision to detect if there is any decrease in VA
if there is discharge look for the type (watery or purulent)
corneal opacification
hypopyon + white infiltrated cornea
How to differentiate b/n corneal ulcer and abrasion?
Corneal Abrasion vs. Corneal Ulcer
Abrasion
Ulcer
Time Course
Acute (instantaneous)
History of Trauma
Cornea
Iris Detail
Yes
Clear White
Clear
Sub acute (days)
Not usually
necrotic area
Obscured
Corneal Thickness
Normal
May have crater defect/thinning
Extent of Lesion
hypopyon
Limited to epithelium
------------------
Extension into stroma
Present
Diabetic Retinopathy
consider DM if unexplained retinopathy, cataract, EOM palsy, optic neuropathy,
sudden change in refractive error.
loss of vision due to:
• progressive microangiopathy leading to macular edema
• progressive diabetic retinopathy -+ neovascularization -+ traction -+ retinal
detachment and
vitreous hemorrhage
Classification:
1• non-proliferative: increased vascular permeability and retinal ischemia
• dot and blot hemorrhages
• microaneurysms
• hard exudates (lipid deposits)
• macular edema
2• advanced. non-proliferative (or pre-proliferative):
• non-proliferative findings plus:
• venous beading.
• intraretinal microvascular anomalies (IRMA)
- IRMA: dilated, leaky vessels within the retina
• cotton wool spots (nerve fiber layer infarcts)
3• proliferative:
• neovasculuization of iris, disc, retina to vitreous
• neovascularization of iris (rubeoais irldis) can lead to neovascular glaucoma
• vitreous hemorrhage from bleeding. fragile new vessels, fibrous tissue can contract
causing tractional retinal detachment.
• high risk of severe visual loss secondary to vitreous hemorrhage. retinal
detachment.
Screening Guidelines for Diabetic Retinopathy:
• Type1 DM
• screen for retinopathy beginning annually 5 years after disease onset
• Type2 DM
• Initial examination at time of diagnosis, then annually
•pregnancy
• ocular exam in 1st trimester,close follow-up throughout as pregnancy can
exacerbate Diabetic retinopathy.
• gestational diabetics not at risk for retinopathy
Treatement:
Diabetic Control and Complications Trial (DCCT)
• tight control of blood sugar decreases frequency and severity of microvascular
complications.
• blood pressure control
• focal laser for clinically significant macular edema
• panretinallaser photocoagulation for proliferative diabetic retinopathy: reduces
neovascularization, hence reducing the angiogenic stimulus from ischemic retina by
decreasing retinal metabolic demand thus reduces risk of blindness
• vitrectomy for non-clearing vitreous hemorrhage and retinal detachment in
proliferative diabetic retinopathy
• vitrectomy before vitreous hemorrhage does not Improve the visual prognosis.
Complications:
Lens Changes:
•earlier onset of senile nuclear sclerosis and cortical cataract
•poor controlled blood glucose levels can suddenly cause refractive changes
Extra Ocular Muscle (EOM) Palsy:
•usually CN III infarct
Optic Neuropathy:
•visual acuity loss due to Infarction of optic disc/nerve.
Eye Trauma
Site Of Injury
" According To Anatomy"
1/ eyelid
:
1. Mechanism of injury: YOU need to determine if the laceration involve the lid margin
and how close the cut to canalicula ( TEAR DRAINGE ) system .
2. Diagnosis
Hx
Ocular examination
3. Management
Wash the bleeding
Rule out ruptured globe
If no rupture globe is present look if the laceration is deep or not , if deep laceration
means that there is fat prolapse , so if its deep don’t suture and refer to an
ophthalmologist
if there is laceration at the medial canthus don’t suture it as you may block the
lacrimal drainage system present there and refer to ophthalmology
if there is a missing part don’t suture it
If the laceration is at the margin ( e.g. eye lash )don’t suture
Suture only superficial laceration
" Very important "
2/ cornea & conjunctiva
1. Mechanism of injury
defect of thin epithelial layer which cover the cornea , usually due to trauma (fingernails
,twigs ,paper ) or by contact lenses
2. Clinical features
Very painful
Tearing
Photophobia
foreign body sensation
3. Diagnosis
de-epithelialized area stains with fluorescein dye,(green cornea )
4. Management
ABX ointment
patch the eye
"Don’t patch eye if the patient wear contact lens"
Cycloplegic to relive pain of photophobia
5. complication
Infection
Ulceration
secondary iritis
1. Mechanism of injury
Injury go deeper into the stroma not only the epithelium
2. Diagnosis
Seidel test 'test by fluorescein day 'You have to rule out rupture globe and perforated
cornea ,because its most of the time associated with opening globe .
