NOte Book

SOA
S: Subject
O: Objective
A: Assessment
P: Plan
Subjective Note
 Family complain Diarrhea for 2 days more than 5 times per day , watery
 Night events with medical diarrhea large amount association abdominal cramping.
 Health comments
Vomiting 2 days non-projectile vomiting colour what
Objectives type of food eat, aggravated by due to feeding.
 Vital signs Fever for 2 days low grade fever intermittent relieve
 Physical Examination by paracetamol syrup.
 Investigations / daily weigh monitor
O/E : Conscious , alert , sing of dehydration , sunken
Emergency signs eye , dry mouth , skin goes back rapidly.
3C Diagnosis: Some dehydration
 Convulsion
 Coma
 Cynosis
3S
o Severe dehydration
o severe respiratory distress
o signs of shock e.g. Cold hand , weak pulse and refile ˂3s
O
Obstructive breathing or airway
PAGE \* MERGEFORMAT 81
Priority sign
3P
 Pallor
 Pain
 Poisoning
3R
 Restless
 Respiratory distress
 Referral
Assessment
o Introduction
o Status ( stable / unstable/ improve / non-improve)
Plan
Plan depend on status
1- New treatment
2- New diagnosis
3- Patient Education
Admission criteria
1- Danger signs Total admission
2- Emergency signs
3- Priority signs
Totally admission 24 hour admission then discharge
Danger signs
1- unable to food /drink
2- Vomiting of everything
3- Convulsion
4- Lethargic / unconsciousness .
Solution: Drop/ minute = Amount × drop factor
Hour or Minute
Example: 500ml × 15 ml = 3 drop / minute

240 min
 Drop factor of colloid : 15 - 20 ml

 Drop factor of blood : 10- 15 ml
 Drop factor of Dexymitta : 60 ml
Fluids
1- Nutrient solution - D5%
2- Electrolyte solution - Ringer solution /Normal saline solution
3- Volume Expanders - Colloids and Dextran, plasma and albumin.
Nutrients
 D5% , D10% and D50% - To prevent dehydration and ketone.

It is Monosaccharide it loss of body protein and nitrogen it uptake of K+ into cell s causes
Hypokalemia.
Electrolyte ( Crystalloid)
 Normal saline , Ringer and Mixed Colloid )

 Dextran : Volume Expanders it reduces blood viscosity and inhibition aggregating of
RBC.
Maintenance fluid are fluid composed water ,glucose ,sodium and K+ - mixed or ringer.
Goals of Maintenance fluid
 Prevent dehydration
 Prevent electrolytes disorder
 Prevent Ketoacidosis
 Protein degration
MOB
o Malnutrition
o Oedema
o Burn
Daily monitor signs in inpatient
 Improvement
 Complications
 Failure of treatment
Drug calculations
Syrup + injection: Kg × required dose × ml

Dose of Hand
Tablet : Required dose × kg

Dose of Hand
Choice of I.V fluid
 Resuscitation Normal saline / Ringer solution

 Maintenance Mixed solution ( NS/D5) or ringer with D5%.
Drug calculation formula:
Results:=
No Drug Name Hand Dose Required Dose Diluted Frequency
1 Ampicilin 250mg/500mg(5ml)/1000mg(10ml) 100-300mg/kg Three times
7 days
2 Gentamycin 80mg/2ml/40mg/20mg 5-8mg or 4-7mg/kg 6ml One times
saline 5 days
3 Ceftriaxone 250mg/500mg(5ml)/1000mg(10ml) 80-100mg/kg
4 Artisunate 1Box( 60mg pow, 5ml sal and 1ml <20Kg= 3mg > 20kg 2.4mg 0 hr -12hr-
24hr if not
respond
cont once 24
hr. start fr
zero hr
5 Co- 20mg /120mg 1- 5-15 Kg-> 6 tab= 3days 1-0hr( 1)-
artem( artemet 2- 15-25->12 tab = 3days >8hr(1)first
her 3- 25-35kg-> 18 tab= 3day day->12(1)-
+lumefantine) >12(1) next
2days. other
same but no
drug
changed
6 Quinine 600mg/2ml Loading dose: 20mg/kg
Maintenance dose:
10ml/kg
7 Diazepam Rec: 2.5/10/20mg IV/IM: 5mg/ml IV: 0.3MG/kg Rec: 0.4-0.5 Div result 3
8 Phenobarbital 80mg iv or tab 30mg Iv or tab 1-2 mg/kg
9 Amox Syr 125mg/5ml 250mg/5ml 50ml/kg
10 Pracetamol 120mg/5ml 10mg/kg
11- Ibuprofen 125mg 10mg/kg
12- Penicillin G 5meg/3meg( 1mg:1000000mg/kg) 100000-300000mg/kg 4 times
13- Dexamethson 4mg/ml 0.6-0.8mg/kg
14- Ferro-folic 60mg 4-6mg 3 times
15- Amox tab 125mg/5ml 50mg/kg
16- Lasix inj 20mg/2 0.5mg/kg
17- Metra syr 200mg/5ml Syr/tab 20-30mg/kg
18- Chloraph syr 1-2yr: 2-3ml 3-4yr: 4ml 7yr: 7-20ml
19- Cefazolin inj 500mg 50mg-100mg
20- Erythromycin 200mg/5ml 50mg/ml
21 Co-trimoxazole 250/5ml RD = 40mg /kg
syrup
22 Arthemeter 40- 80 mg loading dose = 3.2mg/kg
injection
Maintenance = 1.6mg/kg
23 Albendazole 200mg -400mg RD = 1-2 year = 200mg
single dose ˃ 2 year =
400mg
24 Zinc tablet ˂ 6 month = half tablet
(10mg ) × 14 day
˃ 6 month = 1 tablet
(20mg ) ×14 day
25 Vitamin A ˂ 6 month = 50,0000 ug
˃ 6 month = 100,000 ug
˃ 1 year = 200,000 ug
History taking/pediatric
Should Ask
 Informed consent
 Growth and development
 Immunization history
 Birth History
1) Personal Data
Name , Age and address for last 6 months.
2) Chief complain - on mommy own words
3) History of present illness
4) Past medical History
o History of chronic disease
o Hospitalization
o Drug allergy
o Blood transfusion
5) Immunization History
 Complete
 Incomplete
 Up to date
6) Drug History - present taking drugs and past taking drugs
7) Birth History
Antenatal :
 Vaccination
 blood sugar
 Blood pressure of the mother
 Conditions of the mother
 HIV
Natal:
o Location of birth
o way of deliver
o presentation of the child
o TIN
Postnatal
 Cry
 Colour
 Apgar Score
8) Feeding History
 Type of feeding
 Frequency
 Time of feeding - at least 10 month
9) Growth and development
 Growth History
 Measure weight /Heigh / Head circumference/ Chest circumference
 Developmental
o Speech
o Motor ( Gross , fine)
o Social
Family History
 Name of the mother
 Age
 Any sibling - yes - ask number
 Consequenty
Social
o Housing
o Numbering of housing
o water sources
Physical Examinations
1- General Appearance
 Conscious
 Colour of the skin
 Oedema
 Lumphnates
2- HENT
o Hair
o Fontanella /sutures
o Eyes - sunken or puffy
o Nose- discharge
o Mouth- cown, ulcer
o Tonsil - oedema , pus
o Neck - lymphnode
3- CHEST
 Inspection - indrawing, deformity
 Palpitation - mass
 percussion- dullness/tumpan
 Ausculatation - wheeze, crepitation and Rhonhi
Malaria
Complain
I. Fever - high grade ˃ 37.5

