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@marimphil wrote:

key points in case presentations
(natboard)
SPECIALITY : PAEDIATRICS
CASE : RASH
NAME OF EXPERT : Dr. D. RAM MOHAN RAO, PROF. & HEAD OF DEPT. OF PAEDIATRICS, G-36, MADHURA NAGAR, S.R.NAGAR(PO), HYDERBAD – 500038
A CASE OF RASH
HISTORY :
 H/o Repeated infections-unusual infections.
 Immunization status.
 Medication
 Exposure to Domestic pets, other animals.
 Arthopod bites, animals bites.
 Exposure to sick individual.
 Exposure to allergens, contaminated water & animal urine.
 Site of onset, direction & rate of spread.
 Associated with fever, period between appearance of rash and fever.
 Rash with fever, Irritability, Convulsions, Headache and Neck Stiffness.
 Rash with Joint pains, (Polyarthritis migratory)
 Associated with Joint paints, Pain abdomen, Red Colour Urine, Mylagia.
 Rash come/go on different parts of the body, with itching.
 Associated with bleeding points.
 Site of injury (Bleeding diathesis – Lichen planus).
 H/o Sorethroat.
 Aggravating factors.

CLINICAL EXAMINATION :
Type Location, Distribution, Colour Desquamation, other findings.
Type :
Petchiae, Purpura, Blanchable, Nonblanchable Purpura, Macule, Papule, Pustules, Plaque, Vesicle, Nodule, Confluent Desquamating rash.
Location :
• Ear-Measles
• Face
• Scalp – Atopic
• Extensor Surfaces
• Buttocks – HSP
• Site of Trauma
• Truncal – Measles, Rebella, Erthema infections
• Peripheral (Acral)
• Diaper Area.
Distribution Progression :
• Sun Exposed Areas
• Site of Exposure
• Hands Soles.
Colour:
• Erythematous
• Thickening
Gen Physical Examination:
• Eyes – Congestion
Exudate
Photophobia
Hemorrhage
• Pharynx – Congestion
Exudate
• Regional Lympladenopthy
• Lips – Fissuring of lips (Kawasaki)
• Tongue – Central Coating
Strawberry
• Hand, Feet – Desuamation
• Ear – Discharge
• Joint – S/o Inflammation
• Pallor
• Vitals – Temp, PR, HR, BP, CFT
Systemic Physical Examination :
• GIT – Hepato Splenomegaly
• Other Organomergaly
• Tenderness
• CVS – New Murmurs
• CNS – Photophobia
Investigations
• CBP, ESR
• Urine Analysis
• Platelet Count
• Coagulation Profile
• Allergic skin test
• Microscopic examination of a sample of the affected skin
• Skin biopsy
• Other specific tests – for various disease

DIFFERETIAL DIAGNOSIS :
Centrally distributed maculopapular rash
• Measles
• Rubella
• Erythema Infectiosum
• Examthem subitum
• Infectious Mononuclesous
• Drug induced eruption
• Typhus
• Leptospirois
• Lymes disease
• Typhoid fever
• Dengue fever
• Ery thema marginatum
• SLE
• Stills disease
Peripheral Eruption
• Secondary syphills
• Erythema muliforme
• Bact endocarditis
• Confluent desquamative rash
Scarlet fever (second dis)
Kawasaki Disease
TSS (Toxicshock Sydnormes)
SSSS(Staphylococcal Scaled Skin Syndrome)
Vesiculiobulious
• Varicella
• Disseminated herpes virus infection
• Ecthyma gangrenosum
Urtricarial
• Serum Sickness
• Erythermomdosum
• Acute febrile neutrophilic dermatosis
Purpuric
• Infective endocarditis
• Dengue fever
• Typhus fever
• HUS
• HSP
• Viral haemorhagic fever
Non Surgical Management:
• Isolation
• Oral hygiene
• Nutritious Diet
• Bed Rest
• Injection Vit ‘A’
• Stop – offering Drug
• Antibiotics
• Antihistarmines
• Specific Treatment

SPECIALITY : PAEDIATRICS
CASE : VOMITING
NAME OF EXPERT : Brig. M N G NAIR
COMMANDENT
MILLITARY HOSPITAL
SECUNDERABAD – 500015

APPROACH TO A CASE OF VOMITING
DEFINITION : All retrograde ejection of gastrointestinal contents from the mouth.

HISTORY
• Characteristics :
 Frequency
 Volume
 Colour
 Smell
 Contents
 Association with nausea
 Triggering and relieving factors
 Cyclical
• Associations :
1. Fever
 Gastroenteritis
 Otitis Media
 Systemic Infecitons
2. Loose Stools
 Gastroenteritis
 Food Poisoning
3. Projectile Nature with:
a) Abnormal Neurological Examination
i. CNS infection
ii. ICSOL
b) Signs of Intestinal Obstruction
i. Intussusceptions
ii. Pyloric Stenosis
iii. Adhesions
iv. Appendicitis
v. Hernia
4. Poor growth / weight loss
- Renal Metabolic Disease
5. Headache / Nausea
- Migraine
- Psychogenic
6. Cough
- Whooping Cough
- Bronchial Asthma
7. Drug Ingestion

EXAMINATION
1. Nature of Vomitus
- Colour
- Contents
- Amount
- Smell
2. CNS Examination
- Head Circumference
- Eye Examination for :

Loss of disc cupping
Absent venous pulsations
Raised disk margins
Papilledema
- Macewen’s / Carackpot sign
- Cranial nerve deficits
- Focal Neurolgocial deficits
- Investigations – MRI / CT
3. P/A Examination
- Visible peristaltic waves
- Distension
- Tenderness
- Palpable Mass
- Emptiness in any quadrant
- Bowel sounds
- Investigations – X-ray / USG / Endoscopy

DIFFERENTIAL DIAGNOSIS
• Neonatal
1. Atresia / Stenosis - Abdominal Distension
Failure to pass Meconium
2. Malrotation - Distension, meconium not passed
3. Volvulus - Distension, meconium not passed
4. Necrotizing Enterocolitis
i. Distension, Bilious vomiting
ii. Blood / Mucus PR
5. Meconium Plug - Distension, III-defined mass palpable
6. GE Reflux - Effect of posture and cough
7. Inborn errors of metabolism
- Adrenogenital syndrome etc.
8. Birth Asphysia - Irregular, slow gasping breathing with bradycardia / normal HR
9. Hyprocephalus - HC > 97th percentile for GA
- Bulging
10. Faulty Feeding Technique
• Infancy
1. Congenital Hypertrophic Pyloric stenosis
- Vomiting starting in the 2nd / 3rd week of life
- Becoming increasingly projectile
- Visible gastric peristaltic waves
- Palpable pyloric mass
2. Volvulus
- Abdominal distension
3. Intussusception
- Paroxysmal pain causing loud outcries
- Red-currant jelly stools
- Elongated, sausage – shaped in right upper quadrant
4. GE Reflux
5. Overfeeding
6. Gastroenteritis
- Fever
- Loose Stools
- Pain abdomen
7. CNS Infections
- Bulging fontanelle
- Headache
- Convulsions
8. Peritonitis
- Fever, pain abdomen
9. Inborn errors of metabolism
• Childhood
1. Gastroenteritis
- Fever, loose stools, pain abdomen
2. Medications
3. Toxins
4. Hepatitis
- Fever, jaundice, anorexia, pain abdomen
5. Pneumonia
- Fever, Cough, expectoration
- Dull percussion note
- Crepitations audible
- Consolidation on X-ray
6. ICSOL
- Headache, vomiting, papilloedema, focal signs
7. Appendicitis
- Fever, vomiting, pain abdomen
8. Peritonitis
9. Intestinal Obstruction
- Hernia /intussusception / peritonitis/foreign bodies/ rumors.
10. Intussusceptions
11. Psychogenic

MANAGEMENT
• Non – Surgical
- Sips of cold, clear fluids
- ORT
- Drugs

Metoclopramide
Domperidone
Phenothiazines
- Antibiotics for Infecitons
• Surgical
1. CHPS – Ramstedt’s operation.
(Pyloromyotomy)
2. GERD – Nissen’s Fundopication Prosthesis
3. Appendicitis – Appendicectomy
4. Hydrocephalus – Shunts
5. Intussusceptions – Hydrostatic pressure with Enema Exploration
6. Intestinal Obstruction – Exploration

SPECIALITY: PEDIATRICS
CASE : HEMIPLEGIA
EXPERT: DR. K. RAMAKRISHNAN

HISTORY
Most importance should be given for a proper and accurate history taking, since it gives the clue for a correct diagnosis, in CNS cases, unlike other systems where a proper diagnosis may be made even by clinical findings alone.