3. Management
Need an urgent referred to ophthalmologist
1. Mechanism of injury
Foreign material in or on cornea may have associated rust ring if metallic
2. Clinical features
May note tearing,
photophobia,
Foreign body sensation
red eye
AC flare, corneal edema, conjunctival injection.
3. Diagnosis
HX: Ask about mechanism of injuryhgih : speed perforation or Low speed no
perforation
Ocular examination: Visual acuity & check pupil
Rule out rupture of globe & prolapsed iris and rule out intra ocular foreign body by x-ray
or thin slice CT scan of the head if you have suspicion for penetrating injury and to look
for metal pieces not obvious on exam. MRI is contraindicated
4. Management
If its superficial and no perforation Remove under magnification using local anesthetic
and sterile needle, give antibiotic drop after removal and refer to ophthalmology
(depending on depth and location)
But if it deep and you suspect rupture globe
Treat it Initially:
1. ABC
2. Don’t take IOP
3. check the vision
4. Ask for diplopia
5. Apply rigid eye shield to minimize further trauma
6. Keep NPO
7. Don’t remove the foreign body
8. Give tetanus toxoid
9. Give IV antibiotic.
5-complication:
abrasion, infection, scarring, rust ring, secondary iritis.
3/ Conjunctiva
1. Mechanism of injury
Very common and usually caused by blunt trauma or HTN
2. Clinical features
red eye
3. Diagnosis
1/ Hx(HTN, bleeding disorder, trauma, idiopathic, aspirin)
2/ Ocular
examination to rule out rupture globe : VA first, pupil size and reaction, EOM (diplopia),
external and slit-lamp exam, Ophthalmoscopy .
4. Management
If the examination is unremarkable reassure & follow up (resolves spontaneously 2-3w)
if recurrent, medical & hematologic work up
4/ Iris and ciliary body
1. Mechanism of injury
A blood in anterior chamber often due to damage to root of the iris, May occur with blunt
trauma Can associated with Iritis which resulting of sphincter tearing (mydriatic pupil) .
2. Clinical features
Red eye
If there is Iritis pain, photophobia
3. Diagnosis
1) HX(trauma, sickle cell disease).
2) Ocular examination: VA first, pupil size and reaction, EOM (diplopia), external and slitlamp exam,
ophthalmoscopy
•if VA normal or slightly reduced, globe less likely to be perforated
• if VA reduced may be perforated globe, corneal abrasion, lens dislocation, retinal
tear.
4. treatment:
-refer to ophthalmology.
-shield and bed rest for 5d.
-sleep with head upright.
-may need surgical drainage if hyphema persist or if re-bleed.
-never prescribe Aspirin as it increase risk of re-bleeding.
5. complications:
risk of re-bleed on day 2-5, resulting in 2ndry glaucoma, corneal staining, iritis
necrosis.
5/Lens
1. Mechanism of injury
• Trauma to the lens can cause cataract resulting in traumatic cataract It can be seen
immediately at the time of injury or can occur gradually
• lens dislocation (ectopic lentis) occur due to blunt trauma, dislocated into anterior
chamber ,inferiorly or into the retina.
(decrease VA, abnormal red reflex)
2. Management
Urgent Refer to ophthalmology (surgical correction +/- lens displacement)
6/ vitreous
1. Mechanism of injury
Trauma cause vitreous hemorrhage
2. Clinical feature:
sudden loss of VA
Reduce red reflux and retina not visible during examination.