II. Vomiting Uncomplicated malaria
III. diarrhea
IV. Chills
Complication malaria
Signs of Uncomplicated malaria plus
 Unable to feed
 Convulsion
 Vomiting due to weight loss
 lethargic
 Hypoglycemia
 Respiratory distress
 Anemia
 Malnutrition
Malaria Treatment
( uncomplicated)
1st line
Co- artem ( 20mg arthemeter , 120 lumfatrine ) - 1st day 1 stat then 8 hour.
 ˂ 5 kg donot give 1×2 ×3
 5-14 kg : 6 tablet -- 1 stat then 8 hr then 1×2
 15-24 kg : 12 tablet
 25-34 : 18 tablet -- First 3 tablet stat then 8 hr- give 3 tablet then 3×3
 ˃ 35 kg : 24 tablet --4 stat tablet stat then 8 hr - 4×4.
Complicated malaria
 1st line : Artesunate
 2nd line : Quinine 600mginjection
 3rd line : Arthemeter injection 40, 80mg
Arthemeter
Loading dose 3.2
5 day
Maintenance 1.6
Quinine 600mg /2ml
Loading dose 20mg × kg× 2ml
7 day
Maintenance 10mg × kg× 2ml
Plus Dextrose 10ml /kg
Example : 20 × 10 ×2ml = 0.66
60
Malaria
Malaria is protozoal disease caused by genus of plasmodium including:-
 Plasmodium falciparum
 Plasmodium malaria
 Plasmodium Vivax
 Plasmodium Ovale
 Plasmodium Knowles
Life cycle
o Asexual phase or Erytrocytic phase (Schizogony) in human
o Sexual phase (Sporogony ) in mosquito
Incubation period 6 30 days
Transmission by female anospheles mosquito
Plasmodium vivax and ovale are dominant liver hypnozoite which are not killed most drugs
and mostly relapse.
Plasmodium malaria and falciparum mostly not damage hepatocyte or liver infect so they
have not (hepatocyte phase ) mostly they are in erytrocytic.
Long term relapse:- Mostly Plasmodium vivax and ovale whch are resistance in liver and
Plasmodium malaria persistance in RBC.
Plasmodium falciparum mostly identity from blood.
The most characteristic feature of malaria and differentiate other infections
Malaria febrile paroxyms
paroxyms occurs in rupture of RBC of every 48 hours in P.vivax and ovale (tertian periodic) and
every 72 hours of p.malaria (quartan periodian)
Clinical features of malaria
Classical symptoms
Fever, rigors, sweat, headache ) plus anemia and splenomegaly
Stages
Cold stage
decrease headache, nausea ,chilly followed by rigors ( 1 hour and 15 minute)
Hot stage
Patient feels burning hot skin , hot touch, headache in the pulse increase ( 2-6 hours)
Sweating stage
Fever comes down with profuse sweating , pulse slowers patient feels relieved (2-4 hours)
Investigations
 Thin and thick smear
 CBC
Differential diagnosis
Tuberculosis , Typhoid , Brucellosis ,meningitis, tetanus , relapsing kalazar, liver abscess and
toxoplasmosis.
Pneumonia
Complain
 High grade fever
 Cough
 Fast breath
 Crepitation
 indrawing and flaring - severe
Respiratory rate
 ˂ 2 month : 60 breath/minute
 2-12 month : ˃ 50 b/minute
 1-5 year: ˃ 40 breath/minute
Treatment
1. Ampicilline
2. Gentamicine
3. SAlbutamol - if respiratory distress
 Ventoline 2.5mg
 Ventoline 1.5mg + 2.5 ml of N.S = 4ml
If not responding to Ampicilline and Gentamicine
4. Ceftraixone
Not responding its atypical pneumonia
5. Erytromycine/ Azithromycin
Pneumonia
Pneumonia is inflammtion of parenchymal of the lungs.
Causes of Pneumonia
Bacteria
 Streptococcus pneumonia all age
 Chylamdia infants
 Mycoplasma ˃ 5 years
 haemophilus influenza and stphylococcus aures non vaccine
Clinical feature
 Fever
 Tchypnea
 Respiratory distress ( intercostal and Subcostal retraction)
 Nasal flaring
 Indrawing
 Cyanosis
 Crackle
 Wheeze or crepitation
 Bronchial breathing
Types of pneumonia
No pneumonia
Fever and Cough
Pneumonia
Increase fever, Cough , Fast breathing , crackle /crepitation and ˃ 50 breath /min
Severe pneumonia
Pnemonia + chest indrawing , nasal flaring , grunding O2 saturation ˂90 mmhg
Very pneumonia
Severe pneumonia + Cyanosis , inability to drink or breast feeding and O2 saturation ˂80mmhg
Differentiate Viral and Bacterial pneumonia
Viral Bacteria
 High grade fever

 Low grade fever
 WBC 15,000-40,000
 WBC ˂ 20,000
 ↑ ESR / CRP
 ↓ ESR / CRP
V.S X-ray
X-ray
 Peri hilar changes  Bilateral lobar pneumonia
 Lung abscess
 Pleural
Peri bronchial
effusion thicky
 Pneumothora
Complication of pneumonia
 Empyema
 Pleural effusion
 Pneumonia
 Sepsis
Investigation
 CBC
 Malaria
 blood culture
 CXR
Management
 Very severe pneumonia and Severe pneumonia
 O2 neoplazer / salbutamol
 Hospitalization
 O2 neoplazer / salbutamol
 Ventoline 2.5mg
 Ventoline 1.5mg + 2.5 ml of N.S = 4ml
 Correct shock, hypoglycemia /dehydration
 Fluid maintenance
 Ampicilline 500mg - 100mg/kg
 Gentamicine 40mg = 5mg/kg or cefotaxime
No pneumonia
Home treatment
Amoxicillin 50mg/kg /12
Augmentine 125mg
90 mg ×kg × 7 days
 If pneumonia is staphylococcus use cloxacillin 100mg/kg
 If pneumonia is mycoplasma use erytromycin
 if pneumonia is viral use acyclovir.
Differential Diagnostic of pneumonia
 Bronchitis
 Asthma
 Pulmonary edema caused by Heart failure
Anaemia
Anemia is reduction of hemoglobin blood or RBC count below average value for age and
sex.
Hp: is oxygen carrier capacity.
Causes of anemia :
1- Decreased production
A. Bone marrow failure
 Pure red cell anemia
 Aplastic anemia
 Marrow infiltrate = leukemia mydofi
B. Decreased production and normal RBC
 Anemia of chronic disease
 Chronic inflammation
 Chronic infection
 chronic renal failure
C. Specific factor deficiency
o Iron deficiency
o B12 ad folic acid
o protein deficiency
2- Increased destruction ( Hemolysis)

A- Intracorpuscular
Membrane defect Hemeglobinopathy

Enzyme defect
 H.spherecytosis  α thalasemia  G6 PD deficiency

 H.Eliptocytosis  β thalasemia  Pyruvate kinese defect
 Paroxymal nocturia  Extra corpuscular
sickle cell disease
 Hemoglobinemia
Immologic Non-immologic
Combs - ve
Iso immologic Auto immonologic
Combs + ve
Microangiopanic H.A
DIC, HUS
Iso immune Auto immune
renal vein thrombosis
Passively acquired antobody Actively forming antibody

 Sepsis
 Malaria
 Wilson disease
 Drugs
 Hypersplenism
3- Hemorrhagic anemia
 Acute Hemorrhagic
 Chronic Hemorrhagic
Classification of anemia
MCV ˂ 80 MCV 80-100 MCV ˃ 100
Microcytic hypochromatic anemia Normocytic anemia Macrocytic hypochromatic anemia
 B12 deficiency
 Iron deficiency  Hemoly tic anemia  Folate
 Thalasemia  anemia of chronic due renal failure deficiency
 lead poison  Aplastic anemia
Clinical feature of anemia

Symptom
 Anorexia weigh loss
 Easy fatiguability
 Headache
 Tinnitus
 Sweating
 Fainting
Signs of anemia
 Pallor
 Tachycardia (Hemic murmur)
 Systolic follow murmur
 Heart failure
 Kolilonchia ( spooning)
 Angular stomatitis Iron deficiency anemia
 Glased Shing tender tongue
 Brittle nails
 jaundice
Hemolytic anemia
 Splenomegaly
 Leg ulcer Sickle cell anemia
 Neurological manifestation B12 deficiency
 Purpuric eruption and throat ulcer A plastic anemia
Types of anemia in Clinical

A. Mild anemia 10-12g/dl
B. Moderate anemia 9-10g/dl
C. Severe anemia ˂7g/dl
Investigation
 CBC
Low MCV , Low MCH and Normal RDW
Management of anemia
Treat underlying cause
Ferrofollic 60mg
For 3 month
RD : 4-6 mg
If Ferro B- complex syrup
Child ˂ 1 year : 3-4 ml × 2
Child ˃ 1 year : 5-7 ml × 2
 ˂7 Hp with normal appetite and not malnutrition Ferrofollic
 ˂7 Hp with normal appetite and malnutrition Ferrofollic phase 2
 ˂7 Hp with stress and lethargic and not malnutrition Blood transfusion
15 ml - 20ml × kg for 4 hours then
furesemide 1-2 mg × kg
 If he has malnutrition or CHF
Blood transfusion
10ml ×kg / 4 hours + furesemide
 ˂ 4 HP in malnutrition = Blood transfusion
 ˃ 4 HP in malnutrition = Nutritional assessment
Furesemide 20mg 0.1× kg 30 minute before and after
Gastritis
 If the child has only vomiting is Gastritis
 If the child has vomiting + diarrhea is Gastroenteritis
Investigation
CBC , Malaria, , Smear and Stool Examination
Treatment
I. ORS
II. Zinc
III. Albendazole
IV. Penicilline G + Gentamicine
V. Ranitadine 50mg/2ml
RD: 1.2mg/kg Add mixed solution 20-30mg/kg
Dextrose 10% , RD: 2.5mg/kg bolus
ICU
 Comma
 DKA
 Shock
 Asphyxia
 Premature
 Severe pneumonia
IMCI ˂ 2 months
1. Clump cord
2. Suction
3. Hambag ( ambu bag) 40/minute
4. Cardiac compression and adrenaline use ˂ 100 b/minute
5. Tetracycline eye ointment
6. Vitamin K
If Pregnancy women taking T.B treatment in ˃ than 2 month of gestational age treat give
Neonatal INH in 6 month.
If pregnant taking T.B treatment in ˂ 2 months of gestational age neonatal full treatment of b in 6
months.
If pregnant women has HIV in delivery Neonate give Rifampicin the take PCR.
Management of Neonatal jaundice
Admission
Ǫ therapy
IV canula
If hypoglycemia give 10% dextrose
3ml × kg / 1hour
NGT tube for feeding
o Jaundice ˂ 24 hour age is pathological jaundice
o Jaundice ˃ 24 hour age is physiological jaundice encourage breast feeding.
Neonatal Asphyxia ( Perinatal asphyxia)