Following points must be stressed in the presenting complaints: Was the onset acute, sub acute or gradual? Was it associated or preceded with fever and/ or a seizure?
Any severe headache, vomiting or change in consciousness, preceding the onset of hemiplegia. If so, sudden or gradual? Is the condition deteriorating, static or improving?

Past history: Any history suggestive of vasculitis, rheumatic fever, trauma or thrombosis or bleeding disorders.
Review of developmental history, antenatal, perinatal, and post natal should always be recorded. Family history and consanguinity must be noted.

CLINICAL EXAMINATION

A detailed general examination, including temperature, pulse, BP and anthropometric measurements should be noted. Any facial dysmorphism, cutaneous lesions like café au lait spots, angiomas or depigmentation and condition of teeth have to be noted. Look for any mid line defect. Examination of chest, abdomen and palpation of femoral pulse must always be a part of general physical examination. Note for unusual body order. Palpation of anterior fontanel, and auscultation for bruits done in erect posture-over both globes, temporal fossae, and mastoid region (six sites).

CNS examination:
Higher function assessment according to the age of the patient.

Cranial nerves.

Olfactory(I) rarely assessed, Optic nerve (II): Elicit the blink reflex, (in a child>3 mon.old) Fundi examination: optic disc, retinal hemorrhage, chorioretinitis,
Look for visual acuity, and field of vision depending on the age, and sensorium of child.
III, IV, VI Cranial nerves: Enophthalmos ptosis, meosis, lack of sweating, on the ipsilateral side of face.. See the papillary reflex, If ptosis is present, look for ‘Marcys Gunn sign,’ Test the movements of all extraocular muscles. If the child is unconscious see the ‘doll’s eye movement. Examine for internuclear ophthalmoplegia by looking for defective adduction of the medial rectus and nystagmus of the abducting eye.
See for nystagmus, and if present stage it (stage 1,2,3)

V Nerve: Look for deviation of jaw.. corneal and conjunctival reflexes. Test sensation of face.
VII Nerve: Is the facial nerve affected. If so, ipsilateral or contralateral to the side of hemiplegia..Look for’emotional ‘facial weakness. Confirm whether UMN or LMN type of involvement.. Look at the naso labial fold and wrinkling of fore head. Is the taste salivation and/ or tear production affected?
Look for the strength of orbicularis occuli. Elicit ’Mc Carthy reflex’

VIII (Cochlear and Vestibular).
Rinne’s test for defective hearing. Test for vertigo

IX and X : Any nasal regurgitation or change in voice? Movement of palate.
XI Nerve: Test the sterno mastoid and trapezius muscles
XII Nerve: Look for deviation of tongue when protruded, fasciculations when the tongue is inside the mouth, and/ or atrophy.

Motor system: Look for abnormal movements
Muscle power (0-5- MRC scale). Tone, pronator sign for upper extremities and Barre sign. for lower limbs, depending on the age of the child.. Look for coordination by applying specific tests for cerebellar function: Finger nose test,’ tapping in a circle (one cm.diameter) test’, look for rebound phenomenon.

Sensory system in older child
Temperature, light touch, crude touch, based on a dermatomal distribution. Examine for position and vibration sense, and elicit Roberg’s sign.

Reflexs: Elicit superficial and major tendon reflexes, knowing its root value, and cutaneous nerve involved..Elicit plantar reflex and ankle clonus

Infants:
Posture and muscle tone, primitive reflexes: Moro reflex, Tonic neck reflex, Righting-reflex, palmar and plantar grasp reflexes, Vertical suspension, and Landau reflex

INVESTIGATIONS:
Besides, routine CBC, Mantoux and X Ray chest, the following investigations should be done:
CSF examination.
Electrolyte estimation (Na, K, Cl2 )
PT, APTT.

Antiphospholipid antibodies (in SLE), ANA,
Estimation of antithrombin III level, protein C, S, and factor V Leiden.

ECG, ECHO, EEG, NCV, and CT brain
Cerebral angiogram, or MR angiography (MRA)/ Functional MRI
Evoked potentials VERs/BAERs and, SSEPs)
Radiography of Spine and Myelography
Diffusion-Weighted Magnetic Resonance Imaging in acute stroke conditions
Magnetic Resonance Spectroscopy (MRS), when cerebral metabolites are of significance.
Positron-emission tomography (PET), esp. in children for surgical programmes.. Single – photon – emission computerized tomography (SPECT) for conditions where regional blood flow study is important.

DIFFERENTIAL DIAGNOSIS

The following conditions should be kept in mind to arrive at a provisional diagnosis. Of the following, only 3 most probable conditions judged by history and clinical signs must be discussed in differential diagnosis.:

(i) Hemiplegic cerebral palsy
(ii) Infantile hemiplegia (to be considered only in a child up to 6 years)
(iii) Vascular causes, including IEM (haemarrahage, thrombosis, vasculitis, trauma, hemiplegic migraine)
(iv) Infective causes: bacterial, viral, fungal (Meningitis, encephalitis, TBM)
(v) Demyelintng: Acute Desseminated Encephalo Myelitis (ADEM)
(vi) Todd’s paralysis also may be considered, if hemiplegia follows a prolonged seizure.
(vii) Space occupying lesions

Non-surgical management
Depends on etiology. Measures to reduce cerebral edema, correction of fluid and electrolytes imbalance, if any has to be done.
Long term management like physiotherapy, speech therapy, and rehabilitative measures may be required in some cases. Referral to a child development center (CDC) is advisable for selective patients.

Surgical management
Surgical management will be required in space occupying lesions and selective cases of spastic cerebral palsy.

Any other: Site of the lesion, (Localisation) must be discussed before considering the differential diagnosis..

SPECIALITY: PEDIATRICS
CASE: CEREBRAL PALSY
EXPERT: DR. KURIAN THOMAS

CLINICAL EXAMINATION

HISTORY

The candidates should be very clear about the duration of the illness – present illness.

A patient with recurrent episodes of almost identical illnesses with symptom free intervals – the last episode to be described in full and others included under the heading of past illness.

All events (including treatment) should be described in the chronological order - as the disease develops
Describing each symptom separately is not desirable.

Illnesses which have origins in the neonatal period to be described from birth e.g. birth asphyxia with seizures leading to Cerebral palsy.

Describe in detail only relevant history. Discredit for spending too much time on irrelevant history.

All aspects of history to be discussed and documented. At postgraduate level they must know which is relevant and which is irrelevant.

At the end of history the candidate should be able to draw some conclusions regarding the problem.
e.g. Degenerative diseases of brain
Intracranial space occupying lesion
Chronic liver disease

PHYSICAL EXAMINATION

General physical examination

Observation about general appearance

Diagnostic clues – positive and negative

Growth

Detailed measurements only in growth problems.