3. Management
(if child, R/o Abuse)
Urgent Refer to ophthalmology.
-U.S to R/O RD
-expectant: non-urgent cases, blood resorbs in 3-6m.
-Surgical: vitrectomy +/- retinal endolaser to possible bleeding sites/vessels.
7/ Retina
1. Mechanism of injury
Blunt trauma can cause;
Retinal hemorrhage or detachment
Macular hemorrhage or detachment
2. Management
Urgent Refer to ophthalmology
8/ blow out fracture (fracture of orbital floor )
1. Mechanism of injury
Blunt trauma causing fracture of orbital floor and herniation of orbital contents into
maxillary Sinus
orbital rim remains intact
inferior rectus and/or inferior oblique muscles may be incarcerated at fracture site
infraorbital nerve
courses along the floor of the orbit and may be damaged
2. clinical features
pain and nausea at time of injury
diplopia,
restriction of EOM
infra orbital and upper lip paresthesia (CN V2)
enophthalmos( sunken eye), periorbital ecchymoses
3. Diagnosis
plain films: Waters’ view and lateral
CT: anteroposterior and coronal view of orbits .
4 . Management
•refrain from coughing, blowing nose
•systemic antibiotics may be indicated
•surgery if fracture >50% orbital floor, diplopia not improving, or enophthalmos >2 mm
• may delay surgery if the diplopia improves
8 /Chemical Burns
1. Mechanism of injury
•Alkali burns have a worse prognosis than acid burns because acids coagulate tissue and
inhibit
further corneal penetration
• Poor prognosis if cornea opaque, likely irreversible stromal damage
• Even with a clear cornea initially, alkali burns can progress for weeks (thus, very guarded
prognosis)
"Alkaline burn "
"Acid burn"
No blood vessels
Limbus—blood vessels— this is a good sign .
because all steam cells are located in the Limbus .
2. Management
1) immediately irrigate at site of injury by normal saline , ringer lactate or tap water for
30 minutes ƒ
2) give local anesthesia eye drop and remove the particles
3) do not attempt to neutralize because the heat produced by the reaction will damage
the cornea
4) cycloplegic drops to decrease iris spasm ( pain (
5)
Atropine to decrease iris spasm, pain and photophobia
6) If the IOP is high give anti -glaucoma medication
7) Antibiotic prophylaxis to prevent corneal ulcer formation
8) topical steroids (by ophthalmologist) to decrease inflammation .
3. complication
Stem cell deficiency
Neovascularization
Conjctiviazation
9 /Ruptured globe
"laceration"
1. Mechanism of injury
History of injury
2.
Management
1.
2.
3.
4.
5.
ABC
Vision test
Don’t touch the eye
Shield the eye
Call ophthalmologist "very important"
Glaucoma
Definition : progressive optic neuropathy involving
1- characteristic structural changes to optic nerve head
2- visual field changes ( loss of peripheral vision precedes to central loss )
3- high IOP ( not required for diagnosis)
sequence of events: gradual pressure rise g increased C:D ratio g visual field loss
Pathophysiology :
•
aqueous is produced by the ciliary body and flows from the posterior chamber to the anterior
chamber through the pupil, and drains into the episcleral veins via the trabecular meshwork and
the Canal of Schlemm in the angle between the cornea and the iris
Open angle glaucoma ( most common form): due to obstruction of aqueous
drainage within the trabecular meshwork and its drainage into the Canal of Schlemm
Angle closure glaucoma ( Acute glaucoma ):due to pressure gradient peripheral iris
bows forward in an already susceptible eye with a shallow anterior chamber
obstructing aqueous access to the trabecular meshwork
-
sudden forward shift of the lens-iris diaphragm causes pupillary block, and results
in inability of the aqueous to flow from the posterior chamber to the anterior
chamber resulting in a sudden rise in IOP
Investigation :
1- history
2- IOP measurement :by Goldman applanation tonometry ( IOP is determined by the amount of
force required to flatten a constant corneal surface area ) Average IOP = 15 ± 3 mmHg
3- corneal thickness measurement : by Pachymetry (Corneal Thickness can affect pressure
measurement)
4- Fundus examination : by ophthalmoscope
