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Traditional Traditional Medicine,2007 Medicine,2007

Traditional medicine 2007 by ap u kyaw naing

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Page 1: Traditional medicine 2007 by ap u kyaw naing

Traditional Medicine,2007Traditional Medicine,2007

Page 2: Traditional medicine 2007 by ap u kyaw naing

Cervical LymphadenopathyCervical Lymphadenopathy

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Cervical LymphadenopathyCervical Lymphadenopathy

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AnatomyAnatomy

Waldeyer’s ringWaldeyer’s ring palatine tonsils palatine tonsils

lingual tonsillingual tonsil

adenoidsadenoids

lymphoid tissue around lymphoid tissue around the eustachian tubethe eustachian tube

Page 7: Traditional medicine 2007 by ap u kyaw naing

Anatomy 2 Anatomy 2

Horizontal chainHorizontal chainsub-mentalsub-mentalsub-mandibularsub-mandibularpre-auricularpre-auricularpost-auricularpost-auricularoccipitaloccipital

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Anatomy 3Anatomy 3

Vertical chainVertical chain along the internal jugular along the internal jugular veinveinJugulo-digastric nodeJugulo-digastric nodeJugulo-omohyoid nodeJugulo-omohyoid node lymph nodes in the posterior triangle of the lymph nodes in the posterior triangle of the

neckneck

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Slide courtesy of Anton Pozniak

Page 15: Traditional medicine 2007 by ap u kyaw naing

Slide courtesy of Anton Pozniak

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APPROACH TO THE PATIENT WITH LYMPHADENOPATHY APPROACH TO THE PATIENT WITH LYMPHADENOPATHY

Generalized immune proliferation and lymphadenopathy can occur with a

systemic disorder of the immune system,

disseminated infection, or

disseminated neoplasia.

Malignancies of the immune system might be manifested as:

localized or

disseminated lymphadenopathy.

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Causes of cervical Causes of cervical lymphadenopahtylymphadenopahty

InflammatoryInflammatory reactive hyperplasiareactive hyperplasia

InfectiveInfectiveBacterialBacterial

staphylococcalstaphylococcalstreptococcalstreptococcalactinomycosisactinomycosisTB & brucellosisTB & brucellosis

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Causes of cervical Causes of cervical lymphadenopahty 2lymphadenopahty 2

ViralViralinfectious mononucleosisinfectious mononucleosisHIVHIV

ProtozoalProtozoaltoxoplasmosistoxoplasmosis

NeoplasticNeoplasticprimaryprimary lymphoma lymphomasecondarysecondary known primary known primary SCC SCC

unknown primaryunknown primary

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APPROACH TO THE PATIENT WITH LYMPHADENOPATHY APPROACH TO THE PATIENT WITH LYMPHADENOPATHY

LYMPH NODE EVALUATION.a careful history a thorough physical examination laboratory tests imaging studies to determine the extent and character of the lymphadenopathy age of the patientThe occurrence of fever, sweats, or weight lossof a site of infection, a particular medication, a travel history, or a previous malignancy.

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APPROACH TO THE PATIENT WITH LYMPHADENOPATHY APPROACH TO THE PATIENT WITH LYMPHADENOPATHY

physical examination

localized or generalized

size of nodes

Texture

presence or absence of nodal tenderness

signs of inflammation over the node

skin lesions

splenomegaly.

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APPROACH TO THE PATIENT WITH LYMPHADENOPATHY AND SPLENOMEGALY APPROACH TO THE PATIENT WITH LYMPHADENOPATHY AND SPLENOMEGALY

METHODS OF LYMPH NODE EVALUATION

Physical examination

Imaging

Chest radiography

Lymphangiography

Ultrasonography

Computed tomography

Magnetic resonance imaging

Gallium scanning

Positron emission tomography

Sampling

Needle aspiration

Cutting needle biopsy

Excisional biopsy

Page 23: Traditional medicine 2007 by ap u kyaw naing

MycobacteriumMycobacterium

Suspicious when antibiotic Suspicious when antibiotic therapy failstherapy fails

Typical presentation: preschool Typical presentation: preschool aged child, upper cervical or aged child, upper cervical or submandibular mass with submandibular mass with overlying violaceous skin.overlying violaceous skin.