Development

Details only in cases of developmental delay.

System involved

Give all details.

Other systems

Positive findings only.

SUMMARY

The candidates should summarize the case in 4 or 5 sentences – only relevant history, positive findings and important negative findings

DIAGNOSIS

Complete diagnosis to be given.

Substantiate the diagnosis based on history, findings and course of the
disease – both positive and negative.

Differential diagnosis only if there are valid reasons.

Candidates should state why the DD is suggested

INVESTIGATIONS

Relevant investigations only.

The candidates should know why he is suggesting a particular investigation.

TREATMENT

Essential treatment only.

Rationale of treatment should be explained.

SPECIALITY : PEDIATRICS
CASE : COMA/ALTERED SENSORIUM
NAME OF EXPERT : DR. D. VIJAYASEKARAN, DVS HEATH CENTRE
#18/1, HARRIS ROAD, PUDUPET, CHENNAI-600002

COMA

HISTORY

When? How? Under what circumstances? How long? Who were there?
Witness should be questioned.
History of fever - CNS infection, febrile encephalopathy(cerebral malaria, Dengue
encephalopathy, leptospirosis with aseptic meningitis etc)
History of Headache, vomiting – increase in ICP.
History of seizures
If known seizure disorder – whether omission/over dosage of AED
History of fall/head trauma – concussion, intracranial injury
History of drug intake – suspicion is very misleading – family members on drugs
History of Pica – Lead poisoning
Similar episodes before – lethargy, vomiting, Coma – Inborn error of metabolism
Underlying chronic medical conditions – CRF, hepatic encephalopathy etc

CLINICAL EXAMINATION

 ABC
 Glasgow Coma Scale
 Pulse – bradycardia - ↑ ICT
 Temp. – Febrile seizures, CNS infection, febrile encephalopathy
 Respiration – effortless tachypnea-metabolic acidosis, DKA
- slow breathing – respiratory depression
- ataxic breathing – cerebellar herniatino
 BP – HT, hypertensive encephalopathy, increased ICP
 Pupils – asymmetry – unilateral dilated fixed pupil – Tentorial herniation
Pinpoint – OPC, barbiturates
Dilated, fixed – postictal, atropine etc.
3. Differential Diagnosis

 Metabolic
 Trauma, Tumour, Toxins
 CNS infection
 Vascular
 Demyelination
 Postictal
 HIE
 Persistent vegetative state

Management Non Surgical

 ABC
 Draw blood fro biochemistry/drug/toxin
 25% dextrose if hypoglycemia
 IV mannitol if increase in ICP
 IV antibniotics if suspicion of meningitis
 IV anticonvulsants, seixures
 Sublingual nifedipine if hypertensive
 Antidotes for poisoning
 Investigate the cause and manage accordingly

Surgical

 Extradural/subdural tap
 Cerebral abscess – drainage
 Tumous with obstructive hydrocephalus – VP shunt

Any other

 Water & electrolyte balance – look for SIADH/central diabetes insipidus
 Nutrition
 Care of back/bladder/bowel/eye
 Passive physiotherapy
 Parent counseling & support
 Dolls eye movement – Full – brainstem intact
 Fundi – retinal hemorrhages – ICH accidental or non accidental
Palilloedema – increased ICP
 Skin rash – Meningococcal meningitis
Hepatis encephalopathy
 Icterus – Hepatic encephalopathy
 Bruises, subconjuctival haemorrhage, black eye, Battle’s sign, bleeding from ENT – ICH following head trauma
 Focal deficit – opposite hemispherical lesion
 Meningeal signs – CNS infection, subarachnoid hemorrhage

Investigations

 Blood sugar – hypo/hyperglycemia
 Serum electrolytes, ABG
 Blood urea, serum creatinine
 LFT, serum ammonia – Reye’s syndrome, IEM
 Serum lactate pyruvate, toxic screening, serum AED levels
 If fever – QBC, MSAT, Dengue serology, WIDAL(fever workup), NEC, CSF, peripheral smear
 CT brain P & C – Trauma, tumor, vascular, CNS infection, HIE, ADEM
 LP & CSF analysis
 EEG – triphasic waves in metabolic encephalopathy
PLEDS in hepes encephalitis
Spikes and waves in non convulsive status eiplepticus
 MRI brain – ADEM, HSV encephalitis

SPECIALITY : PEDIATRICS
CASE : A CASE OF BLEEDING DISORDER
NAME OF EXPERT : DR. G R SETHI, PROFESSOR DEPARTMENT OF PEDIATRICS, MAULANA AZAD MEDICAL COLLEGE, NEW DELHI

HISTORY

Localized Vs Generalized bleeding
Markers of serious bleed
First presentation Vs recurrent bleeding
Differences in presentation of a bleeding and clotting disorder in relation to:
Age of presentation
Gender
Site of bleeding
Relation with injury (early/late bleed)
Family history(and pedigree chart)
Drugs related with thrombocytopenia/thrombasthenia/pancytopenia
Bleeding disorders due to chronic liver disease, chronic renal disease, autoimmune disorders with vasculitis
Clinical pointers towards HIV in a multi transfused case
Previous history of bleeds with reference to site, amount, need for hospitalization a d transfusion.
POINTS IN EXAMINATION
Significance of Pallor out of proportion to bleed, and lymophadenopathy.
Identification of lesion like petich, purpura, echymosis, nodules and hematoma
Distribution
Hess’s test
Detailed examination of joints and bones
Significance of organomegaly
Markers of vasculitis and autoimmune disease
DIFFERENTIAL DIAGNOSIS OF:
Bleeding due to supectd thrombocytopenia
Bleeding due to thrombocytopenia with other series also affected (Pacnytopenia)
Clotting disorder
Vasculitis Syndromes
MANAGEMENT OF:
Acute bleed
Specific underlying cause

SPECIALITY : PEDIATRICS
CASE : PARAPLEGIA
NAME OF EXPERT : DR. R SHANMMUGHASUNDHARAM, NEW # 100 –OLD # 48 CATHEDRAL ROAD, GOPALAPURAM, CHENNAI 600086

Paralysis or weakness of both lower limbs

Site of lesion
1. Cerebrum : Trauma – Parasagittal
Tumor – Parasagittal meningioma
Thrombosis – of a) Unpaired anterior cerebral A
b) Sagittal sinsus

Spinal Cord

Spinal roots

Peripheral nerve

Muscle

Clinical features and History taking

1) Onset – mode
Acute
Subacute
Chronic
Intermittent(Very rare – T.B.)

2) Progression
Static
Progressive
Improving

3) Cause
Trauma
TB contact
Primary tumor
Vaccine/Dogbite
Family
Similar illness(Hereditary spastic paraplegia)
Drug intake(Causing neuritis/myopathy)

Complications
CNS
PNS
Automatic
Other systems

SYPMPTOMS AND SIGNS

Spinal paraplegia
- clumsiness of gait
- refusal to stand or walk
- loss of bower/bladder control
- loss of sensation

Signs

Scoliosis
Note: Presence of scoliosis in females before puberty and males of all ages should strongly suggest neuro muscular disorder of spinal cord pathology

Sking abnormalities over spine

tuft of hari

pigmentation

sinus

mass

Pes cavus

Tropic ulcers

Posture

Hip flexion corresponds to L1, L2 so is affected in high lesions. Thus in thoracic lesions – assume a from – legged posture

Preserved L3 allows some knee flexion and extnsion

Lower lumbar lesion results in preserved hip/knee movements and ankle dorsiflexion

Hip extension corresponds to L5, S1, S2 and so is affected in all but lower sacral lesions

Lesions at S3 or below completely spare lower limb sensory and motor function, but cause paralysis of bladder and anal sphincters and saddle anesthesia

Muscle bulk/joint deformity/contractures

Head size/shape/fontalnelles

Scar on abdomen(VP shunt)

Tender spine

Cutaneous markers of T.B.