Neonatal Asphyxia is the medical condition resulting from deprivation of oxygen to a newborn
infant that causes physical harm , mainly to the brain or lack of breathing at one minute of life.
Pathophysiology
When fetal asphyxia happens , the body will show a self -defended mechanism which
redistribute blood flow to different organs called '' Inter-organs shunt '' in order to prevent some
important organs including brain , heart and adrenal from hypoxic damage.
Pathology
Lack of adequate breathing lack of oxygen supply to heart inability of heart to pump
adequate blood hypoxia + ischemic to organs ( particularly brain).
ETIOLOGY
I- Intrapartum or antepartum ( 90%)
1. Maternal factors
1. Obstetric factor
 Diabetic mellitus
 Placenta previa
 Toxemia
 Cord prolapse
 Hypertension
 Pacental insufficiency
 Cardiac disease
 Polyhidramnion
 Infections
 Chorioamnitis.
 Iso immunication
 Drug addiction
II- Inpartum conditions
III- Fetal or neonatal conditions
 Abnormal presentation
 Prolonged delivery  Prematurity
 Respiratory distress syndrome
 Difficult delivery
 meconium aspiration syndrome
 Post term delivery  Sepsis, pneumonia
 Forceps or vacum delivery  cardiac or pulmonary anomalies.
Clinical feature
 Respiratory depression at birth
• Lack of crying
• bluish or gray skin color
 Poor heart rate
 Poor muscle tone
 Acidosis ( PH ˂ 7)
 seizure
Investigation
Apgar score 0 -10
 The doctor may suspect your baby has asphyxia neonatorum if they have an apgar score
of 3 or lower for more than minutes.
Initial Management
 Admit in newborn unit ( Intensive care unit / ICU)
 Oxygen/ ventilation
 Maintenance of temperature
 Check vital signs
 Check hematocrit , sugar , ABG , electrolyte
 I.V line
Complication
 Hypoxia - encephalopathy
 Cerebral palsy: affects a child body movement , muscle control , muscle coordination,
muscle tone, reflex and posture and balance.
 Perventricucular leukomalacia : involves the death, or necrosis , to the white matter of
the brain.
 Developmental delay : cause delays in child's motor, physical , speech and mental
development.
 Mental retardation
 seizure disorders
 paralysis
Tetanus
Toxic infection of the nervous system caused by clostridium tetanus .
Pathophysiology
Wound Clostridium tetanus - spores germinate Proliferation locally
Produce 2 toxin ( tetanospasmin and tetanolys Travel along nerve trunk ( motor nerve
ending and motor nerve cell) then to blood stream.
The involvement of anterior horn cells results in rigidity and convulsion.
Incubation period : 6-10 days
Clinical feature of tetanus
1. Mild tetanus
Pain and stiffness of the site of injury for few week occur in patient who received anti toxin,
mortality ˂ 1%.
2. General tetanus
o Spasm occur in descending form with intact conscious.
o Spasm participated by visual or auditory stimuli.
Special signs
 Risus sardonicus
Grimacing face due to facial muscle spasm.
 Trismus
 Difficult of mouth opening due to masseter spasm.
 largeal spasm
Stridor and may be suffocation.
 OPsthotonus
Arched back
 Tonic seizure
Fixed adducted arms and extended lower limb with colonic.
3. Cephalic tetanus
Followed by head injury or otitis media, short incubation period with high mortality , involved
cranial nerve palsy may be generalized.
4. Tetanus neonatorum
Due to contaminated umbilical stump.
Diagnoses
 History of wound and Atypical species
 Normal CSF
 Wound culture
Investigation
o No specific lab test for tetanus.
Differential diagnostic
 Meningitis
 Rabies : Dysphagia associated with spasm s of inspiratory and pharyngeal muscles, but
there is no trismus.
 Poisoning e.g. dystonic reaction drugs such as Phenothiazine and metocloropramide - other
cause muscle spasm.
 Hysterical : Trismus without generalized rigidity.
Management
 ICU
 Oxygen
 Diazepam
 Tetanus immunoglobim I.M 500 -2000 iu single
 Metronidazole 40mg
 Dressing or wound care
 N.G tube
Prevention
Tetanus toxoid vaccine I.M 0.5ml
Complication of tetanus
Respiratory
 Largeal spasm suffocation
 Aspiration pneumonia ( Broncho- pneumonia )
 Pneumothorax
 Lung collapse
Mechanical
 In severe seizure
 Tongue laceration
 Vertebral fracture
 Muscle hematoma
Burn
Burn is damage to your body's tissue ad caused by thermal ,chemicals , electrical, sunlight,
radiation.
Clinical manifestation
 First degree:- Red , painful, dry non-blister , non-scar is epidermis and superficial.
 Second degree:- Painful, blister , non-scar is partial thickness.
 Third degree:- Painless , non-blister , scar is full thickness and require skin graft if ˃
1cm diameter.
 Fourth degree: In fascia , muscle and bone
Admission criteria
 ˃ 10% of BSA
 Special areas :- Face , hands , buttock ,groin, feet , neck and perineum.
Investigation
o CBC
o Electrolytes
o Blood sugar
Management
If BSA ˃ 10% or special areas
 First aid
 ABC
 Fluid management
 Dressing and sulfadiazine
 Surgery
 Physiotherapy
 Rehabilitation
 Antibiotic
If BSA ˂10% or Non- special areas

 Rehydration
 Oral antibiotc
 Sulfadiazine or silver nitrate
 Tetanus toxoid
Fluid management
Using rule of nine
 Head /neck = 18%
 Front = 18%
 back = 18%
 hand = 9%
 hand = 9%
 leg = 14%
 leg = 14%
Rule of palms
Every palms 1%
Fluid management
Bolus
20ml × kg of Ringer
Replacement of deficit
4 ml × kg × BSA/24 of Ringer
give first 8 hour
Second 16 hour
Maintenance ( Mixed)
 First 10 kg = 100 kg /day
 Second 10kg = 50 kg /day
 Apose = 20 × kg
or
Rule 4cc, 2cc and 1cc
o 4cc for first 10kg
o 2cc for second 10 kg
o 1cc for apose
Antibiotics
Penicillin G 100,000 ×kg
Gentamicin 40mg 5mg ×kg
Others
 Tetanus
 Blood transfusion
 Plasma albumin
Tetanus toxoid = vaccination as booster
Tetanus immune = Non-vaccine
DKA
DKA is metabolic disorder due to acute insulin deficiency and common in type 1 DM.
Causes
 Infection
 Trauma
 Psychic
Mechanism of insulin action
↑ lipogenesis
↓ Blood glucose
Suppresses glucose release by the liver inform of glycogen and
glycogelys through and lipido fat by glucogenesis
regulates uptake of glucose by the
cell
Mechanisms of DKA
Lack of insulin
↑ lipolysis
↑ Blood glucose
decreased glucose in the cell ( starvation)
Increase glucose in blood
compensatory mechanism
Hyperglycemia
glycogenolysis
renal threshold ˃ 180
insufficient lipolysis
osmotic diuretic
Release FFA
polyuria
Converted into ketone bodies by the liver

dehydration
body uses as energy

compensatory mechanism
Then in the blood (ketonemia)

Thirst and polydipsia
Acetone
Aceto acitic
acid B-hydroxy butyric acid
Lungs
Kidney
Metabolic acidosis Acetone odor
 Pain
Ketonuria  vomiting
 Kussamal breathing
Compensatory mechanisms or puffering system
 Polyuria : from hyperglycemia - kidney compensate mechanism
 Vomiting : from metabolic acidosis - GI compensate mechanism
 Kussmaul's respiration: from metabolic acidosis to excreate more CO2 - Respiratory
compensate mechanism.
 Ketonuria : from ketonemia or acids in the blood - kidney compensate mechanism
 Thirst and polydipsia :from dehydration of polyuria
 Abdominal pain : due to hypokalemia and distension.
Clinical featureof DKA

Clinical History ( symptoms)
 Polyuria
 Polydipsia Classical signs
 Polyphagia
 weight loss
 Abdominal pain
 Vomiting
Clinical signs
 Dehydration
 Deep sighing respiration (Kussmaul's respiration:)
 Lethargy / drowsiness + Vomiting
Biochemical signs
o Ketone in urine
o Blood glucose ˃ 300 or 11 mmol
o Acidemia PH ˂7.1
Investigation
 Blood glucose
 Electrolyte / Urea ( K+ and Na+ )
 Serum ketone
 Blood glucose
 CBC and blood culture
 ECG
 PH , HCO2 PACO2 ( blood gas)
Diagnoses
Keto Acidosis
Diabetic
 Blood glucose ˃300g/dl  Ketonemia  Metabolic acidosis

 Glucosuria  Serum ketone ˃ 3 mmol  PH ˂ 7.3
 Ketonuria  HCO3 ˂ 15
 ↓ Paco2
Differential diagnoses of DKA