Infected nodes may suppurate, Infected nodes may suppurate, and lead to persistent sinus and lead to persistent sinus drainagedrainage

PPD will help TB vs NTBPPD will help TB vs NTB Treatment: complete excision if Treatment: complete excision if

possible vs. long term medical possible vs. long term medical managementmanagement

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TB LymphadenitisTB Lymphadenitis

common in developing countriescommon in developing countries affects children & young adultsaffects children & young adults deep upper cervical nodes are commonly deep upper cervical nodes are commonly

affectedaffected human strain of Mycobacterium tuberculosis > human strain of Mycobacterium tuberculosis >

bovine strainbovine strain atypical mycobacteria in HIV patientsatypical mycobacteria in HIV patients direct entry from tonsilsdirect entry from tonsils haematogenous spreadhaematogenous spread

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TB Lymphadenitis 2TB Lymphadenitis 2

limited to affected group of lymph nodeslimited to affected group of lymph nodesmatted lymph nodes due to matted lymph nodes due to

perilymphadenitisperilymphadenitisnatural resistance natural resistance calcification calcification if failed if failed cold abscess cold abscess

collar stud abscesscollar stud abscess

discharging sinus discharging sinus

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TB Lymphadenitis 3TB Lymphadenitis 3

InvestigationsInvestigations laboratory……..T & DC laboratory……..T & DC lymphocytosis lymphocytosis ESR ESR high high Tuberculin testTuberculin test Sputum for AFBSputum for AFBImaging……….. CXR ( PA )Imaging……….. CXR ( PA )Excisional biopsy Excisional biopsy for confirmation by for confirmation by

histology & microbiologyhistology & microbiology

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TREATMENTTREATMENT

Anti-tuberculous drugs ( DOTS )Anti-tuberculous drugs ( DOTS ) INHINHRifampicinRifampicinEthambutolEthambutolPyrazinamidePyrazinamide

Antibiotics according to C & SAntibiotics according to C & S Multi-drug resistant tuberculosisMulti-drug resistant tuberculosis NutritionNutrition

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LymphomaLymphoma

malignant tumour arising from the malignant tumour arising from the lymphatic system mainly lymph nodeslymphatic system mainly lymph nodes

ClassificationClassificationHodgkin’s lymphomaHodgkin’s lymphomaNon-Hodgkin’s lymphomaNon-Hodgkin’s lymphoma

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Hodgkin’s LymphomaHodgkin’s Lymphoma

typestypes lymphocyte predominantlymphocyte predominantnodular sclerosisnodular sclerosismixed cellularitymixed cellularity lymphocyte depletedlymphocyte depleted

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Non-Hodgkin’s LymphomaNon-Hodgkin’s Lymphoma

typestypes low gradelow gradehigh gradehigh grade intermediateintermediate

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PresentationPresentation

lymphadenopahtylymphadenopahty regionalregional wide spreadwide spread

enlarged lymph nodes are rubbery & discreteenlarged lymph nodes are rubbery & discrete bilateral cervical lymphadenopathybilateral cervical lymphadenopathy

constitutional symptomsconstitutional symptoms intermittent fever, malaise, aches & pain, wt lossintermittent fever, malaise, aches & pain, wt loss prurituspruritus alcohol induced painalcohol induced pain

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Presentation 2Presentation 2

obstructive symptomsobstructive symptoms due to enlarged due to enlarged lymph nodeslymph nodesHorner’s syndrome Horner’s syndrome compression on the compression on the

sympathetic ganglionsympathetic ganglionmediastinal obstructionmediastinal obstruction intestinal obstructionintestinal obstruction renal failurerenal failure

HepatosplenomegalyHepatosplenomegaly

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HistologyHistology

Reed-Sternberg giant cells are present in Reed-Sternberg giant cells are present in Hodgkin’s lymphomaHodgkin’s lymphoma

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ManagementManagement

historyhistory thorough clinical examinationthorough clinical examination laboratorylaboratory CP, ESR, Urinalysis CP, ESR, Urinalysis imagingimaging CXR, USG abdomen CXR, USG abdomen CTCT LymphangiogramLymphangiogram Bone marrow aspirationBone marrow aspiration Lymph node biopsyLymph node biopsy