Herpetic vesicles(Herpes-myceletis)

Cafa au lait spots(Neuro fibromatosis)

Q. How to differentiate UMN from LMN causes
A.
1. Cortial sensory loss
2. Seizures
3. CNS dysfunction(e.g.) altered senorium, mental retardation

Tumor 1. Vascular

Trauma 2. Transverse myclitis

T.B. 3. Nerotining myclitis

DEVIC’s disease (combination of transverse myclitis
and optic atrophy)

Motor neuron disease

Hereditary opastic paraplgie

Q. In compressive myelopathy what is the order of involvement of tracts?
A.
In general i. Pyramidal tracat
ii. Posterior column
iii. Spinothalamic tract

Differentiation between Intra/Extra medullary lesion

Features Extra Intra

Motor

UMN – spasticity - Common and persist Less common

LMN – a) Atrophy 1-2 segments at the site Wide due to ant.horn
Of involvement

b) Tropic Not common Present
changes

c) Fasciculation Rare Common

Sensory

Root pain Common Rare
Parenthesis Rare Common
Dissociated Absent Present
Sensory loss
Joint position Lost Spared

Autonomic

Bowel, Bladder Late Early
disturbance

Q. How to differentiate between Automatic Autonomous bladder
Automatic Autonomous
Site of lesion UMN LMN
Symptoms Frequency/Urgency Overflow incontinence
Bladder size Decreased Increased
Pyramedal sign + _

Q. What questions do you ask about bladder function
a) Sensation of bladder filling
b) Starting micturition
c) Sustaining
d) Stopping
e) Satisfaction of emptying
Q. What is Paraplegia in flexion
A. Involvement of pyramidal tract + posterior column

Q. What is Paraplegia in extension
A. Involvement of only pyramidal tract

Q. Salient features of Transverse Myectis
A. i) Motor loss of below the level
ii) Sensory loss below the level(all modalities)
iii) Bladder involvement
iv) Most common site – Mid-thoracic region
v) Evolves over a period of several days to weeks

Q. How will you mention the diagnosis
A. 5 levels: 1) Motor level
2) Sensory level
3) Reflex level
4) Vertebral level
5) Autonomic involvement

SPINAL PARAPLEGIA
Etiolgoy
1. Congenital malformation
- Arachnoid cyst
- AV malformation
- Atlanto aial dislocation
- Arnold chiari malformation
- Myclomeningocele

Familial spastic paraplegia

Autosomal Dominant (A.D)

Autosomal Revessive (A.R.)

X linked Recessive (X.R.)

Infections

T.B.

Hopkins paxalysis(Post Mycoplasma)

Diskitis

Epidural abscess

Herpes Zoster

Metabolic

Adrenomyelo neuropathy

Argininemia

Krabbes disease

Transverse Myelities

Devic’s disease

Encephalomyelitis

Idiopathic

Trauma

Consussion

Epidural hematoma

Dislocaton/fracture

Tumors

Astrocytoma

Ependymoma

Neuroblastoma

Ewings sarcoma

INVESTIGATIONS

MRI

Single most important investigation but clinical findings should guide this investigation

CT

Important role in identifying extent of bony defect in spina bifida

Also investgation of choice in Atlantoaxial anomalies or instability

Plain X-Ray – Spina bifida Atlantoaxial anomalies

Lumbar Puncture(L.P)
a. Tuberculosis:
Total Count(T.C) – usually > 500, lymphocyte predominant
Protein – increased
Glucose – decreased
AFB +/- (Acid Fast Bacillus)
PCR +ve (>95%)
Note: LP is contra indicated in acute stage, since it aggravates parapareis

b. Herpes zoster myelitis
TC: Pleocytosis
Protein: mild evelation
Glucose –normal or decreased

c. Tumours (e.g) (Astrocytoma)
(Secondaries –
Acute myeloid leukemia(AML)
Acute lymphocytic leukemia(ALL)

Electromyography(EMG)
a. When suspecting metabolic myopathies (e.g.) Severe Congenital Autosomal Recessive Muscular Dystrophy (SCARMD)
b. To delineate segmented involvement to patchy lesions

Nerve Conduction Velocity (NCV)

When features are suggestive of peripheral neuropathy

Arteriography
A.V. malformation

ANA/Anti ds DNA
SLE – Lupres myciopathy

SPECIALITY : PEDIATRICS
CASE : MONOPLEGIA
NAME OF EXPERT : DR. S. GNANA SUNDRARAM, 43(OLD NO.), IV MAIN ROAD, HOUSING BOARD COLONY, KOTTUR GARDEN, CHENNAI-600085

HISTORY TAKING

Establish if the case is a monoplegia (or) part of hemiplegia, quadriplegia or paraplegia. Then the following history is a must.

(A) Age of onset :

(i) Infant - Brachial plexitis(ERB’s Palsy)
(ii) 10-15 yrs - Monomelic spinal Muscular.
Atrophy(REF.1)
(iii) Any age - Injury to plexus or Nerve – Infection

(B) Sex :

Male - Monomelic spinal muscular atrophy

(C) Family History :

Hereditary brachial plexopathy
Homocystinuria

(D) Birth History :

Birth injury C.P.
ERB’s Palsy

(E) Trauma:

Extended arm during prolonged surgery
Fall & Injury to plexus
Trivical Hereditary brachial plexopathy

(F) Infection:

Poliomyclitis
Osteomyelitis leadin to neuropathy
(Ex.) Osteomyelitis humerus upper end plexitis – neuritis

(G) Immunisation:

OPV

Tetanus Toxiod precipitating hereditary Brachial plexopathy

(H) Asthma(Hopkins syndrome)

Asthmatic Amyotrophy(REF. 2)
Monoplegia following asthma

(I) Site of Involvement:

Promixal muscles

Distal Muscles

(J) Pain

At rest

Increased by movement

(K) Inability to use Limb

Ex. Trauma/others

(L) Pain + Inability to use Limb

Plexitis
Trauma
(M) Sensation : Present/absent/extend of loss of sensation

(N) H/o. Bleeding Diathesis

(O) Duration:

• Acute
• Chronic
• Progressive
• Recurrent eg. Hereditary Brachial Plexopathy
• Improving or not

(P) H/o. ICT:

Headache, Vomiting and seizures

(Q) Contractures:

Foot drop – peroneal nerve palsy

CLINICAL FEATURES
General appearance:
Facies:
Storage disease – mucolipidosis
Causes compression at the carpal tunnel in children
Eyes:
1. Cataract
2. Storage disease subluxation lens – homocystinuria
Lymph adenopathy – Neuroblastoma etc.
Anemia – bleeding disorder
Skin Purpunt Spot
System examination:
HIGHER FUNCTION
CNS:
Conscious/unconscious
Group according to Glasgow coma scale
CRANIAL NERVES
Cr. Nerve:
- Visual impairment – subluxation lens – homocystinciria
- FUNDUS: Bleeding/Chroid tubercle or secondaries
Cranial Nerve:
Fascial palsy a part of ERB’s Palsy
Other Cranial nerves:
Particularly lower cranial nerves at the atlanto accipital region

MOTOR SYSTEM
Inspection:
Nutrition:
Wasting – Poliomyclitis
Wrist Drop – Peroneal Nerve Palsy/Contractures
Faciculation
Trauma
Power:
Tone:
Hypertonia/Hypojonig – Cerebral Palsy
Hypotonia - Poliomyelitis/Plexitis
Reflexes:
DTR
Brish & Exagerrated – CP(Hypotonic)