I. All causes of Acute abdominal pain
II. All causes of metabolic acidosis
 Renal failure
 Organic acidemia
 Lactic acidosis with sepsis
 Acute diarrhoea
 Real tubular acidosis
III. All causes of coma in DM patient
IV. Hyperosmolar ketone
 Blood glucose ˃ 800
 Serum osmolarity ˃350
 No or slight ketone
 Acidose mainly in lacic acid
V. Hypogycemia Coma
 Insulin overdose
 Exercise or delayed meals
 Seizure ( due to glycopenia in CNS)
Management of DKA
 Fluid therapy
 Insulin therapy
 Potassium therapy
 Antibiotic therapy
Fluid therapy
Use
 5% in mild and moderate DKA or PH 7.1 or ˃ 7.1
 10% in severe DKA o PH ˂7.1
DEFICIT
Deficit = % of dehydration × kg
Deficit = % of dehydration × kg × 10
MAINTENANCE ml × kg/ 24 hour
ml × kg /hour o 3 - 9 = 80 ml/kg
 ˂ 10 kg = 2ml/kg/hour Or o 10 -19 = 70 ml/kg
 10 - 40kg = 1 ml /kg/hour o 20 - 29 = 60ml/kg
 ˃ 40kg = give 4 ml /hour o 30 - 50 = 50 ml/kg
o ˃ 50 = 35ml / kg
Use deficit 48 hour + maintenance / hour
Example : 20 kg with 5% or PH ˃7.1
Deficit Maintenance
20 kg × 5 = 1000  20 kg × 1ml = 20 ml
1000 ∕ 48 hour = 21 ml/hour
Deficit + maintenance / hour = 41 ml / hour
OR
20 kg × 5% × 10 = 2000
Maintenance
20 kg × 60ml = 1200/24hr or 2400/48 hr
Deficit + maintenance / hour = 41 ml / hour
2000 + 2400 = 4400/48 hr = 91 ml/hr
Use normal saline or Ringer due to lactic acidosis or Pt is shock

20 ml × kg of Normal saline 20 ml × 20 kg = 400 ml/kg over 1 hour
Next hour
Deficit = 85 ml × kg
Maintenance
100ml ×kg = in first 10 kg
50 ml × kg = in second 10 kg
25 ml × kg = in remaining
Example: 20kg patient

Amount per hour: Deficit + Maintenance - Bolus
23 hour
Deficit : 20 kg × 85 ml = 1700 ml/kg

Maintenance : 1500 ml
Amount per hour: 1700 + 1500 - 400 = 121ml / hour

23 hour
Use Normal saline 045% or 0.9% not use ringer due to lactic acidosis and hypertonic.
 Ringer (R) : Hypertonic
 Normal saline (Na) : Isotonic
 Dextrose (D5%) : Hypotonic
Potassium therapy
Add every 500ml with 20 mEq of K+ phoasphate N.S 0.9%
and 20 mEq of K+ acetate so every 1 liter 40 mEq of K+
OR
Add every 500ml with 20 mmol K+ Chloride so every liter 400 mmol N.S 0.45%
Insulin Therapy
o Use Regular insulin in slow infusion 0.1/kg/hour without bolus dose.
o Use Second liter not 1st liter
o When blood glucose ˂ 250 use D5% to avoid hypoglycemia Add D5% in the Normal
saline.
o Shift 0.2 - 0.4 u/kg every 6 -8 hour of insulin in S.C.
o When PH ˃7.3 , HCO3 ˃ 16 , Na 135 - 145 and No vomiting
o Give Na+ bicarbonate only in severe acidose unresponse to fluid therapy PH ˂ 7.1
RENAL D ISEASE
NEPHROTIC SYNDROME
Is clinical - laboratory condition characterized by
1. Heavy protenuria
o Protein ˃ 40 mg/ m2/hr
o Albuminemia ˃ 1g / m2 /24 hr
2. Hypoabunemia
˂ 2.5 g/dl
3. Hyper cholesterolemia
˃ 250 mg/dl
4. Generalized oedema
Anasarca - form face to feets
Histological classification
I. Minimal change nephropathy
II. Focal segmental glomerosclerosis
III. Mesencheal proliferation glumeronephritis
IV. Membrano proliferation
V. Membranous glomeronephritis
Causes of nephrotic syndrome
 Idiopathic in 90% ( primary)
Minimal change nephropathy 85% , Focal segmental glomerosclerosis
 Secondary nephrotic syndrome
SLE , Honoch- schonlein purpura , infection , Hepatitis B virus and Hepatitis C virus
 Congenital nephrotic syndrome
Pathophysiology
Glomular membrane damage Glomular memebrane damage Hypoalbunemia
Heavy protenuria loosing 13.5 g/dl Lossing anti thrombin III liver compensate ↑
product of cholesterol
Hypoalbunemia Thrombosis
Hyper cholestemia
Decreased oncotic pressure Renal vein thrombosis
Hyperlipdemia
Increased Hydro static
Na+ and H2O
Edema
 Sometimes loose RBC and globuline = anemia
Clinical feature nephrotic syndrome
o Pitting oedema periorbital edema in early morning.
o Sudden on weight gain
o Ascites
o Abdominal pain
o Vomiting and Diarrhea- due to intestinal edema
o Respiratory distress due to pulmonary edema
Differential diagnosis
Congestive Heart failure
Liver cirrhosis
Protein loosing enteropathy
Investigation
 Urine
 Serum albumin
 Low - density lipoprotein
 Raised ESR
 Blood sugar
 Hepatitis B serology
Treatment
Hospitalization and monitor
Urine output 24 hour
Blood pressure
Daily weight
Diet
 Salt restriction
 Fluid
 Increased protein intake
Avoid infection
Avoid thrombosis
 Low dose aspirin
 Avoid excess diuretic
Salt free abumin
Important drugs steroid without renal biopsy
Prednisolone in 12 week
2mg / kg mostly 50% children 1 - 7 respond steroid
If not responding in 12 weeks make renal biopsy.
Renal biopsy is contra indicated :
 Children under 10 years
 Known diabetic
 patient on drugs e.g. penicillamine ( only stop the drug)
Complication
 Thrombo embolic
 Infection
 Pulmonary oedema
 Hypothydroidism
 Vitamin D deficiency
 Cushing syndrome
NEPHRITIC SYNDROME
Renal disease in which immunological mechanism triggers inflammation and proliferation
glomerular tissue that result damage of basement membrane messengium or cappilary
endothelium.
Causes of nephritic syndrome
Post infection ( strep, viral parasite , and fungi)
Systemic cause ( vascular collagen, and vascular disease)
Renal disease ( G.N and Berger disease)
Clinical feature
 Hematuria
 Protenuria
 Hypertension
 Uremia - due to retention waste product
 Azotemia - due to destruction protein to amino acid to nitrogen - renal insuficient.
 OLiguria
Investigation
 CBC
 Anti streptolysin O titre (ASO )
 Urinalysis --- red cell cast and Protenuria
 Urine culture
 Complement (C3 and C4)
Diagnose of nephritic syndrome
Clinical sign
Anti streptolysin O titre (ASO) to see streptoccus
I. Focal proliferation
Ig A nephropathy
Chronic liver failure
Celiec sprue
SLE
II. Diffuse proliferation
Membranous proliferation glomerulus
Cryoglobulunemia
SLE
Treatment
Treat underlying cause
Complication
 Micro hematuria persist for years -- Honoch- schonlein purpura.
 Chronic Rhematic fever
Measles (Rubela and morbilli.)
Measles is highly contagious infection of the respiratory immune and skin system.
Etiology
Measles (rubeola) is caused by a single-stranded RNA paramyxovirus of the genus morbillivirus with
one antigenic type. Humans are the only natural host.
Measles virus infects the upper respiratory tract and regional lymph nodes and is spread systemically
during a brief, low-titer primary viremia.
A secondary viremia occurs within 5 to 7 days when virus-infected monocytes spread the virus to the
respiratory tract, skin, and other organs
Virus is present in respiratory secretions, blood, and urine of infected individuals.
Transmission
Measles virus is transmitted by large droplets from the upper respiratory tract and requires close
contact ( person to person) and every patient can transmitted 12- 18 person.
Most young infants are protected from measles by transplacental antibody, but infants become
susceptible toward the end of the first year of life. Passive immunity may interfere with effective
vaccination until 12 to 15 months of age.
Pathophysiology of meaasles
Respiratory droplet of measles
Epithelial cells of the trachea / bronchi
Bind H. protein - then bind CD46 and CD150
Then spread to lung tissue
Then lymph node
Blood ( 1st viremia)
Multiplication
The second Viremia
Then General toxin
causing complication
Pneumonia Diarrhoea Encephalitis
Clinical types of measles

 Typical
 Atypical
 Modified
Clinical stage or phase of typical measles
Measles infection is divided into four phases:
o incubation,
o prodromal (catarrhal),
o exanthematous (rash), and
o recovery.
Incubation period : 8 - 12 develop symptoms
o Prodromal / catarrhal) ( 3 - 5 days)
Characterized by low grade to moderate fever , hacking dry cough
3 C : Cough,Coryza, Conjucntivitis
Kopules spot (gray-white, sand grain-sized dots on the buccal mucosa opposite the lower molars) )
1 -2 days before rash
Exanthematous / Eruptive (4 -5 days)
 Temperature rise 40 - 45 cͦ
 Rash begin behind ear painless not touchable.
Rash is maculapapollar cephalo - caudal
1st 24 hour
Entire face - neck , upper arm and upper part of the chest.
Next 24 hours
Back , Abdomen , Entire arms and Thigh.
2 - 3 days finally reaches the face and begins to fade on face.
In severe cases It may be petechial or hemorrhagic (black measles). there is brownish
discoloration and desquamation called post measles staining and disappears 7 10 after.
Organ involvement
Cervical lymphadenitis, splenomegaly, and mesenteric lymphadenopathy with abdominal pain may be
noted. Otitis media, pneumonia, and diarrhea are more common in infants.

