NBE CME programme for DNB consultants - National Board Of ...

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NBE CME programme for DNB consultantsCerebral PalsyHistory - The candidates should be very clear about the duration of the illness – present illness; Apatient with recurrent episodes of almost identical illnesses with symptom free intervals – the lastepisode 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 developsDescribing each symptom separately is not desirable; Illnesses which have origins in the neonatalperiod 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 knowwhich is relevant and which is irrelevant; At the end of history the candidate should be able to drawsome conclusions regarding the problem e.g. Degenerative diseases of brain -Intracranial spaceoccupying lesion, Chronic liver diseasePhysical 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 findingsDiagnosis - Complete diagnosis to be given; Substantiate the diagnosis based on history, findingsand course of the disease – both positive and negative; Differential diagnosis only if there arevalid reasons; Candidates should state why the DD is suggestedInvestigations - Relevant investigations only; The candidates should know why he is suggestinga particular investigation.Treatment - Essential treatment only; Rationale of treatment should be explained.Coma/Altered SensoriumHistory- When? How? Under what circumstances? How long? Who were there? Witness shouldbe questioned. History of fever - CNS infection, febrile encephalopathy(cerebral malaria, Dengueencephalopathy, leptospirosis with aseptic meningitis etc) ; History of Headache, vomiting – increasein 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 isvery misleading – family members on drugs; History of Pica – Lead poisoning; Similar episodesbefore – lethargy, vomiting, Coma – Inborn error of metabolism; Underlying chronic medicalconditions – CRF, hepatic encephalopathy etcClinical Examination-ABC; Glasgow Coma Scale; Pulse – bradycardia - ‘! ICT; Temp. – Febrileseizures, CNS infection, febrile encephalopathy; Respiration – effortless tachypnea-metabolicacidosis, DKA -slow breathing – respiratory depression, ataxic breathing – cerebellar herniatino;BP – HT, hypertensive encephalopathy, increased ICP; Pupils – asymmetry – unilateral dilatedfixed pupil – Tentorial herniation-Pinpoint – OPC, barbiturates, Dilated, fixed – postictal, atropineetc.Differential Diagnosis- Metabolic; Trauma, Tumour, Toxins; CNS infection; Vascular; Demyelination;Postictal; HIE; Persistent vegetative stateManagement -Non Surgical - ABC; Draw blood fro biochemistry/drug/toxin; 25% dextrose ifhypoglycemia; IV mannitol if increase in ICP; IV antibniotics if suspicion of meningitis; IVanticonvulsants, seixures; Sublingual nifedipine if hypertensive; Antidotes for poisoning; Investigatethe cause and manage accordinglySurgical - Extradural/subdural tap; Cerebral abscess – drainage; Tumous with obstructivehydrocephalus – VP shuntAny other - Water & electrolyte balance – look for SIADH/central diabetes insipidus; Nutrition;146
NBE CME programme for DNB consultantsCare of back/bladder/bowel/eye; Passive physiotherapy; Parent counseling & support; Dolls eyemovement – 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 hemorrhageInvestigations - Blood sugar – hypo/hyperglycemia; Serum electrolytes, ABG; Blood urea, serumcreatinine; 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 & CSFanalysis; EEG – triphasic waves in metabolic encephalopathy; PLEDS in hepes encephalitis;Spikes and waves in non convulsive status eiplepticus; MRI brain – ADEM, HSV encephalitisBleeding DisorderHistory- Localized Vs Generalized bleeding; Markers of serious bleed; First presentation Vsrecurrent 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), Familyhistory(and pedigree chart) ; Drugs related with thrombocytopenia/thrombasthenia/pancytopenia;Bleeding disorders due to chronic liver disease, chronic renal disease, autoimmune disorderswith vasculitis; Clinical pointers towards HIV in a multi transfused case; Previous history of bleedswith reference to site, amount, need for hospitalization a d transfusion.Examination - Significance of Pallor out of proportion to bleed, and lymophadenopathy; Identificationof lesion like petich, purpura, echymosis, nodules and hematoma; Distribution; Hess’s testDetailed examination of joints and bones; Significance of organomegaly; Markers of vasculitis andautoimmune diseaseDifferential Diagnosis -Bleeding due to supectd thrombocytopenia; Bleeding due tothrombocytopenia with other series also affected (Pacnytopenia); Clotting disorder; VasculitisSyndromesManagement -Acute bleed; Specific underlying causeParaplegiaParalysis or weakness of both lower limbsSite of lesion - Cerebrum - Trauma – Parasagittal, Tumor – Parasagittal meningioma, Thrombosisof a) Unpaired anterior cerebral A b) Sagittal sinsus; Spinal Cord; Spinal roots; Peripheral nerve;MuscleClinical features and History taking Onset – mode; Acute; Subacute; Chronic; Intermittent(Veryrare – T.B.);Progression-Static,Progressive,Improving;Cause-Trauma,TBcontact,Primary tumor,Vaccine/ Dogbite, Family Similar illness (Hereditary spastic paraplegia), Drug intake(Causingneuritis/myopathy)Complications- CNS; PNS; Automatic; Other systemsSypmptoms and Signs - Spinal paraplegia -clumsiness of gait, refusal to stand or walk, loss ofbower/bladder control, loss of sensationSigns - ScoliosisNote- Presence of scoliosis in females before puberty and males of all ages should stronglysuggest neuro muscular disorder of spinal cord pathology -Sking abnormalities over spine, tuft ofhari, 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 preservedhip/knee movements and ankle dorsiflexion; Hip extension corresponds to L5, S1, S2 and so isaffected in all but lower sacral lesions; Lesions at S3 or below completely spare lower limb147
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