DTR Plexitis/neuropathy
Superficial reflexes
Plantar extensor – C.P.
Neonatal Replexes: (Ex.) Moro present or absent
SPINE:
- Local tenderness/swelling
- Abnormality eg. Short neck
Gait:-
Assessing Recovery:
Proximal to distal. This is plotted by Tinel Sign(Tingling in the distal part of a limb caused by tapping over the regenerating segment of a nerve).
RESP SYSTEM:

Wheeze – Asthma

Paradoxical breathing – Diaph paralysis

As part of ERB’s (T1 Involvement)

CARDIOVASCULAR SYSTEM:

Myxoma of the heart recurrent Monoplagia
Cynotic heart disease eg. Fallots producing Thromoembolism

ABDOMEN:

Hepato splenomegaly – storage disease

DIFFERENTIAL DIAGNOSIS D/D

Hypotonic Cerebral Palsy:
Tone but DTR exaggerated. Plantar extensor/H/o of birth injury

Plexopathy/Neuropathy:
Involvement of proximal muscles with or without sensory loss. There is gradual improvement over the years Eg. Brachial Palsy

Aneterior Horn Cells:
Poliomyelitis

Tumours:
Primary – malignanat schwannoma secondary – neuroblastoma

Trauma: Eg. 1. Neonatal brachial Neuropathy

To plexus

To bone Osteomyelitis - neuritis

In born error of Metabolis:

o Homocystinuria
o Storage disorder – Carpal tunnel syndrome

Spinal abnormality:

Cervical & lumbar

Degenerative disorder (Monoplegia + fasciculation, Tremar, Blindness + Consanguinity)

(a) monomelic spinal muscular atrophy. This is a rare disorder Fasciculation common
(b) SCHINDLER’s Disease Acute, Sudden on set
Monoplegia/Hemiplegia + Blindness

INVESTIGATIONS

Hemogram

Hb
PCV – increased in cyanotic heart disease
TC
DC
Smear – abnormal cells/Blast cells or B.T.C.T.

Blood culture & Antibiogram – Oseteomycitis – Neuritis

Nerve Conduction

(eg) Normal in spinal muscular atrophy
But EMG is consistent with denervation

CT/MRI/Sonogram

For spinal tumours

Electromyogram(EMG)

To distinguish between plexus injury and nerve injury

Screening test : For Amino Aciduria

(eg) Homocystinuria

Muscle Biopsy: Monomelic spinal muscular atrophy

CSF: (Eg.) Normal except for a mild elevation of protein in lumbar plexitis
TREATMENT

Non Surgical:

Antibiotics if necessary

Physiotherapy

Electrical Stimulation

Others

Surgical:

Removal o tumour

Eg. Malg. Schwannoma

Restoration of injured nerve
Others:

Prevention:
 Prevention of EB’s Palsy by careful delivery of baby
 Takin precaution to avoid trauma, infection etc. in Precipitating Heridatory Bracial Plexopathy
 Avoiding prolonged extension of upper limb/arm during Surgery – to avoid trauma to plexus

REFERENCES

REF. 1

Tandon R Chronic segmental spinal Muscular Atrophy of upper extremities in identical twins. Neurology 1990; 40: 236-239

REF. 2

Shahar EM – Poliomyelitis – like paralysis during recovery from Acute Bronchial Asthma. Possible ethiology and risk factors.

Paediatrics 1991;88: 276-279

SPECIALITY : PEDIATRICS
CASE : A CASE OF GASROINTESTINAL
BLEEDS
NAME OF EXPERT : DR.(MRS.) MAYA MUKHOPADHYAY, 11 DR. BIRESH GUHA STREET, KOLKATA – 700017

HISTORY: Age of baby
Nature and site of bleeding-epistaxis/hematemasis/malena/hematochezia
Onset-Acute/Chronic
Amount of bleeding
History of ingestion of spurious compounds eg. Bismuth, Iron preparation etc
Any other bleeding manifestation-Petechiae, Purpura
Urine output

CLINICAL EXAMINATION:
General Survey:
Consciousness
Anemia/Jaundice/Cyanosis/Neck glands/Neck veins/Jaundice/Cold peripheri/BP/Pulse/Respiration
Systemic Examination:
Inspection
Abdominal distention/Prominent superficial veins
Local Examination of Anal fissure
Palpation
Free fluids
Flow of veins
Organomegaly
Palpable mass
PR examination
Percussion
Shifting dullness
Auscultation
Peristalsis sound

Investigation
APT test
Hb%, TC, DC, ESR, CRP, Platelet count, BT, CT, Grouping, Cross-matching
Blood Urea/Creatinine
LFT
PT, PTT
Blood C/S
Urine C/S
Stool fro Ocult blood
USG Abdomen
Barium Swallow
Endoscopy
Colonoscopy
Detection of H Pylori
Radio nuclide study to determine site of bleeding of GIT where endoscopy and barium study have failed
Angiography in selective cases and to detect vascular malformation

Differential Diagnosis
Varicose vein
Exraphepatic Portal Hypertension
Cirrhosis
Meckel’s diverticulum
Polyp
H Pylori

Management
Non-Surgical
O2 Administration

IV drip 10-20 ml/kg of Ringer Lactate or NS rapidly, repeat SOS till urine output, pulse & BP improves and cutaneous perfusion normalized
Hematocrit to maintain at 30o

Blood transfusion if needed accordingly

NG tube suction

Bleeding site to be determined-mucosal lesion/varicela bleed
Treatment of Mucosal lesion,
Antacid/Ranitidine/Omeprazole
Treatment of causes-ITP etc

Treatment of variceal bleed

Vasopression/Nitroglycerin/
Glypression/Somatostatin
Octreotide
Beta blockers fro recurrent variceal bleed

Ballon tamponade

After patient is stabilized - Endoscopic sclerotherapy-every week for 3-6 wks
Observe for ulceration/stricture/disphagia

If bleeding continues emergency surgery-
Shunt surgery or
Portal decompressive surgery

Factory indicating poor prognosis-
[Massive hematemesis
Initial hematocrit<20o
HB<7gm%
Transfusion exceeding 85ml/kg
Failure to identify source of bleeding
Coexisting coagulation disorder
Associated liver disease of other systemic disease]

SPECIALITY : PEDIATRICS
CASE : FEVER AND RASH
NAME OF EXPERT : DR. ARVIND SAILI, PROFESSOR OF PEDIATRICS
LADY HARDINGE MEDICAL COLLEGE, NEW DELHI

FEVER AND RASH
Fever is one of the common presentations of children admitted to the hospital. Very often fever is of viral origin and lasts fro a short duration. Quite often fever becomes a diagnostic enigma. However, when fever presents with rash or rash associated with fever, the diagnosis becomes relatively easier because rash acts as a clue to the diagnosis of the disease. The skin rash with fever may reflect the effect of toxin(scarlet fever), bacteria(meningococcemia), virus(dengue), inflammation(drug rash) or vasculitis(henoch scholein purpura).

The onset of rash relative to the course of underlying illness if any should be ascertained. The temporal relationship of fever with rash should be seeked. Associated features should be looked for e.g. diarrhoea(enteroviral) and severe illness(meningococcal). Lcocatino of rash would also give a clue about the aetiology. History of similar illness in the neighborhood or siblings, and the use of drugs must be noted.

A systematic history, clinical examination further aided by investigations would assist in the diagnosis of the disorder. A pertinent differential diagnosis can at least be deduced, thus making the management easier. The following key issues need to be addressed while discussing/presenting a case of fever with rash.