Clinical stage or phase of Atypical measles
Atypical measles: who received vaccination with original killed virus vaccine.
1- Mild measles
2- Severe measles ( Toxic and shock type)
3- hemorrhagic measles
4- Variant measles
Modified measles
Modified measles : Measles for vaccinated child , who received serum immnoglobin
o Milder symptoms
o Incubation periods 21 days
Risk factors for measles
 Age 6 months - 5 years
 developing country
 Un vaccinated
 History of contact
 HIV
 Malnutrition
 Poor socioeconomic
 More in winter
Diagnoses of measles
 Clinical symptoms
mouth : koplik spot on mucousa membrane in first 24 hours
Skin: muculopopular rash - definitive diagnose
Eye : Corneal loading and conjuntival line Stemson line)
 Laboratory
 CBC : ↓WBC , ↑ lymphocyte and ↓ plt
 Serological: ↓ testing for IgG and Igm - 7
 PCR - Visualizing measles RNA virus
 X-ray - Pneumonia
 Lumbar puncture
 Skin biopsy
 Spicemen from ( nasopharynx urine)
Diffrential diagnostic
 Rubella
 Chicken pox - rash of painful and touchable
 Ruseola
 Scabies
 Toxoplasmosis
 Kawasaki disease
 Serum sick ness
 Mono nucleosis
 Drug rash
Treatment
There is no specific therapy for measles.
 Routine supportive care includes
 Oxygen
 NGT tube 150ml/kg
 maintaining adequate hydration and antipyretics.
 Oral scar - First normal saline wash , then Gemsa violation then oral nystatin drop.
 High-dose vitamin A supplementation .
Complication
o Otitis media
o Interstitial pneumonia
o Malnutrition
o Secondary TB
o Mesenteric lymphadenitis
o Anemia
o Encephalitis
o Corneal loading and conjuntival ulcer
Deaths most frequently result from bronchopneumonia or encephalitis.
Prevention
1. Vaccination
2. Control source
3. Protection of susceptible person
Vaccination
Measles Mumps rubella vaccine (MMR)
Live attetunated vaccine
Dose1 : 9 month or ˃ 6 month in outbreak
Dose 2: MMR 4 -6 years or may be ˃ 4 week effect dose.
Contraindicated in pregnancy
 Re vaccination indicated
 Vaccination before 1st birth
 Vaccinated with kwed vaccination
 Vaccination with K1
 Become active in 2 weeks use upto 5 years
Whooping cough
the whooping cough syndrome, usually is caused by B. pertussis, a gram-negative pleomorphic bacillus
with fastidious growth requirements.
The mean incubation period is 6 days. Patients are most contagious during the earliest stage.
Classic pertussis is the syndrome seen in most infants beyond the neonatal period through school age.
The progression of the disease is divided into:-
 Catarrhal,
 Paroxysmal, and
 Convalescent stages.
The catarrhal stage
marked by nonspecific signs (injection, increased nasal secretions, and low-grade fever) that last 1 to 2
weeks.
The paroxysmal stage
 Coughing occurs in paroxysms during expiration, causing young children to lose their breath.
coughing is due to the need to dislodge plugs of necrotic bronchial epithelial tissues and thick mucus. It
lasts approximately 2 to 4 weeks and worsening at night.
 The forceful inhalation against a narrowed glottis that follows this paroxysm of cough produces
the characteristic whoop.
 Post-tussive emesis is common ( Vomiting after cough) and
 Periodic apnea are common stage causing Hypoxic then hypoxic ischemic encephalopathy.
The convalescent stage
Coughing becomes less severe, and the paroxysms and whoops slowly disappear. Although the disease
typically lasts 6 to 8 weeks, residual cough may persist for months, especially with physical stress or
respiratory irritants.
Laboratory
 absolute number and relative percentage of lymphocytes in the peripheral blood
(lymphocytosis).
 The WBC count may increase from 20,000 cells/mm3 to more than 50,000 cells/mm3.
 parainfluenza virus, and
 C. pneumoniae
Treatment
 Erythromycin, given early in the course of illness, eradicates nasopharyngeal carriage of
organisms within 3 to 4 days.
 Azithromycin and clarithromycin
Complication
 hypoxia,
 apnea,
 pneumonia,
 seizures,
 encephalopathy, and
 malnutrition.
Criteria of admission whooping cough

Symptoms of whooping
+
danger sign
+
Complication
Meningitis
Meningitis is inflammation of the membranes (meninges) covering the brain and the spinal cord.
The most common causes are infection (bacterial, viral, fungal or parasitic),
Most common neonate bacterial meningitis
 Group B streptococci
 Escherichia coli
 Klebsiella
 Enterobacter
Most common ˃ 1 month bacterial meningitis
o Streptococcus pneumoniae
o Neisseria meningitidis
Viral meningitis is caused principally by entero-viruses, including coxsackieviruses, echoviruses.
Fungi caused by Cryptococcus neoformans and Candida.
Pathophysiology
Most often, the body’s immune system is able to contain and defeat an infection. But if the
infection passes into the blood stream and then into the cerebrospinal fluid that surrounds the
brain and spinal cord, it can affect the nerves and travel to the brain and/or surrounding
membranes, causing inflammation. This swelling can harm or destroy nerve cells and cause
bleeding in the brain.
Clinical feature of meningitis
High grade fever continues
Convulsion continues ˃ 15minutes or ˃ one times / hour
Projectile vomiting indicate ↑ICP
Headache Increased intracranial pressure
diplopia( Squant or nystigma)
photophobia (intolerance of bright light)
Neck stiffness
Feeding history ( unable to feed)
Conscious level : unconscious, stupor, lethargic and delirium.
Bulging fontanella with excessive crying may be present in infant.
irritable
Ptosis, sixth nerve palsy, anisocoria( unaequal pupil size) , bradycardia with hypertension, and
apnea are signs of increased intracranial pressure with brain herniation.
Symptoms
Kernig's sign: Severe stiffness of the hamstrings causes an inability to straighten the leg when
the hip is flexed to 90 degrees.
Brudzinski's sign: Severe neck stiffness causes a patient's hips and knees to flex when
the neck is flexed.
Differential diagnoses of meningitis
1. Complicated malaria
Some unsconsciousness but has no pulging fontanella ( meningeal irritataion)
2. Encephalitis has coma

3. History of viral disease but no meningeal
4. Febrile convulsion ( 6 month - 6 years)
 Convulsion is one m/2h
 Convulsion ˂ 15 minutes
 Convulsion + fever
5. Tetanus - has lock jaw , wound and consciousness
6. Salmonella typhi - Fever + bradycardia + Convulsion and constipation
7. Toxoplasmosis - fever + organomegaly + lymphadenopathy + rash if HIV positive.
Investigation
In Somalia lumbar puncture not available so that we request only :
 CBC
 ESR
 Malaria
 Electrolyte
 blood sugar
 X - ray
 CT scan
 MRI
Treatment of meningitis
If bacterial meningitis
• Dexamethasone injection give 30 minute before antibiotic for 2 - 4 days.

Uses:To Reduce Inflammation and to prevent Increase Intracranial Pressure(ICP).
• Ampicillin Injection for 7 to 14 days & Cefatriaxone Injection for 14 days
Uses: To Prevent Septicemia and Complication.
• Ibuprofen tab Or Syrup : For Inflammation
• Diazepam Injection 10mg 0.3mg/kg every convulsion to prevent Brain Damage.
• Phenobarbital tab 30mg ,at Night RD: 1-2mg/kg or 4-6 mg If convulsion > 2 times per day.
If viral meningitis
• Acyclovir 200mg 20-30mg/kg for 4-6times per day for 7 days ( 1 ×4)
• Supportive Treatments
Tubercular ( TB ) Meningitis:
• HRZE tab ¼ tab < 10kg ½ tab 10-14kg 1 tab 15-19kg for first 3 months
• HR tab ¼ tab < 10kg ½ tab 10-14kg 1 tab 15-19kg for second 8 months
• Prednisolone tab 5mg 2mg/kg, divide at morning & afternoon for first 1 month
Complications
 cerebral edema,
 venous sinus thrombosis,
 brain abscess ,
 septicemia,
 DIC and
 multi-organ failure (MOFS)
Pulmonary Tuberculosis
T.B infection is in active infection only exposure to contain of diseased person and there is no
clinical feature and skin test+.
T.B disease is active form , there is contact and clinical feature are positive with X-ray, sputum
and skin test positive.
Tuberculosis : is infection disease caused by mycobacteium tuberculli which mostly occur in
lung.
Types of T.B
 Primary : initial infect mostly in children ( Pulmonary T.B)
 Secondary : Re-infection mostly in adult (( Pulmonary T.B))
 Millary : outside of the lung ( Extra pulmonaryT.B)
Pathophysiology of T.B
Pneumonia Granuloma with fibrosis Caseous necrosis Calcification( Ca + and salt
deposit Cavitations.
Predisposing factor T.B
 ˂ 5 years
 Malnutrition
 Lymphom Steroid use ( Nephrotic and Asthma )
 Post measles ˂ 6 weeks
 HIV
 Down syndrome
High risk group of T.B
 ˂ 3 years
 C.H.D : poor feeding due to when he feeds he feels dyspnea.
Poor feeding malnutrition anemia ↓ immune TB
Diagnose of T.B
1. Carefully history taken
 Clinical symptoms suggest T.B
 History Contact of T.B
- Timing - last 2 years
- Closed contact Mother or sleeping in 1 room.
- Type of T.B contact
smear + T.B , X-ray + T.B and MDR T.B contact.
2. Clinical features
 Chronic Cough ˃14 days - not remitting not responding to antibiotics or
bronchodilator.
 Night sweat
 Fever , ↑ Respiratory rate
 Measure weight, height , Muac and record on growth chart
 Weigh loss or flattened growth curve is signal chronic respiratory disease Like
T.B.
 Respiratory Wheeze - which is unilateral and is not responding to bronchodilator
or percussion - dullness is sign of pleural effusion.
 Fatigue reduced play fullness
3. HIV testing
HIV + and 2 or more
Symptom of T.B : Treat the pt 2 symptoms of T.B + T.B contact +No BCG vaccination
+ ˂ 5 year : treat the patient.
4. Bacteriological confirmation by using gene expert
 RR + and MTB+ = MDR
 RR- and MTB + = MDR risk ( treat pulmonary T.B or new case)
5. T.B investigation
o X-ray
o Sputum
o CT
o Skin tuberculi test
Management of T.B
T.B Category
1. Category A
 Pulmonary T.B or new case
 Treat 6 month
 Phase 1: initial 1-2 month
 Phase 2: continuous 4 - 6 month
2. Category B
o Treatment failure:
Child taking Phase 1 ( 2 month) and taken sputum if it is positive
o Relapse MDR risk
o Defaulted : If child taking T.B treatment in 1 week and stops.
Differentiate MDR risk from MDR by using gene expert
 MTB ( Mycobacterium TB)
 RR ( Rifampicine resistance)
Treat in 9 month with steptomycine injection - 7 month -2 month streptomycine
If MTB and RR are positive
3. Category C
Outcome of T.B treatment
Cure
Complete
Failure
Death
Defaulter
Transfer
Drug calculation of T.B