5- visual field assessment: by confrontation manually - Normal C:D ≤0.4
or automated by perimetry Humphrey field Analyzer - Suspect glaucoma if C:D ratio >0.6,C:D ratio
between eyes >0.2, or cup approaches disc margin
- slow, progressive, irreversible loss of peripheral
- vertical thinning and notching of the inferior and
vision( paracentral defects, arcuate scotoma, and
superior rims (ganglion atrophy)
nasal step) are characteristics
-
Central vision usually spared unless untreated
6- Anterior chamber depth : by slit lamp (for closed
Angle glaucoma risk factor )
Follow up : every 1-2 months
1- iop measurment
2- fundus exam
3- visual field assessment
Normal
Shahd Alshareef 2016
glaucoma
Management for open angle glaucoma
•
medical treatment: decrease IOP by
1- increase aqueous outflow
1. topical cholinergics (pilocarpine)
2. topical prostaglandin analogues (latanoprost)
3. topical α-adrenergics ( epinephrine)
2- decrease aqueous production
1. topical β-blockers ( timolol)
2. topical and oral carbonic anhydrase inhibitor( acetazolamide)
3. topical α-adrenergics (apraclonidine)
•
Surgical: indicated when there’s no improvement for 3-4monthes.
1-laser trabeculoplasty (for refractory cases)
2-Trabeculectomy creation of a new outflow tract from anterior chamber to under conjunctiva
Management for Angle closure glaucoma
• OCULAR EMERGENCY: refer to ophthalmologist for acute angle closure glaucoma
•
•
medical treatment like above
systemic hyperosmotic agents : to deacrese corneal edema
1– oral glycerine
2– IV mannitol
•
laser iridotomy : create a hole in the edge of the iris so the fluid can flow to the anterior chamber
strabismus
Ocular misalignment in one or both eyes, objects no visualized simultaneously by fovea of
each eye.
HETEROTROPIA : Manifest deviation: deviation not corrected by the fusion mechanism (i.e.
deviation is apparent when the patient is using both eyes)
Types: Exo (lateral) - eso (medial) – hyper (up) – hypo (down)
Accommodative esotropia
normal response to approaching object is
the triad of the near reflex: convergence,
accommodation and miosis
Hyperopia
over activation of near
reflex
age: 2-5 years
reversible with correction of refractive
error
Non- accommodative esotrpoia
Idiopathic.
Early onset. (4,6,8 monthes)
Monocular visual impairment (cataract, corneal
scarring, anisometropia ,retinoblastoma or
divergence insufficiency (ocular misalignment
that is greater at distance fixation than at near
fixation)
Surgery as soon as possible before 2 years for
fear of amblyopia.
PSEUDOSTRABISMUS : thick epicanthal folds, appearance of esotropia, normal corneal
light reflex.
HETEROPHORIA : latent deviation: deviation corrected by the fusion mechanism (i.e.
deviation not seen when patient is focusing with both eyes) majority are asymptomatic.
Exacerbated with asthenopia (eye strain, fatigue)
Concomitant (nonparalytic)
angle of deviation is equal in all directions, no
restriction, Monocular, alternating, or
intermittent
Causes:
Sensory deprivation
EOM: normal
Amblyopia is common/Diplopia is uncommon
Age: Childhood, gradual
Incomitant (paralytic)
angle of deviation varies with direction of gaze,
restriction of eye movement.
Causes:
Neural (CN III, IV, VI): ischemia, MS, aneurysm,
brain tumor, trauma
• Muscular: myasthenia gravis, Graves’ disease
• Structural: restriction or entrapment of extraocular
muscles due to orbital inflammation, tumor, fracture
of the orbital wall
Diplopia is common/amblyopia is uncommon
Any age (acquired), sudden
Risk factors
Family history of strabismus, amblyopia, type of eyeglasses and history of wear,
extraocular muscle surgery or other eye surgery, and genetic diseases
Investigation
1- Hirschberg test (corneal light reflex: normal in heterophoria, asymmetrical in
heterotropia, lateral to central cornea indicates esodeviation; light reflex medial to
central cornea indicates exodeviation
2- cover-uncover test
3- alternate cover test (reveal both latent and manifest)
Management
1- Glasses: for refractive error, to put the eye in straight position.