History
1. Age of the child.
2. Temporal relationship of fever with rash
3. Prodromal symptoms
4. Site of onset of rash and its distribution
5. direction and rate of spread of rash
6. Morphology of rash(macular, popular, pustular)
7. Progression/Course of rash
8. +/- Pruritis photosensitivity(waxing & waning pattern in erythema infectiousness)

Associated systemic symptoms:
Cough, coryza, conjunctivitis, arthritis, LN pathy, diarrhoea, abdominal pain, chest pain, bleeding from any other site, carditis.

Did the patient become toxin at any point int h4 course of illness.

Immunization history(rules out vaccine preventable exanthems)

H/o contact with individuals with similar illness(infectious aetiology)

Is the individual immunocompromised

H/o intake of drugs, food allergy(drug rash)

Travel history to endemic areas vital(viral hemorrhagic fevers)

H/o animal or arthropod bites(body lics, rat fleamite, rat bite)

Similar illness in the nighbourbood or siblings

H/o joint pains

H/o Pica

Examination
Fully expose the area preferably in natural light.
Rash
Morphology - Colour, size consistency, margins, surface characteristics
Distribution - Symmetrical/arymms, centrifugal/centripetal
Flexor/Extensor configurations - Nummular/discoid, annular, circiant4e, arcirate, gyrati/serpiginous, linecir, grouped, reticulate
Are onlythe exposed areas affected.
Are the genitals/mucous membrane also involved.
Nikolskyi sign(positive in SSSS, TEN)

Vitals
Signs and symptoms of sepsis.
Shock – Strep Toxic Shock Syndrome(TSS), staph TSS, ecthyma gangrenosum, purpura fulminans, dengue hemorrhagic fever, meningococcemia.
Oral Examination
Koplik spots – Measles
Forchheimer spots – palatal petichiae – German measles, Infectious mononucleosis, scarlet
fever.
Pharyngitis – Rh fever, IMN
Strawberry tongue – Scarlet fever, Kawasaki disease
L.N.
Post auricular and sub-occipital group-German measles
Joints
Arthritis in German measles
Meningitis
Enteroviruses, meningococcemia, aseptic meningitis.
Hepatosplenomegaly – infectious mononucleosis, typhoid, TORCH infectious(neonates)
Heart – Murmur(Rh. Fever, SABE)

Measles Rubella Exanthema Subitum Fifth Disease Varicella
Incubation period 8-12 days 2-3 weeks 5-15 days 4-14 days 10-21 days
Etiological agent Pramyxovirus RNA-Toga virus HHV- Parvoirus-B-19 Varicels-zostor virus
Prodrome Upper respiratory syndrome, Conjunctivitis, Fever, Koplik Spots Mild fever and coryza Sudden onset of high fever Low grade fever Brief illness headache and fever
Rash characteristics and Location Maculopapular starts from face behind the ears goes down till feet in next 2 days Macular confluent begins on face and spreads Rah 3-4 dyas after fever begins on trunk and spread oil Slapped check appearance later spreading to trunk and limbs more prompt-extensive surface Papular rash later changing to clear vesicles. Appears in crops. Starts from trunk and then spreads
Post rash staining Fades in some order Fades quickly and nil Maculopapular fades within 3 days-nil Lasts fro 1-3 weeks. Lacy reticular pattern on fading-may was and wane Scrab formation after 4-7 days hypopigmented lesion
Fever and associated symptoms Fever at peak when rash appears and remains high grade x 2 days after rash Mild fever, Post occipital and retroauricular lymphadenopely Sudden onset of high fever. Fever falls along with appearance of rash Fever is mild Fever rises with each fresh crop of rash
Complications Pneumonia, Encephalitis, Diarrhoea, Malnutrition Embryopathy Febrile seizures Arthropathy and myalgia. Aplastic crises in patients with hemolytic anaemia Pneumonia, encephalitis in Immunocom-promised. Severe illness in adolescent and adults

INVESTIGATIONS
1. Hb, TLC, DLC, ESR, platelet count
2. Chest X-ray
3. Blood culture(bacterial infection)
4. Tourniquet test
5. Viral serology
6. TORCH screen
7. LE cell, rheumatoid factor
8. ECHO(cardiac involvement)
9. ECG(rheumatic fever)
10. Urine analysis(Bacterial endocarditis)
11. Lumbar puncture

MANAGEMENT
1. Maintenance of vitals (oxygenation, BP, blood sugar, temperature, airway, etc.)
2. Temperature control
3. Intravenous fluids
4. Antibiotics fro bacterial infections (rational antibiotic therapy)
5. Blood/blood product transfusion as per requirement
6. Specific therapy for specific disorders

SPECIALITY : PEDIATRICS
CASE : ANEMIA - GUIDELINES FOR THE RESOURCE PERSONS/FACILITATORS

NAME OF EXPERT : DR. MKC NAIR, DIRECTOR, CHILD DEVELOPMENT CENTRE, MEDICAL COLLEGE CAMPUS, THIRUVANANTHAPURAM-695011

Anemia – Salient Points
HISTORY:
Present – Acute or Chronic
- Lethargy
- Fatigue
- Scholastic backwardness
- Frequent infections
- H/o Exertional dyspnoea breathlessness
- H/o Bleeding – any site e.g. PR
Past
- H/o Pallor
- H/o bleeding disorders
- H/o Malaria
- H/o Blood transfusions
- H/o Worsening of pallor with infections
- H/o Chronic infections – bronchicetasis, osteomylitis, dactylitis
- H/o Connective tissue disorders – Rhumatoid arthritis, SLE
- Chronic renal Diseas
- Chronic diarrhea
- H/o Surgery – involving stomach/terminal clieum(B12 def)

Personal History
- H/o Chewing pencil(lead)
- H/o Pica-mud, ice cube, etc.
- Hook work – H/o walking barefoot – open defecation

Family History
- Anemia
- Blood transfusions
- Splenectomy
- Bleeding disorders
Birth History
- Preterm birth
- H/o bleeding in the newborn period

Dietetic History
- Strict vegan (B12 def.)
- Iron def. Diet
- Duration of breast feeding
- Time of cow’s milk introduction
- Milk protein introlerance
- H/o goat’s milk intake(folate def.)

Drug History
- Phenytoin
- Methotrexate
- Pyrimethamine

CLINICAL EXAMINATON
General
- Stunted growth
- Thin built, marasmic/obese(rare)
- Pallor-nails-bulbar conjunctiva-tongue, Blue line of gums
- Eyes-blue sclera
- Tongue-papillae are atrophied red painful tongue(pernicious anemia)
- Nails-longitudinal-ridges
- Koilonychia
- Thins, brittle nails
- Bony abnormalities
- Triphalangeal thumb(Diamond Blackfan anemia)

CVS
- Tachycardia
- Cardiomegaly
- Murmurs
- Venous hum

Abd
- Splenomegaly
- (Mother’s Splenomegaly)

CNS
- Alaxia
- Hyporeflexia
- Clonus
- Babinski positive
INVESTIGATIONS
Blood

Haemoglobin – low

Red cell indices – MCV, MCH, RDW

Retic count – Decrease in Diamond Blackfan, Increased in hemolytic anemia

TC, DC

Neutropaenia

Hypersegmented(>5 segments) nucleated neutrophils>5% - folic acid def.