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Management 2Management 2

treatmenttreatmentmainly chemotherapymainly chemotherapystage IA, IIA stage IA, IIA Radiotherapy….90% survival Radiotherapy….90% survivalstage IIIA, IIIB stage IIIA, IIIB Chemoradiation ChemoradiationCHOP CHOP cyclophosphamide cyclophosphamide doxorubicindoxorubicin oncovin( vincristine )oncovin( vincristine ) prednisoloneprednisoloneextensive extra-nodal d/sextensive extra-nodal d/s poor prognosis poor prognosis

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Metastatic Lymph NodesMetastatic Lymph Nodes

from primary sites from primary sites head & neck head & necknasopharynxnasopharynx tonsiltonsil tonguetonguepyriform fossapyriform fossasupraglottic larynxsupraglottic larynx

history & clinical examination to find out history & clinical examination to find out the primary lesionsthe primary lesions

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Metastatic Lymph Nodes 2Metastatic Lymph Nodes 2

InvestigationsInvestigations imaging imaging FNACFNAC

TreatmentTreatmentsurgery for primary lesion is required & node surgery for primary lesion is required & node

> 3 cm > 3 cm en blocen bloc dissection dissection

--radiotherapy --radiotherapy advanced tumours advanced tumours

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AnatomyAnatomy

Blood Supply Blood Supply Superior and inferior Superior and inferior thyroid arteriesthyroid arteries

Venous drainage Venous drainage Superior, middle and Superior, middle and inferior thyroid veinsinferior thyroid veins

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Overview of MethodOverview of Method General InspectionGeneral Inspection Around the bed, patientAround the bed, patient

HandsHands Acropachy, sweaty palmsAcropachy, sweaty palmstremortremor

PulsePulse

Face Face Peaches and cream Peaches and cream complexioncomplexion

EyesEyes Eye diseaseEye disease

NeckNeck Thyroid, trachea, and lymph nodesThyroid, trachea, and lymph nodes

LegsLegs Pretibial myxoedemaPretibial myxoedemaReflexesReflexes

Page 44: Traditional medicine 2007 by ap u kyaw naing

General InspectionGeneral Inspection

Thin / fatThin / fatMuscle wastingMuscle wastingNervous / agitatedNervous / agitatedUnder-clothed and sweatyUnder-clothed and sweatyOverdressed but coldOverdressed but coldHoarse (Hoarse (RLNRLN) / fatiguable voice () / fatiguable voice (ELNELN))StridorStridor

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General InspectionGeneral Inspection

• Inspect from the Inspect from the frontfront

•BMIBMI

•Tremor / Restless / Tremor / Restless / AgitationAgitation

•EyesEyes

•Hair and EyebrowsHair and Eyebrows

•SCARSSCARS

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NeckNeck

InspectionInspection Stand in front of ptStand in front of pt

Visible?Visible? Enlarged?Enlarged? Symmetrical?Symmetrical?

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IsIs ThisThis aa ThyroidThyroid??

•Ask patient to stick tongue out while Ask patient to stick tongue out while palpating:palpating:

•Ask patient to swallow water:Ask patient to swallow water:

Should NOT move

Should move

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Inspection of HandsInspection of Hands

•TemperatureTemperature

•Palmar ErythemaPalmar Erythema

•Thyroid AcropachyThyroid Acropachy

•TremorTremor

•Pulse (AF / Tachy)Pulse (AF / Tachy)

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HandsHands

Thyroid acropachyThyroid acropachy

clubbingclubbing

digital swellingdigital swelling

periosteal new boneperiosteal new bone

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HandsHands

Sweaty palmsSweaty palms

PulsePulse rate, rhythmrate, rhythm

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EyeEye DiseaseDisease

Examine Examine from from in frontin front

from from aboveabove

from from the sidethe side

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EyeEye DiseaseDisease

LidsLids Lid retractionLid retraction Lid lagLid lag

MusclesMuscles ExophthalmosExophthalmos ProptosisProptosis OphthalmoplegiaOphthalmoplegia Periorbital swellingPeriorbital swelling