1. 4 - 6 kg
Phase 1 : 1 HRZ + 1 E
Phase 2 : 1HR
2. 7 - 10 kg
Phase 2 : 2 HR
3. 11 - 14 kg
Phase 1 : 3HRZ + 2 E
Phase 2 : 3HR
4. 15 - 19 kg
Phase 2 : 4 HR
5. 20 - 24 kg
Phase 1 : 5HRZ + 4E
Phase 2 : 5 HR
Subgroup of ˃ 25 kg
A. 25 - 39kg
Phase 1 : 2 HRZE
Phase 2 : 2HR
B. 40- 54kg
Phase 1 : 3 HRZE
Phase 2 : 3 HR
C. 55-70 kg
Phase 1 : 4 HRZE
Phase 2 : 4 HR
D. ˃ 70 kg
Phase 1 : 5 HRZE
Phase 2 : 5 HR
Extra pulmonary T.B

occur 25% of T.B among children ˂ 5 year.
The most common forms :-
Peripheral Lymphnode T.B ( T,B adenopathy)
 Assymetrical painless mostly 2 - 10 years
 Mass ˃ 3 cm and more the 1 month
 Discharge sinus mostly in the neck area
 use fine needle aspiration
Pleural T.B
Dullness on percussion
Chest pain
Reduced breath sound
CXR and Pleural aspiration
Meningitis T.B
 Sign of meningitis
 Lumbar puncture , CSF and CXR
 ˃ 5 years
Abdominal T.B
 Abdominal swelling ,Ascites , pain
 Ultrasound: Ascites fluid analyse
Spinal T.B
 Deformity of spine Lower limb weakness
 Paralysis , unable to work
 X -ray spine
Pericardial T.B
Cardial failure
distant heart murmur apex beat
CXR and Cardiac ultrasound
Malnutrition is a state resulting from nutritional inadequacy or over nutrition related to excess
intake in which an individual’s physiological and physical functions are impaired.
Triage for acute malnutrition
 Severe acute malnutrition (SAM)

 Moderate acute malnutrition (MAM)
 At risk of malnutrition
 Health
Severe acute malnutrition (SAM) or PEM
Complicate
 Medical complication Criteria for SAM
 No appetite o MUAC ˂ 11.5 cm
 Oedema ++ or +++ o Z-score ˂ -3 SD
Manage for SC o Bilateral pitting edema
Uncomplicated
 No edical complication
Criteria of admission Malnutrition
 Good appetite
 Oedema +  General danger sign
Management for OTP  Oedema
 Poor feeding
MAM
 No weigh gain
Criteria for MAM
 Any child ˂ 3 kg
o MUAC 11.5- 12.5 cm  Anthrometric measurement
o Z-score ˃ -3 SD or -2
The different types of malnutrition

Wasting Shunting Underweight
(W/H) ( H/A) W/A
Short stature Chronic malnutrition

Kwashkor Marasmus
Protein colorie malnutrition or Protein energy malnutrition
Classification
1. Wellcom Classification
using W/A and presence edema
 WFA ˃ 80% + oedema = Kwashikor
 WFA 60 - 80% and No edema = Simple under weigh
 WFA 60 - 80 % and No edema = Kwashikor
 WFA ˂ 60 and no edema = Marasmus
 WFA ˂ 60 and edema = Marasmus / Kwashikor
2. Water law Criteria
a) Changes in weight may indicator of acute malnutrition
Actually wt (Kg)
Expected wt for ht at 50th percent
 Grade 0 = ˃ 90% Normal

 Grade I = 80 -89% Mild
 Grade III = 70 - 79% Moderate
 Grade IV = ˂ 70 % Severe
b) Changes in height may be indicator of chronic malnutrition

c) Grade 0 = ˃ 95% Normal
d) Grade I = 90 -94% Mild
e) Grade III = 85 - 89% Moderate
f) Grade IV = ˂ 85 % Severe
3. WHO criteria
 Wasting = ↓ WFA below median

 Stunting = ↓ HFA below median
4. Kanawahi criteria
Using MUAC
H.C
 Mild = ˂ 0.31
 Moderate = ˂ 0.28
 Severe = ˂ 0.25
 Bilateral edema
 Z-score ˂ -3
Kwashikor  MUAC ˂ 11.5
It is acute protein deficiency with normal or even high coloric intake.
This sickness the baby gets when new baby comes
Causes of kwashiokor
Primary
 Sudden weaning on starchy
 Maternal deprivation
 1st baby when 2 nd baby comes
 Depressed child
Secondary
 Pertusis - recurrent vomiting
 Chronic diarrhea - protein loss in stool
 Measles - complicating enterocolitis
 Parasitic infection - Giardiasis
Pathology of kwashikor
Acute protein loss lead
1. Decreased plasma protein
2. Brain slowly atrophy
3. Delayed bone growth - which causing reduction of total mass of bone
Osteoporosis
4. skeletal muscle - degenerative changes compensate ↓ plasma proteins
5. Liver - fatty infiltration ( steotosis) but usually no necrosis or cirrhosis
6. Gastro-intestinal tract - atrophy of villi decreased digestive and absorptive
enzymes
7. Pancreas - atrophy of acini ↓ digestive enzyme Steotorhea
8. Heart degenerative changes in cardiac muscle weakness( Heart small in
early stage) .
Clinical feature of kwashikor
1. Constant feature
2. Variable feature
Constant feature
1. Oedema
 Starts in dorso of feet and hands then
 the upper and lower limbs
 Bilateral pitting and painless
 Shiny overlying skin
 facial oedema produce prominent pale cheeks ( Doll facies)
 Periorbital edema
 No ascites and pleural effusion
Kwo Hypoalbunemia Reduced plasma osmotic pressure Decreased anti-

oxidant (V.E , V.A, gluthaton) Free radical damage increased capillary permeability
Increased ADH Na+ and water retension.
Grade of oedema
Grade 1 : + both feet or ankle
Grade 2: ++ both feet , lower leg , hand and lower arm
Grade 3 : +++ generalized all limb and face
2. Mental change
Patient looks apathic , Miserable
3. Growth retardation
failure to thrive weigh follow by weigh loss
4. Muscle wasting
o Muscle are thin , atrophic and weak
o Decreased MUAC ˂ 12cm
o H.C / C.C ratio ˃1
Variable kwashikor
1. Hair changes - hair brittle - easy pickable
Black Brown yellow Gray
Brittle hair :Flag sign - Alternating bands of lights color and normal color occurs in long haired
with multiple relapsed due to tyrosine deficiency .
Copper and tyrosonie Essential for melanin synthesis.
2. Dry scaling skin
 Erythems - hyper pigment
 Desquamation ( razy prving or flacky pint dermatosis)
Skin infectious come due to :
o Vitamin A deficiency
o Essential fatty acids deficiency
o Zinc deficiency
o oedema fluid
o Fissuring
kin infection sites :
Pressure area
 buttock
 Knees
 Ankle
Irritated area
 Groin
 Perineum
3. Hepatomegaly
o Reversible for treatment , No cirrhosis
o Fatty liver due to high fatty acid synthesis
4. Diarrhea
o Infectious - Gastroenteritis
o Non-infectious - due to malabsorption e.g. Lactulose intolerance
5. Abdominal distension
o Malabsorption
o Hypokalemia
o Toxic ileus with infection
o Gaseus
6. Anemia due to
o Iron deficiency - microcytic anemia
o Folic acid deficiency and B12 deficiency (megablatic anemia)
o Prothrombin deficiency (Heamorrhagic anemia)
o Protein deficiency ( Normochromatic mormocytic anemia)
7. Vitamin deficiency
Eye:
 Bitot spot s, Corneal ulcer
Mouth :
Stomatitis
Vitamin B12:
 Angular Stomatitis
 Cheilosis
Vitamin D
 Rickets
Vitamin K
 Bleeding tendency
Vitamin C
 Spong gum bleeding
INVESTIGATION OF KWASHIKOR
Confirm diagnosis
 Plasma protein o Plasma protein
Albumin ˂ 2.5 o Non-essential aminoacids
 CBC o Low urinary urea/ Creatinine
 Electrolyte
MANAGEMET OF KWASHIKOR
˂ 6 month
Phase Objective Product Protocol Meal time