Platelet increased in iron def. Anemia

Blood smear – study morphology of RBC, nucleated RBC, basophilic stippling(lead poisoning)

Decrease in c/c infections

Iron binding capacity – increased in iron def., decrease in c/c injections

Serum ferritin – decrease in iron deficiency

Adenosine deaminase activity in RBC, increased in Diamond Blackfan

Lactate dehydrogenase increased in hemolysis

Serum folate level

Bore Marrow – Aspiration
- Morphology of cells
- Erythroid hyperplasia(iron def.)
- Meglablastic precurcessor
- Absent harmodiderin slain
- Ring sideroblasts
- Culture – reduced no. of erythrocyte colony forming units
- Biopsy if indicated

Urine
- Methyy malonic acid excretion orotic acid crystal – orotic aciduria

Schelling test
- to confirm absence o intrinsic factor in pernicious an anemia

Approach
- Anemia alone or other marrow elements involved. In aplastic anemia only anemia is seen.
- Is there reticulocytosis? Seen in hemolysis and bleeding
- Peripheral smear-
• Spherocytosis-hereditary spherocytosis, Wilson disese, Autoimmune hemolytic anemia
• Sickle cells-sickle cell anemia
• Target cells
• Nucleated RBC
• Microangiopathy
• Bite cells-G6PD deficiency
- RBC size-
• Microcytic(lead poisoning, thalassemia, irondefeciency)
• Macrocytic anemia(folate deficiency, B122 deficiency, Pearson syndrome
• Normocytic-Chronic disease, renal failure, hypothyroidism

DIFFERENTIAL DIAGNOSIS
Infancy
- Diamond Blackfan
- Transient erythro blastopaenia of childhood
- Physiological anaemia of infancy
- Red cell hypoplasia
- Drug induces – eg; Chloramphenicol

D/d of Microcytic an anemia
- Iron def anemia
- Sideroblastic anemia
- Lead poisoning
- A trans ferinanimia

D/d of Megaloblastic anemia
- Folic acid deficiency
- Abnormalities of folate metabolism
- Drug induced eg; Methotrexate, Pyrimethamine
- Vitamin B12 deficiency
- Orotic aciduria
- Thiamnie responsive anemia

Haemolytic anemias
- Membrane defects(spherocytosis, elliptocytosis)
- Enzyme deficiencies, G6PD deficiency
- Auto immune haemolytic anemias
- Hyper splenism
- Hemoglobinopathies(Sickle cell anemia)
- Thalassemias
Pancytopenias
- Constitutional/acquired

MANAGEMENT
- Iron def. Oral ferrous iron.(sulphate, gluconate, fumarate)
- Parenteral Iron-only in cases of malabsorption
- Imrove diet-decrease milk ot 500ml/day, Iron rich foods, combination foods with Vitamin C
- Severe anaemia – blood transfusion packed cells
- Frank CCF-Exchange transfusion with fresh packed cells

Special situation
- Iron chelating therapy
- Steroids in Diamond Blackfan
- Vitamin B12 supplementaion, Folinic acid supplementation
- Folate supplementation in haemolytic anemia
- Recombinant human erythropoietin eg: renal failure,
- Bone marrow transplantation Pancytopenias
- Gene therapy
Surgical management
- Splenetomy

SPECIALITY : PEDIATRICS
CASE : A CASE OF QUADRIPLEGIA
NAME OF EXPERT : DR. V. D. PATIL, PAEDIATRICIAN, 48/49 “SHIVA KRUPA”, HINDWADI, BELGAUM
Must be covered Points
History History of epidemics
History of Recent Viral Infection
Adequate Immunization
History of cousanguinivity
Fetal movement antenataly
March of evens of paralysis
History of Trauma to spinal cord
History suggestive of TB
History of convulsions/altered sensorium
History suggestive of cranial nerve palsies
History of respiratory difficulty
Bladder/bowel disturbances
Clinical Examination Assessment of higher functions
Cranial nerves
S/o Meningitis
Whether UMN for LMN type of Paralysis
Tone
Involuntary movement
Fundoscopy
Investigations Apart from routine investigations
NCV studies
Muscle biopsy
CT/MRI of skull and spine
EEG
Differential Diagnosis Poliomyelitis
G B Syndrome
Spinal dystrophies
Cong. Myopathies
Cerebral palcies hypo and hypertonic
Cord injuries
Non surgical management Role IV IG
Role of rest
Role of physiotherapy
Nutritional management
Care of bladder and bowl
Prevention of bed sores
Role of ATT
Surgical Management Cord decompression
Release of contractures
Selective neurecting

SPECIALITY : PAEDITRICS
CASE : SEIZURE DISORDER
NAME OF THE EXPERT : COL P L PRASAD, HOD, DEPT OF PEDIATRICS, CHCC, LUCKNOW-2

Guidelines for the Resource Personnel/facilitators

SEIZURE DISORDER

1.HISTORY

Aims: (a) to differentiate Febrile seizure from afebrile seizure and age related childhood seizure disorder like infantile spasm
(b) To differentiate provoked seizure from unprovoked seizure
( c) To differentiate Seizures from Pseudo seizure

(i) Situation of episode
ii) Any triggering factor
(iii) Detailed eye witness account (eye witness should be asked to imitate the actions which he has seen)
(iv) Onset
(v) Level of consciousness
(vi) Presence of aura
(vii) Recovery
(viii) Speech
(ix) Bowel/bladder incontinence
(x) Any injury sustained
(xi) Duration of seizure activity
(xii) Presence of fever (whether followed the seizure or preceded the seizure)
(xiii) Drug treatment history
(aa) Any antiepileptic drugs, their dosage and history of discontinuation
~ (bb) Potentially epileptogenic drugs like ciprofloxacin, antimalarials
(cc) Drugs with important interactions
(xiv) History of provoked seizure e.g. drug intoxication
Meningitis / encephalitis
Head Injury
Intracranial hemorrhage
Interruption in treatment
Metabolic events like hypoglycemia, hypocalcaemia,
hypomagnesaemia, dyselectrolytemia, hypoxia etc.
(xv) Special attention should be given to identify
(aa) Absence seizure
(bb) Myoclonic seizure
(cc) Simple partial
(dd) Complex partial seizure
(xvi) History of heart disease, depression, anxiety, head injury, past h/o febrile seizure

Family History

H/o of febrile seizure
H/O afebrile seizure
H/O sudden unexpected death
H/O syncope

Social History

Education
Employment
Driving Status
Home situations
Sports
Use of alcoholic drinks

CLINICAL EXAMINATION:

(i) Look for episodes of seizure /Pseudo seizure by hyperventilation
(ii) Neurocutaneous markers
(iii) Dysmorphic features, micro/ macrocephaly
(iv) Asymmetry in body size
(v) Cerebral bruit
(vi) Tremor
(vii) Hair loss
(viii) Weight gain
(ix) Gum hypertrophy, Hirsutism
(x) Acne, ataxia
{xi) Neonate with neurometabolic disorder, failure to thrive, rash, vomiting etc
(xii) Absent reflexes, visual field defects
(xiii) Neurodevelopmental delay, cerebral palsy, other neurologic disorders
(xiv) Long tract signs, focal neurological deficits, raised intracranial pressure
(xv) Mental retardation, hyperactivity etc.
(xvi) CVS exam if syncope is considered

INVESTIGATION

(a) Hemogram to diagnose evidence of infection
(b) Electrolyte estimation
(c) Metabolic parameters like calcium, magnesium, sugar
(d) EEG
(e) Video EEG
(f) Neuroimaging: MRI is better than CT. Show differentiating features of neurocysticercosis and tuberculoma
(g) Newer modalities like EEG telemetry. MEG. MRI advances. SISCOM

4 DIFFENTIAL DIAGNOSIS

(a) Diagnosis of seizure: absence, myoclonic, febrile etc
(b) Movement disorder
(c) Syncopal attack
(d) Migraine

NON SURGICAL MANAGEMENT

(a) Treatment of acute attack
Emphasis on ABC .
Use of Lorazepam, Midazolam, Diazepam, their doses and method of administration
Use of Phenytoin, and then Phenobarb
Frequency of repeating the drugs to abort an attack

(b) Treatment of neonatal seizure
Use of 10% Dextrose bolus and continuous IV
Use of Calcium, Sodium, Magnesium salt
Use of Phenobarb first and then Phenytoin

(c) Treatment of solitary seizure
Whom to treat?
(i) First seizure if symptomatic due to etiology like atrophy, inflammatory granuloma, infarct, migration defect
(ii) Type of seizure: Choice of drugs depends upon
(aa) type of seizure,
(bb) age
(cc) Economic factors
(dd) Specific epileptic syndromes

(d) Treatment of febrile seizure
(i) Use of Lorazepam, Midazolam, and Diazepam-IV and per rectal
(ii) Method of giving per rectal and doses. Give demonstration
(iii) Use of antipyretics and diazepam during fever episode, if recurrent seizure

(e) Treatment of childhood epileptic syndromes

These are age related. Some may have progressive natural course. Some like Benign neonatal convulsion, benign rolandic epilepsy may not require any treatment. Many syndromes evolve with passage of time and diagnosis may have to be revised.