2- Patching: for amblyopia, must treated before 7 years
3- Surgery: if 2 above not working (recession: weakening muscle or resection:
strengthening muscle)
Complication: Amblyopia
Uveitis and autoimmune Disease
Uveal tract:
Is vascularized, pigmented middle layer of the eye, between the sclera and the
retina ( from anterior to posterior) = iris, ciliary body, choroid.
Uveitis:
defined as inflammation of the uveal tract, subdivided into anterior (iris,
usually accompanied by ciliary body) , Intermediate(vitreous) and posterior
(choroid and/or retina).
Pathophysiology:
The etiology of uveitis is often idiopathic. genetic, traumatic, or infectious
mechanisms are
known to promote or trigger uveitis.
- Infectious: (tuberculosis, syphilis, and AIDS, herps zoster, herps simplex)
- autoimmune disorders: reiter syndrome , juvenile rheumatoid artharitis
(pediatric case ) , inflammatory bowel disease, rheumatoid arthritis, systemic
lupus erythematosus (SLE), sarcoidosis) “ most common etiology”
History: ”not included in blue print”
Important elements of the medical history that should suggest uveitis as the
cause of ocular pain:
- History of autoimmune disease such as inflammatory bowel disease, SLE, and
sarcoidosis
- Sexually transmitted diseases, particularly syphilis and chlamydia
- Tuberculosis
Anterior uveatis:
- Pain , tenderness of the
globe, redness, photophobia
(due to reactive spasm of inflamed
iris muscle), excessive tearing,
and decreased vision; pain
generally develops over a few
hours or days except in cases
Posterior uveitis:
- Absence of symptoms of
anterior uveitis (pain,
redness, and
photophobia).
Intermediate uveitis:
- Similar to posterior
uveitis; painless floaters
and decreased vision
- Minimal photophobia or
external inflammation
- Blurred vision, floaters
physical examination:
1- visual acuity (may be decreased in the affected eye).
2 - extra ocular movement (generally normal).
3 – funduscopic examination:
- intermediate uveaitis:
aggregates of inflammatory cells may condense over the pars plana and
look like
snowballs.
white exudates (snowbanks) gray-white plaque at the pars plana.
4- measure intraocular pressure:
may be normal or slightly decreased.
Iritis typically reduces IOP because ciliary body inflammation causes decreased
aqueous production. But in severe iritis may cause an inflammatory glaucoma
(trabeculitis) by reduction in outflow of aqueous result in an increase IOP.
5- slit-lamp examination (confirm diagnosis):
Examine the epithelium for abrasions, edema, ulcers, or foreign bodies.
Inspect the stroma for deep ulcers and edema.
Scan the endothelium for keratitic precipitates (white blood cells on the
corneal endothelium), a hallmark of iritis in anterior uveaitis.
examin Anterior chamber for : cells ( WBC) , flare (protein
precipitation) and hypopyon (collection of neutrophilic exudates
inferiorly in chamber)
- Corneal Ulceration
in anterior uveaitis
- Emergency Corneal Abrasion
DD: “not included in blue print
- HSV Keratitis
- Intraocular Foreign Body
”
- Scleritis.
- Aute Angle-Closure
Glaucoma
- Acute Conjunctivitis
Work up:
Laboratory:
- in cases of mild, unilateral nongranulomatous uveitis in the setting of trauma,
known systemic disease, or a history and physical not suggestive of systemic
disease, laboratory studies are unlikely to be helpful.
- If the history and the physical examination findings are unremarkable in the
presence of bilateral uveitis, granulomatous uveitis, or recurrent uveitis, a
nonspecific workup is indicated:
CBC count
Erythrocyte sedimentation rate (ESR)
Antinuclear antibody (ANA)
Rapid plasma reagin (RPR)
Venereal disease research laboratory (VDRL)
Purified protein derivative (PPD)
Urinalysis.