ConjunctivaeConjunctivae ChemosisChemosis Occular injectionOccular injection

Optic NerveOptic Nerve Optic neuropathyOptic neuropathy

Page 53: Traditional medicine 2007 by ap u kyaw naing

EyeEye DiseaseDisease

Lid retractionLid retraction

Upper lid pulled back Upper lid pulled back to expose sclera to expose sclera above irisabove iris

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EyeEye DiseaseDisease

Lid lagLid lag

On looking up or On looking up or down, lid doesn’t down, lid doesn’t follow eyeballfollow eyeball

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EyeEye SignsSigns

• Inspect from front - lid Inspect from front - lid retractionretraction

• Inspect from side / Inspect from side / above ....above ....

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EyesEyes - - GravesGraves’ ’ DiseaseDisease

•Due to retro-orbital inflammation Due to retro-orbital inflammation and lymphocyte infiltration.and lymphocyte infiltration.

ExopthalmosProptosis

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EyeEye DiseaseDisease

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EyeEye DiseaseDisease

ExophthalmosExophthalmos

Sclera visible above Sclera visible above and below eyeand below eye

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EyeEye DiseaseDisease

OphthalmoplegiaOphthalmoplegia

1. Weakness of ocular muscles due to oedema & cellular infiltration of these muscles.

2. Superior & Lateral rectus and inferior oblique muscles are affected mostly.

3. Paralysis of these muscles prevents the patient looking upwards & outwards.

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EyeEye DiseaseDisease

ChemosisChemosis

Ocular injectionOcular injection

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PalpationPalpation

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PalpationPalpation

•Palpate from behindPalpate from behind

•Ask about pain!Ask about pain!

•Use bimanual palpationUse bimanual palpation

•Note character of swelling (one lump / Note character of swelling (one lump / multiple lumps / diffuse enlargement)multiple lumps / diffuse enlargement)

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NeckNeck

PalpationPalpation

Stand behind ptStand behind ptThumbs on occiputThumbs on occiputFlex neck slightlyFlex neck slightlyPalpatePalpate

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NeckNeck

PalpationPalpation

Abnormality?Abnormality? SizeSizeTendernessTendernessSurfaceSurfaceConsistencyConsistencyDiscrete nodulesDiscrete nodules

Moves on swallowing?Moves on swallowing?

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NeckNeck

Palpate tracheaPalpate trachea

?central?central

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Neck / ChestNeck / Chest

PercussionPercussion Percuss for a retrosternal goitrePercuss for a retrosternal goitre Pemberton’s testPemberton’s test

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NeckNeck

AuscultationAuscultation

Auscultate for a thyroid bruitAuscultate for a thyroid bruit

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LegsLegs

Pretibial MyxoedemaPretibial Myxoedema

Quad reflexesQuad reflexes

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Summary Risk Factors

Hypothyroidism Hyperthyroidism

Family or personal hx of thyroid disease

Family or personal hx of thyroid disease

Goiter or hx of goiter Goiter or hx of goiter

Prior or current thyroid use Prior or current thyroid use

Hx of other autoimmune disease

Hx of other autoimmune disease

  Recent iodine exposure

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Clinical Findings

Hypothyroidism HyperthyroidismFatigue Fatigue

Weight gain Weight loss without change in appetite

Cold intolerance Heat intolerance

Depression or memory impairmentDepression or nervousness, irritablility,anxiety or agitation

Menstural irregularities (menorrhagia), infertility Menstural irregularities (oligomenorrhea)

Weakness, muscle cramps, joint pains Weakness, tremor

  Palpitations

  Exertional dyspena

Constipation Hyperdefecation

Hoarseness Anterior neck pain

Hypersomnolence Insomnia

Page 72: Traditional medicine 2007 by ap u kyaw naing

Physical Exam: Thyroid----Related Findings

Hypothyroidism Hyperthyroidism

Xerosis (dry skin) Moist palms (increased perspiration)

  Thickening of skin, especially pre-tibial

Preorbital puffinessBulging eyes (lid retraction or proptosis), unblinking stare

 Eye irritation, periorbital edema, diploplia, change in visual acuity**

Delayed relaxation phase, deep tendon reflex

Hyperreflexia

Dry Coarse hair or alopecia  

Bradycardia Tachycardia, atrial fibrillation

Non-pitting edema  

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WOUNDSWOUNDS

AP U Kyaw NaingAP U Kyaw Naing

SUIISUII

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DefinitionDefinition

A wound can be caused by almost any A wound can be caused by almost any injurious agent and can involve almost any injurious agent and can involve almost any tissue or structure.( due to trauma)tissue or structure.( due to trauma)

A woundA wound is a breach in continuity of is a breach in continuity of epithelium epithelium due to traumadue to trauma..