(i) West Syndrome: ACTH/Steroids
Sod Vallproate
Clonazepam
Vigabatrin
Pyriodoxin

(ii) Lennox Gestaut Syndrome Lamotrigine
Sod Valproate
Vigabatrin

(iii) Landau Kleffner Syndrome Sod Valproate
Steroids

(iv) Juvenile Myoclonic epilepsy' Sod Valproate

(f) Treatment of inflammatory granuloma, Neurocysticercosis, tuberculoma
Treat seizure disorder with appropriate AED. Treat Neurocysticercosis and tuberculoma as per protocol.
(g) Treatment of other seizure disorder
(i) For generalized tonic clonic seizure: Phenyotin
Sod Valproate
Carbamazepine

(ii) Partial Seizure: Phenobarbitone
Carbamazepine
Phenytoin

Discuss cost of drugs, their availability, efficacy, side effects before taking final decision. Carbamazepine is a good first choice and superior to Sod Valproate for partial seizure

Discuss drug interactions and adjustment of drugs doses.

(h) Duration of treatment
(i) Generalized epilepsy: 2 years
(ii) Partial seizures due to granuloma: 18-24 months
(iii) Absence attacks 18-24 months
(iv) Symptomatic epilepsy due to underlying disease process like mental retardation, atrophic lesion, post traumatic causes: longer duration

Relapse rate has been found t be varying from 20-30 %. The longer the seizure free duration the greater is the chance of having achieved a cure and lesser the chance for relapse.

Tapering is done over a period of 6-12 weeks.
Monotherapy / Poly therapy:

Follow up: every 3-6 months. Basically to identify side effects of drugs and adjustments of their doses, if required.

SURGICAL MANAGEMENT

Indication: failure of medical therapy
Intractable epilepsy
Surgical procedure likely to give more benefit in control
Patient is significantly disabled due to seizure

Contraindication: Generalised interictal discharges
Epileptogenic focus inaccessible to surgery
Multiple seizure patterns
Types of surgery:
Ant temporal lobectomy for mesial temp sclerosis
Corpus callosotomy for drop attacks
Lesionectomy for tumors, hemartoma
Hemispherectomy

ANY OTHER
Ketogenic diets: Diets rich in fats and with low protein and carbohydrates will produce ketosis like situations, which is beneficial in seizure disorder by reducing its incidence. He has been useful in mentally retarded and handicapped children where compliance can be ensured. Due to high fat children refuse t take such diets.

SPECIALITY : PAEDITRICS
CASE : HEMIPLEGIA
NAME OF THE EXPERT: DR. K RAMAKRISHNA, “ASHTAPATI”, KADAVANTHRA, KOCHI-682020

I. HISTORY
Most importance should be given for a proper and accurate history taking, since it gives the clue for a correct diagnosis, in CNS cases, unlike other systems where a proper diagnosis may be made even by clinical findings alone.

Following points must be stressed in the presenting complaints: Was the onset
acute, sub acute or gradual? Was it associated or preceded with fever and lor a seizure? Any severe headache , vomiting or change in consciousness, preceding the onset of hemiplegia. .If so ,sudden or gradual? Is the condition deteriorating, static or improving?

Past history: Any history suggestive of vasculitis, rheumatic fever, trauma or thrombosis or bleeding disorders.
Review of developmental history, antenatal, perinatal, and post natal should always be recorded. Family history and consanguinity must be noted.

CLINICAL EXAMINATION

A detailed general examination, including temperature,pulse,BP and anthropometric measurements should be noted. Any facial dysmorphism, cutaneous lesions like cafe au lait spots, angiomas or depigmentation and condition of teeth have to be noted.
Look for any mid line defect. Examination of chest, abdomen and palpation of femoral pulse must always be a part of general physical examination .Note for unusual body order. Palpation of anterior fontanel, and auscultation for bruits done in erect posture- over both globes, temporal fossae, and mastoid region ( six sites)

CNS examination:
Higher function assessment according to the age of the patient.

Cranial nerves.

Olfactory(I) rarely assessed, Optic nerve(II):Elicit he blink reflex,(in a child> 3 mon.old) Fundi examination: optic disc,retinal hemorrhage ,chorioretinitis,
Look for visual acuity, and field of vision depending on the age ,and sensorium of the child.
III,IV, VI Cranial nerves: Enophthalmos ,ptosis ,meosis ,lack of sweating, on the ipsilateral side.offace.. See the pupillary reflex, If ptosis is present, look for 'Marcus Gunn sign,' Test the movements of all extraocular muscles. If the child is unconscious see the 'doll's eye movement. Examine for internuclear ophthalmoplegia by looking for defective adduction of the medial rectus and nystagmus of the abducting eye. See for nystagmus, and if present stage it ( stage 1,2,3)
V Nerve: Look for deviation of jaw. .corneal and conjunctival reflexes. Test sensation of face.
VII Nerve: Is the facial nerve affected. If so ,ipsilateral or contralateral to the side of hemiplegia.. Look for 'emotional 'facial weakness. Confirm whether UMN or LMN type of involvement.. Look at the naso labial fold and wrinkling of fore head. Is the taste ,salivation and lor tear production affected?
Look for the strength of orbicularis occuli. Elicit 'Mc Carthy reflex'

VIII (Cochlear and Vestibular).
Rinne's test for defective hearing. Test for vertigo

IX.and X : Any nasal regurgitaion or change in voice? Movement of palate.
XI Nerve: Test the sterno mastoid .and trapezius muscles
XII Nerve:Look for deviation of tongue when protruded, fasciculations when the tongue is inside the mouth ,and lor atrophy.

Motor system: Look for abnormal movements
Muscle power (0-5- MRC scale). Tone, pronator sign for upper extremities. and Barre sign. for lower limbs, depending on the age of the child.. Look for coordination by applying specific tests for cerebellar function: Finger nose test,’ tapping in a circle (one cm.diameter) test' ,look for rebound phenomenon. .

Sensory system in older child
,Temperature,light touch, crude touch ,based on a dermatomal distribution. Examine for position and vibration sense, and elicit Romberg's sign.

Reflexes: Elicit superficial and major tendon reflexes, knowing its root value, and cutaneous nerve involved. Elicit plantar reflex and ankle clonus

Infants: ,
Posture and muscle tone, primitive reflexes: Moro reflex, Tonic neck reflex,Righting - reflex, palmar and plantar grasp reflexes, Vertical suspension, and Landau reflex

INVESTIGATIONS

Besides, routine CBC, Mantoux and X Ray chest ,the following investigations should be
done:
CSF examination.
Electrolyte estimation (Na + ,K+ ,Cl -)
PT, APTT.
Antiphospholipid antibodies(in SLE) 1 A. NA
Estimation of antithrombin III level, protein C , S,and factor V Leiden.
ECG, ECHO, EEG, EMG ,NCV, and CT b