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NBE CME programme for DNB consultantsNote- LP is contra indicated in acute stage, since it aggravates parapareis Herpes zoster myelitis—TC- Pleocytosis, Protein- mild evelation, Glucose –normal or decreased;Tumours (e.g)(Astrocytoma) (Secondaries –Acute myeloid leukemia(AML), Acute lymphocytic leukemia(ALL)Electromyography(EMG)- When suspecting metabolic myopathies (e.g.) Severe CongenitalAutosomal Recessive Muscular Dystrophy (SCARMD) ; To delineate segmented involvement topatchy lesionsNerve Conduction Velocity (NCV)-When features are suggestive of peripheral neuropathyArteriography- A.V. malformationANA/Anti ds DNA—SLE – Lupres myciopathyMonoplegiaHistory - Establish if the case is a monoplegia (or) part of hemiplegia, quadriplegia or paraplegia.Then the following history is a must.Age of onset -Infant-Brachial plexitis(ERB’s Palsy); 10-15 yrs-Monomelic spinal Muscular;Atrophy; any age-Injury to plexus or Nerve – Infection; Sex - Male-Monomelic spinal muscularatrophy; Family History - Hereditary brachial plexopathy; Homocystinuria; Birth History -Birth injury-C.P; ERB’s Palsy-Trauma-Extended arm during prolonged surgery; Fall & Injury to plexus; Trivical-Hereditary brachial plexopathyInfection- Poliomyclitis; Osteomyelitis leadin to neuropathy; Osteomyelitis humerus upper endplexitis – neuritis;Immunisation-OPV; Tetanus Toxiod precipitating hereditary Brachial plexopathy;Asthma(Hopkins syndrome-Asthmatic Amyotrophy; Site of Involvement-Promixal muscles; DistalMuscles; Pain- At rest; Increased by movement; Inability to use Limb - Ex. Trauma/others; Pain +Inability to use Limb - Plexitis; Trauma; Sensation - Present/absent/extend of loss of sensation; H/o. Bleeding Diathesis; Duration-Acute; Chronic; Progressive; Recurrent eg. Hereditary BrachialPlexopathy—Improving or not; H/o. ICT- Headache, Vomiting and seizures; Contractures; Foot drop– peroneal nerve palsy;Clinical Features - General appearance- ( Facies-Storage disease – mucolipidosis, Causescompression at the carpal tunnel in children; Eyes- Cataract, Storage disease subluxation lens –homocystinuria; Lymph adenopathy – Neuroblastoma etc.; Anemia – bleeding disorder; SkinPurpunt Spot;System examination-Higher Functio; CNS- Conscious/unconscious; Group accordingto Glasgow coma scale; Cranial Nerves— Cr. Nerve- Visual impairment – subluxation lens –homocystinciria, FUNDUS- Bleeding/Chroid tubercle or secondaries; Cranial Nerve- Fascial palsya part of ERB’s Palsy; Other Cranial nerves - Particularly lower cranial nerves at the atlanto accipitalregion; motor system- Inspection-; Nutrition-; Wasting – Poliomyclitis; Wrist Drop – PeronealNerve Palsy/Contractures; Faciculation; Trauma; Power-; Tone-; Hypertonia/Hypojonig – CerebralPalsy; 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 alimb 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 producingThromoembolism; Abdomen- Hepato splenomegaly – storage diseaseDifferential Diagnosis - Hypotonic Cerebral Palsy-Tone but DTR exaggerated. Plantar extensor/H/o of birth injury; Plexopathy/Neuropathy-Involvement of proximal muscles with or without sensoryloss. There is gradual improvement over the years Eg. Brachial Palsy; Aneterior Horn Cells-Poliomyelitis; Tumours-Primary – malignanat schwannoma secondary – neuroblastoma; Trauma-Neonatal brachial Neuropathy ; To plexus;To bone Osteomyelitis - neuritis; In born error of Metabolis-Homocystinuria,Storage disorder – Carpal tunnel syndrome; Spinal abnormality- Cervical & lumbar;Degenerative disorder (Monoplegia + fasciculation, Tremar, Blindness + Consanguinity)—monomelic spinal muscular atrophy. This is a rare disorder Fasciculation common, SCHINDLER’s150
NBE CME programme for DNB consultantsDisease Acute, Sudden on set Monoplegia/Hemiplegia + BlindnessInvestigations - Hemogram – Hb; PCV – increased in cyanotic heart disease; TC; DC; Smear abnormalcells/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 – Forspinal tumours; Electromyogram(EMG) - To distinguish between plexus injury and nerve injury; Screeningtest - For Amino Aciduria- (eg) Homocystinuria; Muscle Biopsy- Monomelic spinal muscular atrophy;CSF- (Eg.) Normal except for a mild elevation of protein in lumbar plexitisTreatment- Non Surgical-Antibiotics if necessary; Physiotherapy; Electrical Stimulation; Others. Surgical-Removal o tumour; Eg. Malg. Schwannoma; Restoration of injured nervePrevention-Prevention of EB’s Palsy by careful delivery of baby; Takin precaution to avoid trauma, infectionetc. in Precipitating Heridatory Bracial Plexopathy; Avoiding prolonged extension of upper limb/arm duringSurgery – to avoid trauma to plexusGasrointestinal BleedsHistory- 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 outputClinical Examination- General Survey- Consciousness; Anemia/Jaundice/Cyanosis/Neck glands/Neck veins/ Jaundice/Cold peripheri/BP/Pulse/RespirationSystemic Examination- Inspection - Abdominal distention/Prominent superficial veins; LocalExamination of Anal fissure. Palpation - Free fluids; Flow of veins; Organomegaly; Palpable mass;PR examinationPercussion - Shifting dullness. Auscultation - Peristalsis soundInvestigation - 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 determinesite of bleeding of GIT where endoscopy and barium study have failed; Angiography in selectivecases and to detect vascular malformationDifferential Diagnosis - Varicose vein; Exraphepatic Portal Hypertension; Cirrhosis; Meckel’sdiverticulum; Polyp; H PyloriManagement - Non-Surgical - O 2Administration; IV drip 10-20 ml/kg of Ringer Lactate or NS rapidly,repeat SOS till urine output, pulse & BP improves and cutaneous perfusion normalized; Hematocritto maintain at 30 o ; Blood transfusion if needed accordingly; NG tube suction; Bleeding site to bedetermined-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, Portaldecompressive surgery. Factory indicating poor prognosis-[Massive hematemesis; Initialhematocrit
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