HIV test.
Treatment:
Anterior:
- Mydriatics: dilate pupil to
prevent formation of
posterior synechiae and to
decrease pain from ciliary
spasm.
-
Steroids: topical, subtenon, or systemic
Systemic analgesia.
Complication:
Intermediate:
Posterior:
- systemic or subtenon/intravitreal steroids and
immunosuppressive agents
- Vitrectomy, cryotherapy, or
laser photocoagulation to the
“snowbank”
- Steroids: retrobulbar , or
systemic if indicated (e.g.
threat of vision loss)
“Not included in blue print”
Anterior:
-
-
inflammatory glaucoma
Posterior synechiae:
Adhesions of posterior iris to
anterior lens capsule
Indicated by an irregularly
shaped pupil
If occurs 360°, entraps
aqueous in posterior chamber,
iris bows forward “iris bombé
” angle closure glaucoma
Peripheral anterior synechiae (rare):
adhesions of iris to cornea secondary
angle closure glaucoma
Cataracts
Band keratopathy (with chronic iritis):
Superficial corneal
calcification
keratopathy
Macular edema with chronic iritis
Intermediate:
Cystoid macular edema,
cataract, and glaucoma
Posterior:
-
Macular edema
Vitritis
Neovascularizatio
n
Visual field
loss/scotoma
Ocular Manifestations of Autoimmune Disease:
DISEASE:
Connective tissue
disorder:
- Rheumatoid
arthritis
1
-
Juvenile
rheumatoid
arthritis
(pediatric
case)
-
Sjögren's
syndrome
-
Systemic
lupus
erythematos
us:
pediatric:
renal disease
(nephritic or
nephrotic)
OBGYN:
Spontenous
abortion ,
premature
birth IUGR ,
fetal death
and
preclampsia
OCULAR MANIFISTATION:
- most common ocular manifestation: dry eyes (keratoconjunctivitis
sicca):
aqueous-deficient (lacrimal pathology)
Clinical Features
• dry eyes, red eyes, foreign body sensation, blurred vision, tearing
• slit-lamp exam: decreased tear meniscus, decreased tear break-up time
(normally should be 10 s), Superfacial punctate keratitis.
Investigations
• surface damage observed with fluorescein/Rose Bengal staining
• decreased distance in Schirmer's test.
Complications
• erosions and scarring of cornea.
Treatment
• medical: preservative-free artificial tears up to q1h and ointment at
bedtime (preservative toxicity becomes significant if used more than q1h
PRN) #for severe cases, cyclosporine ophthalmic emulsion 0.05%
(Restasis®) can be used.
procedural: punctal occlusion (punctal plug insertion), lid taping,
tarsorrhaphy (sew lids together) if severe
treat underlying cause.
2
– episcleritis:8
Clinical Features:
- usually asymptomatic; may have discomfort, heat sensation, red
eye (often interpalpebral), rarely pain
- sectoral or diffuse injection of radially-directed vessels,
chemosis, small mobile nodules blanches with topical
phenylephrine (constricts superficial conjunctival vessels). To
differentiate between episcleritis and scleritis, place a drop of
phenylephrine 2.5% in the affected eye. Re-examine the vascular
pattern 10-15 min later; episcleral vessels should blanch,
scleral vessels should not
Treatment:
• generally self limited, recurrent in 2/3 of cases
• topical steroid for 3-5 d if painful
3
- scleritis:
usually bilateral: diffuse, nodular, or necrotizing
• anterior scleritis: pain radiating to face,( may cause scleral thinning in
some cases necrotizing strongly associated with RA called “
scleromalacia perforans”
• posterior scleritis: rapidly progressive blindness, may cause exudative
- ankylosing
spondylitis.
- polyarteritis
nodosa
-
Multiple
sclerosis
RD
Clinical Features
severe pain, photophobia, red eye, decreased vision
pain is best indicator of disease progression
inflammation of scleral, episcleral, and conjunctival vessels
may have anterior chamber cells and flare, corneal infiltrate, scleral
thinning
sclera may have a blue hue (best seen in natural light), due to
rearranged scleral fibers
scleral edema or thinning
failure to blanch with topical phenylephrine.