used
Phase 1 To restore metabolic F 75 75 kcal× kg every 3 hour
function, stabilizer , treat = 100ml for 24 hours
and prevent complication /kg/day
Transition  To change  F100 75 kcal× kg
Phase therapeutic milk  Plumpy- = 100 ml
 Observe the nut /kg/day
increase in food
intake
 To test the RUFT
Phase 2  Intent to promote RUTF 200 4 milk meals
Rehabilitatio rapid weight gain kcal/kg/day + 2 RUFT =
n and catch growth. 6 meal
˃ 6 month

used
Transition  To change  F100 75 kcal× kg every 3 hour
Phase therapeutic milk  Plumpy- = 100 ml for day
increase in food
intake
Rehabilitatio rapid weight gain (B- 100) OR kcal×kg/500kcl + 2 RUFT =
n and catch growth. PLUMPNET /day 6 meal
Days of phases:
 Phase 1: Maximum 7 days
 Transition phase : 1 to 3 days
 Phase2 : 7 day
MARASMUS
Marasmus is a form of severe malnutrition characterized by energy deficiency . child with
marasmus looks emaciated.
Body weight is reduced to less than 60% of the normal ( Expected ) body weight for age.
Marasmus occurrence increases prior to age 1.
Clinical feature of marasmus
 Thin face or old face
 Muscle and subcutaneous fat wasting
 Dry skin and brittle hair
 Prominence of the scapula , spine and ribs
 irritable
The following can also occur :
 Mental change - intellectual disability (Growth retardation)
 Chronic diarrhea
 Respiratory infection
 Stunt growth.
Treatment of marasmus

used
Transition  To change  F100 130 kcal× kg
Phase therapeutic milk  Plumpy- = 130 ml
increase in food
intake
Rehabilitatio rapid weight gain kcal/kg/day + 2 RUFT =
n and catch growth. 6 meal
 In phase 2: assess progressive of the weight gain.

Every 3 days calculate
 5 kg Bad
 5-10 kg Moderate gain
 ˃ 10 kg Good weigh gain
If the child cannot take half amount of RUFT in 12 hrs - stop RUFT and give F75 1-2 days
then start RUFT.
Routine medical treatment at admission

Disease Treatment D1 D2 D3 D4 D5 D6 D7
Bacterial infection Amoxacillin X X X X X
Intestinal worms Albendazole X
Folic acid Folic acid X
deficiency
Malaria Systemic RDT X
Vaccines Measles X
PCV 10 X
Pent valent ( day of transfer
ATFC)
Vitamin A Retinol X
deficiency Minimum 4 month after last
dose
Contra indication of Iron in malnutrition

 It promotes bacterial overgrowth
 Body tries to prevent itself by converting tree iron tofferitine and need ATP and amino acid.
 Free iron promotes promotion free radical leading to uncontrolled chemical react.
10 STEPS FOR CHILD WITH COMPLICATION SAM
1. Hypoglycemia
Unconsciousness
Give:-
 D50% 1ml × kg
 D10% 5ml × kg
 D5% 10ml × kg
If you have not these : -
 Use on Rounded Teaspoon of sugar in 3 teaspoon of water ( 100ml) orally or 50ml

Dextrose 10% by NG tube Then start to re-feed F75 130× kg = /8 every 3 hour.
Example : child 10 kg
5×10 = 50 ml of D10% - 1: 4 Ratio
10% of 50 % + 40 of normal saline = 50 ml of 10%.
If you have not Dextrose 50% but you have D5% use 1:9 Ratio
Example: child 15 kg
 5×15 =75 ml of D5% - 1: 9 Ratio
 10% of 75 % = 7.5 of 50%. = 75 ml.
Rule 4: 1 Ratio : If does not have 10% you have 50% and 5%.
Rule 1: 9 Ratio : f does not have N.S of water and you need 10% , you have 5% and 50%.
2. Hypothermia
 Conguro method
 Warming
3. Dehydration: look tearing without history diarrhea.
 Resomol 5 ml × kg every 30 minute for 2 hour
 Shock give Mixed solution 0.20 ml/kg or 15 ml
Example : child 4 kg
 5 ml × 4 kg = 20 ml
 20 ml every 30 minute for 2 hour
 20 ml × 4 tmes ( 30 minute) = 80 ml for 2 hours.
4. Electrolytes & Minerals
 ˂ month : Zn 10mg ˃ Zn 20mg
 Potassium
 Magnesium
5. Infection
Penicillin G + Gentamicine
6. Micronutrient
Ferrofolic acid 60 mg
Vitamin A
Only marasmus - Not kwashikor
Kwashikor only if eye sign
 ˂ 6 month 50,000 IU
 ˃ 6 month 200,000 IU
And ˂ month Post measles.
7- Initial feeding
Kwashikor F75 100ml/kg
˂ 6 month
Marasmus F100 130ml/kg
˃ 6 month Both start F75 phase 1.
Criteria of discharge inpatient :

 Completed antibiotics
 Good appetite and gaining weight
 Lost any oedema
 Appropriate support in the community or home
 Mother / carer:
- Available
- Understands child’s needs
- Able to supply needs
Dehydration
LOOK ( GEMS)
I. General appearance - e.g. alert, irritable and lethargic

II. Eye - e.g. Normal , Sunken ,Deep sunken and puffy
III. Mouth - e.g. Drink normal ( moisture) , eagerly drink and unable drink
IV. Skin pinch - e.g. Rapid return , slowly , and very slowly.
Classification of dehydration
1) No dehydration
 General appearance - alert
 Eye - e.g. Normal
 Mouth - e.g. Drink normal ( moisture)
 Skin pinch - e.g. Rapid return
2) Some dehydration
o General appearance - e.g. irritable/ restless
o Eye - e.g. Sunken
o Mouth - e.g. eagerly drink
o Skin pinch - e.g. slowly <2sec
o Week pulse
o Urine_eg: Oligouria
3) Severe dehydration
 General appearance - lethargic
 Eye - e.g. Deep sunken
 Mouth - e.g. unable drink
 Skin pinch - e.g. very slowly.
Shock
capillary refill ˃ 3 second

Cold hands /feet
unconsciousness
Weak pulse and Hypotenson
Management of dehydration
1. No dehydration
Plan A : ORS
50ml × kg for 4 hours
˂ 2 year Give 50- 100ml / stool
˃ 2 year give 200ml /each stool
For the worm use Albendazole 400mg
 ˂ 1 year Contraindication
 1-2 year give ½ = 200mg
 ˃ 2 give 1 tablet stat single dose

Zinc
 ˂ 6 month give ½ = 10mg
 ˃ 6 month give 1 tablet = 20mg
2. Some dehydration
Plan B : ORS- Ringer solution

- Use oral ORS or NGT
80ml /kg for 4 hours
- If vomiting increase
use Ringer 80ml /kg for 4 hours
- If the patient is malnutrition
Give Resamol 5 ml /kg every 30 minute for 2hours
Also give Albendazole 400mg
 ˂ 1 year Contraindication
 1-2 year give ½ = 200mg
 ˃ 2 give 1 tablet stat single dose

Zinc
 ˂ 6 month give ½ = 10mg
 ˃ 6 month give 1 tablet = 20mg
Erytromycin 250mg
 ˂ 6 month give ½ × 2 for 3 days
 ˃ 6 month give 1×2 for 3 days
3. Severe Dehydration
Plan C I.V fluids
 Ringer lactate solution
 If missed Normal saline
 Mixed solution for malnutrition
 SAM + Cholera + Severe dehydration Give Ringer solution.
Ringer solution 100ml ×kg
Phase 1
30ml×kg
 ˂ 1 year : for 1 hour. Amount^Drop/Time or mins
 ˃ 1 year : for 30 minutes
Ask urination if then Oliguria
Return 3o ml × kg
Phase 2
70 ml × kg
 ˂ 1 year : for 5 hour—300 mins
 ˃ 1 year : for 2.5 hours—150 mins
Give Albendazole , Zinc And erythromycin same as Plan B.
Also give ORS 5ml × kg
 Infant : 3- 4 hour
 Child : 1-2 hour
Ongoing loss
Vomiting :10 ml × kg
Diarrhea : 15ml × kg
Deficit
 ˂ 2 year : 50 - 100ml/Stool
 ˃ 2 year : 200ml/Stool
Maintenance
100l ×kg
Bolus
30 ml × kg
 Do not give dextrose because it causes Hyponatremia .
Shock
1. Dehydration + Malnutrition
15 ml × kg = bolus for mixed solution for 1 hour
Not responding
Repeat 15 ml ×kg
Not responding
Cholera Suspect
Use Ringer 15 ml × kg ( unconsciousness) or consciousness use Resomal + F75
Not responding There is no hypovolemic
Suspect septic shock

Maintenance 4ml ×kg/hr
Blood transfusion
10 ml ×kg for 4 hours ( Whole blood + lasix 1ml ×kg)
2- Dehydration only
20ml × kg : Bolus
For Ringer lactate only
Not responding
Repeat 20 ml ×kg
Not responding there is no hypovolemic
Suspect septic shock
Blood transfusion
15ml ×kg for 4 hours
Example: 10kg × 15 ml × 10 = 6 drop /minute