An ulcerAn ulcer is a breach in continuity of is a breach in continuity of epithelium.epithelium.

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Classification of woundClassification of wound

Tidy woundTidy wound Inflicted by sharp instrumentInflicted by sharp instrumentContain no devitalized tissueContain no devitalized tissueCan be closed primarily with exception of P’ Can be closed primarily with exception of P’

healing . Eg. Surgical wound, cut from glass healing . Eg. Surgical wound, cut from glass and knife.and knife.

CleanCleanRepair is possible.Repair is possible.

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Untidy woundUntidy woundResult from crushing, tearing, avulsion Result from crushing, tearing, avulsion

vascular injury or burnvascular injury or burnContained devitalised tissueContained devitalised tissue IrregularIrregularMust not be closed primarilyMust not be closed primarilyT – wound excisionT – wound excision

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Healthy Healing Surgical Healthy Healing Surgical WoundWound

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Wounds may be classified as Wounds may be classified as CleanCleanPotentially contaminatedPotentially contaminatedContaminated – eg. Bowel perforationContaminated – eg. Bowel perforationDirty – eg. fecal contaminationDirty – eg. fecal contamination

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Types of woundTypes of wound

1.1. IncisedIncised

2.2. Lacerated Lacerated

3.3. PenetratingPenetrating

4.4. crushedcrushed

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Wound HealingWound Healing

Wound healing is the summation of a Wound healing is the summation of a number of processed which follow injury number of processed which follow injury includingincludingPhase 1 : inflmmationPhase 1 : inflmmationPhase 2 : cell proliferation & matrix formationPhase 2 : cell proliferation & matrix formationPhase 3 : matrix remodellingPhase 3 : matrix remodelling

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Phase 1 : InflammationPhase 1 : Inflammation

Coagulation cascadeCoagulation cascadePMN polymorpho-nuclear leucocytesPMN polymorpho-nuclear leucocytes3 – 4 days3 – 4 days

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Phase 2 : Cell proliferation & matrix Phase 2 : Cell proliferation & matrix formationformation

Fibroblast migrateFibroblast migrate EndothelialEndothelial New capillary & matrix systhesisNew capillary & matrix systhesis Collagen, proteoglycan & glycoproteinCollagen, proteoglycan & glycoprotein Granulation tissueGranulation tissue

Phase 3 : Matrix remodellingPhase 3 : Matrix remodelling Reorientation of collagen fibrilsReorientation of collagen fibrils

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ProcessProcess Cell TypeCell Type MediatorMediatorWoundingWounding injured cellinjured cell phospholipase of phospholipase of

prostaglandinprostaglandin

CoagulationCoagulation plateletsplatelets IL-1, PDGF, TGF-BIL-1, PDGF, TGF-B

InflammationInflammation LL FGFFGF

MM

AngiogenesisAngiogenesis GrGr TGF-BTGF-B

Proteoglycan SynProteoglycan Syn FibroblastFibroblast

Collagen depositionCollagen deposition

Epithelialisation Epithelialisation Epithelial cellEpithelial cell EGFEGF

RemodellingRemodelling FibroblastFibroblast

( Biological Process in wound repair )( Biological Process in wound repair )

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Healing by Primary IntentionHealing by Primary Intention

Haemostasis – clotting cascadeHaemostasis – clotting cascade Pro: of inflammationPro: of inflammation Cell proliferation and migrationCell proliferation and migration Epidermal eventEpidermal event

Epidermal cell migration - coveringEpidermal cell migration - covering Dermal eventDermal event