Treatment
- systemic NSAID or steroid (topical steroids are not effective)
- treat underlying etiology
4 – uveatitis.
Clinical feature:
- blurred vision and decreased color vision: secondary to optic neuritis
- central scotoma: due to damage to papillomacular bundle of retinal nerve
fiber
- diplopia: secondary to INO
- RAPD, ptosis, nystagmus, uveitis, optic atrophy, optic neuritis
white matter demyelinating lesions of optic nerve on MRI
treatment:
- IV steroids with taper to oral form for optic neuritis
DO NOT treat with oral steroids in isolation as this increases
likelihood of eventual development of MS
Giant cell
neuritis
/temporal
arteritis
Graves' disease
(OB/GYNE)
( abnormal
menstrual
cycle) ,
miscarriage,
preterm birth,
fetal thyroid
dysfunction,
poor fetal
growth,
maternal heart
failure and
preeclampsia.
Clinical feature:
- more common in women >60 yr
- abrupt monocular loss of vision, pain over the temporal artery, jaw
claudication, scalp tenderness, constitutional symptoms, and past
medical history of polymyalgia rheumatica
- ischemic optic atrophy (50% lose vision in other eye if untreated ).
Diagnosis:
- temporal artery biopsy + increased ESR (ESR can be normal, but likely 80100 in first hour) and CRP
- if biopsy of one side is negative, biopsy the other side
Treatment:
- high dose corticosteroid to relieve pain and prevent further ischemic
episodes
- if diagnosis of GCA is suspected clinically: start treatment + perform
temporal artery biopsy to confirm diagnosis within 2 wk of initial
presentation (DO NOT WAIT TO TREAT)
Clinical feature:
- (lid retraction, lid lag)
- Soft tissue swelling (periorbital edema)
- Proptosis (exophthalmos)
- Extraocular muscle weakness (causing diplopia)
- Corneal exposure(keratitis).
Sight loss
treatment:
- treat hyperthyroidism
- monitor for corneal exposure and maintain corneal hydration
- manage diplopia, proptosis and compressive optic neuropathy with one
or a combination of:
steroids (during acute phase)
orbital bony decompression
external beam radiation of the orbit
- consider strabismus and/or eyelid surgical procedures once acute phase
subsides.
Antiphospholipi
d syndrome
(OB/GYN)
pregnancy
complications,
including preecla
mpsia,
thrombosis,
autoimmune
thrombocytopeni
a,
fetal growth
restriction, and
fetal loss
Kawazaki
disease.
(
pediatric).
Central or branch vein occlusion.
Clinical feature:
painless, monocular, gradual or sudden visual loss
• ± RAPD
fundoscopy :
- “blood and thunder” appearance , diffuse retinal hemorrhages,
cotton wool spots, venous engorgement, swollen optic disc,
macular edema
two fairly distinct groups :
-ischemic retinopathy
no RAPD, VA approximately 20/80
ld hemorrhage, few
cotton wool spots, resolves spontaneously over weeks to months
, may regain normal vision if macula intact
- hemorrhagic/ischemic retinopathy
usually older patient with deficient arterial supply , RAPD, VA
approximately 20/200, reduced peripheral vision, more
hemorrhages, cotton wool spots, congestion , poor visual
prognosis.
Treatment:
no treatment available to restore vision
treat underlying cause/contributing factor
laser photocoagulation, or intravitreal anti-VEGF injection to reduce
neovascularization and macular edema.
-
Conjunctivitis: bilateral, non-exudative conjunctival injection.
References :Toronto note and Medscape.
- notes:
blue print :
optha/pediatric ( data interpretation and management)
optha/obgyn ( data interpretation , management and communication).
-
notes for reviewrs:
- I write all the ocular manifestation of autoimmune disease , regardless the
case is related to pediatric or OBGYN. , and all of them present in Toronto
note , except antiphosopholipid syndrome as obgyne case but I don’t know
if is important , so if isn’t you can delete it.
- also I write all about disease regardless the blue print.