4 hour ( 240 minute)
Differentiation between Malnutrition and dehydration
 Dehydration
 Dry mouth
 Oliguria
 Lack of tear
 Depressed fontanella in ˂ 18 mm
Cholera /Acute water diarrhea Case Management

Cholera has only patient aged 5 year or more presenting acute water diarrhea.
Confirmed cases: Those suspected for Vibro cholera or 0.39 has been confirm by culture or PCR.
Rice water + fever + No pain + Odorless = Cholera
Cholera kill the patient within 7 hours.
Assessment of diarrhea
I. Ask 5 questions
1. Duration
2. Frequency/ hour
3. Amount- large/small
4. Character - Colour/ consistent
5. Order
Ask urination To confirm degree of diarrhea
Anuria = ˂ 100 ml /24 hour
Oliguri = ˂ 300 ml/24 hour
Any case that hydrate water if not urinate 6 - 8 hour suspect Renal failure.
II. Look For General Condition
Convulsion + Abdominal distension + muscle paralysis = Hypokalemia
Eye , Mouth and skin
Approach for Cholera
1. assessment of dehydration
2. Rehydration
3. Use of antibiotic
4. Management Complication
5. Treat Co-morbidities
6. Discharge
Case management
 Replacement
 Maintenance
 Antibiotics
IMMUNIZATION
OPV0 Birth upto 15 day
BCG Birth upto 15 day - give BCG in left hand ( deltoid muscle) intradermal.
If missed BCG 45 days - 1 year
OPV1 Give 45 days
Penta1 Give 45 days - on the right thigh Site of injection
OPV2 30 days after dose  Penta 1 and 2 : Right thigh

Penta2  Penta 3 : Left thigh
OPV3 30 days after second dose

Penta3
Measles 9 month on the right hand + Vitamin A up to 5 years

In outbreak measles give ˃ 6 month.
BCG you can give until 11 month
OPV upto 5 years
Penta upto 2 years
Growth parameters
 Weight
 Height
 Head circumference
 Chest circumference
Growth measurement in length

o Recumbent length
o statuew
Growth in length and stature
 Zygote 0.14 mm in diameter
 Birth: Boy: 50.5 cm
Girl: 49.9 cm
 Year : Boy: 76.6.5 cm
Girl: 75 cm
Growth in Length and Stature
 At birth: 50 cm
 6 months: 68 cm
 1 year : 75 cm
 2 years: 87 cm
 3 years: 94 cm
 4 years: 100 cm (2 times birth length).
 Between 4-8 years, the height increases about 7 cm/year.
 5 years: 107 cm
 6 years: 114 cm
 7 years: 121 cm
 8 years: 128 cm
 Between 8 -12 years, it is about 5 cm/year.
 9 years: 135 cm
 10 years: 140 cm
 11 years: 145 cm
 12 years: 150 cm (3 times birth length).
For a quick estimation of height/length,
length from 2-12 year = (age in years × 6) +77 cm.
Formula for average weight

Age Weight
 3 - 2 month : Age ( month ) + 9/2
 1 - 6 year : Age ( year) × 2 + 8
 7 - 12 year : Age ( year) × 7 -5 /2
Head Circumference
o 0 month 35 cm + 8
o 6 month 43 cm + 4
o 1 years 47 cm + 2
o 2 years 49 cm + 2
o 6 years 51 cm + 2
o 12 years 53 cm + 2
Permanent Teeth
 6 years : First molar
 7 - 8 years : Primary teeth
 12 years : second molar
 ˃ 18 month : Third molar
Growth failure
 Primary : Low birth weigh
 Secondary : Normal Body weight due to organic 10% or inorganic 80%.
Growth Charts
Height for age : Stunting
Weigh for age: Under weight
Weigh for length: wasting
Weigh for height : wasting
BMI
Stage of development
o Neonate = 0 - 1 month
o Infancy = 1 month - 1 year
Early childhood
When to screen:
o Toddler = 1 - 3 year
At least 3 times before age 3
o Preschool = 3 - 6 year
 9 month
Mild childhood
 18 month
o School age = 6 -12 years  24 - - 30 month
Late childhood
o Adolescent = 13 - 18 years
Development of milestone
 Fine motor
 Gross motor
 Language
 Social
IQ or Intelligent test = Mental change
Chronological age
130 + = Gifted
145 + = Genies
70- = More
55 - = imbecile
25 - = Idiot
Gross motor
New born = barely able to lift head
6 month = easily lift head ,chest , upper abdomen and can bear weigh on arm.
 2 month = needs assistance
 6 months : can sit alone
 8 month : can sit without support and engage in play.
 9 month: crawl
 1 year : Stand independent
 13 month : walk and toddler
 15 month: can run
 8 - 10 years : Team sports
 10 years : Match sports to physical and emotional .
Fine motor
6 month = Palmar grasp - Uses entire hand to pick an object.
9 month = Pincer grasp - can grasp small object using thumb and fore finger.
Speech milestone
 1 - 2 month : Coos
 2 - 6 month : laugh and squels
 7 - 9 month: Mama and Baba unspecific
 10 -12 month : Mama and Baba specific
 18 -20 month : 20 - 30 words 50% Under
 22 - 24 months : 2 words sentence 75 under
 30 - 36 months: all most all speech
Breast feeding : is the recommended method for feeding normal infants during approximately
the first 6 months of life.
The 24-hour intake of milk varies between mother-infant pairs from 440–1220 ml, averaging
about 800 ml per day throughout the first 6 months
 Exclusive only : breast feeding from 0 - 6 month.
 Complementary : 6 month - 2 years
Early = ˂ 6 month
Late = ˃ 6 month
Adequancy of milk intake :
1. Sixty to 8 times aday
2. Urine should be colourless
3. Loose yellow stool - 4 times /day.
4 positioning in Breast feeding
Cradle holding : Hand support of the infant
Cross- craddle or transitional holding : Support both hand , child 10 kg.
Foot ball or Clutch hold : sitting
Side lying position
Good feeding :
1. Position
2. Good attachment
 Mouth wide open
 More areola above
 Lower limp outward
 Chin touching breast
Baby's reflex
 Rooting reflex : good position and open mouth
 Sucking reflex : Lip touch areola
 Swallowing reflex:
Tell the mother

 0 - 6 months = Breast feed only = complementary
 6 - 8 months = Begin Cereal 200kcl /day 3 times + Breast feed ( 3 spoon )
 9 - 11 months = begin Cereal 300kcal/day times + Breast feed
 1 year = Begin meet carrots, potatoes + breast feed 500 kcal/day plus 2 cup of milk , 3
paze food + salt no good to babies - give micro supplement + dewarming.

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SOA

3C Diagnosis: Some dehydration

1- Danger signs Total admission

Totally admission 24 hour admission then discharge

Solution: Drop/ minute = Amount × drop factor

Example: 500ml × 15 ml = 3 drop / minute

 Drop factor of colloid : 15 - 20 ml

1- Nutrient solution - D5%

2- Electrolyte solution - Ringer solution /Normal saline solution

3- Volume Expanders - Colloids and Dextran, plasma and albumin.

 D5% , D10% and D50% - To prevent dehydration and ketone.

 Normal saline , Ringer and Mixed Colloid )

Daily monitor signs in inpatient

Syrup + injection: Kg × required dose × ml

Tablet : Required dose × kg

Choice of I.V fluid

 Resuscitation Normal saline / Ringer solution

I. Fever - high grade ˃ 37.5

Differentiate Viral and Bacterial pneumonia

 High grade fever

2- Increased destruction ( Hemolysis)

Membrane defect Hemeglobinopathy

 H.spherecytosis  α thalasemia  G6 PD deficiency

Passively acquired antobody Actively forming antibody

Microcytic hypochromatic anemia Normocytic anemia Macrocytic hypochromatic anemia

Clinical feature of anemia

Types of anemia in Clinical

Neonatal Asphyxia ( Perinatal asphyxia)

If BSA ˂10% or Non- special areas

Increase glucose in blood

Converted into ketone bodies by the liver

body uses as energy

Then in the blood (ketonemia)

Clinical featureof DKA

 Blood glucose ˃300g/dl  Ketonemia  Metabolic acidosis

Differential diagnoses of DKA

Use normal saline or Ringer due to lactic acidosis or Pt is shock

Example: 20kg patient

Deficit : 20 kg × 85 ml = 1700 ml/kg

Amount per hour: 1700 + 1500 - 400 = 121ml / hour

Na+ and H2O

 Sometimes loose RBC and globuline = anemia

Respiratory droplet of measles

Epithelial cells of the trachea / bronchi

Bind H. protein - then bind CD46 and CD150

Then spread to lung tissue

Then lymph node

The second Viremia

Then General toxin

Pneumonia Diarrhoea Encephalitis

Clinical types of measles

Criteria of admission whooping cough

Differential diagnoses of meningitis

Some unsconsciousness but has no pulging fontanella ( meningeal irritataion)

2. Encephalitis has coma

In Somalia lumbar puncture not available so that we request only :

• Dexamethasone injection give 30 minute before antibiotic for 2 - 4 days.

Outcome of T.B treatment

Drug calculation of T.B

Extra pulmonary T.B

Triage for acute malnutrition

 Severe acute malnutrition (SAM)

The different types of malnutrition