Arrival of neutrophil and macrophageArrival of neutrophil and macrophage Demolition and removal of exudate and debrisDemolition and removal of exudate and debris

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Restoration of tensile strengthRestoration of tensile strengthSecretion of chemoattractantSecretion of chemoattractantExpansion of fibroblastExpansion of fibroblastStimulation of fibroblast to secrete Stimulation of fibroblast to secrete

extracellular connective tissueextracellular connective tissue AngiogenesisAngiogenesis Granulation tissueGranulation tissue Collagen-tensile strengthCollagen-tensile strength scarscar

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Healing by Second IntentionHealing by Second Intention

A large wound of tissue lossA large wound of tissue lossWound contractionWound contraction

Movement of wound marginMovement of wound marginContraction – myofibroblast fibronectinContraction – myofibroblast fibronectin

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Growth factorGrowth factorAre peptidesAre peptidesEndocrine, paracrine, autocrine pathwayEndocrine, paracrine, autocrine pathwayPDGF, EGF, TGF@ and BPDGF, EGF, TGF@ and B

CytokinesCytokines IL1, TNF-@IL1, TNF-@

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Stages of Bone HealingStages of Bone Healing

1.1. HaemorrhageHaemorrhage

2.2. InflammationInflammation

3.3. DemolitionDemolition

4.4. Granulation tissueGranulation tissue

5.5. CallusCallus

6.6. Woven bone formationWoven bone formation

7.7. remodellingremodelling

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Factors affecting wound healingFactors affecting wound healing

General factorsGeneral factors Local factorsLocal factors1. Age1. Age 1. Blood supply 1. Blood supply

2. Vitamin – C, Zinx2. Vitamin – C, Zinx 2. Infection2. Infection

3. Diabetic3. Diabetic 3. Haematoma3. Haematoma

4. Jaundice & Uraemia4. Jaundice & Uraemia 4. Faulty technique4. Faulty technique

5. Cytotoxic drug5. Cytotoxic drug 5. Tension5. Tension

6. Malignancy6. Malignancy 6. Steriod6. Steriod

7. Infection – pus7. Infection – pus 7. Oxygen7. Oxygen

8. Immunocompromised Pt8. Immunocompromised Pt

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Did this person jump or was he Did this person jump or was he blown out of the building?blown out of the building?

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Somebody knew what was coming...Somebody knew what was coming...

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Do you think just any lawn would hold Do you think just any lawn would hold up like this after a plane crashed on it?up like this after a plane crashed on it?

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Not a Scratch! Perfect Lawn!Not a Scratch! Perfect Lawn!

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Head injuries Head injuries

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Surgical cricothyroidotomy Surgical cricothyroidotomy

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Forearm FasciotomyForearm Fasciotomy

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Lower Limb - FasciotomyLower Limb - Fasciotomy

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A A survivable airway problemsurvivable airway problem

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TourniquetsTourniquets

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Exsanguinating Pelvic Exsanguinating Pelvic Trauma Trauma

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ComplicationsComplications

1.1. Infection , HaemorrhageInfection , Haemorrhage

2.2. Ugly scarUgly scar

3.3. KeloidKeloid

4.4. Incisional herniaIncisional hernia

5.5. PigmentationPigmentation

6.6. Marjolin’s ulcerMarjolin’s ulcer

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TetanusTetanus

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DescriptionDescription

Clostridium tetaniClostridium tetani is the is the bacterium that causes bacterium that causes tetanus, and it is tetanus, and it is mainly found in the mainly found in the soil.soil.

In developed countries, In developed countries, most cases occur in most cases occur in older adults.older adults.

In developing In developing countries, about half of countries, about half of the cases of tetanus the cases of tetanus are found in neonates.are found in neonates.

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DescriptionDescription

There are four main types of tetanusThere are four main types of tetanusGeneralizedGeneralizedLocalLocalNeonatalNeonatalCephalicCephalic

Symptoms of tetanus are cause by Symptoms of tetanus are cause by disinhibition of the nervous system.disinhibition of the nervous system.

The source of a tetanus infection is a wound, The source of a tetanus infection is a wound, where where Clostridium tetaniClostridium tetani enters the body. enters the body.

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The Discovery of TetanusThe Discovery of Tetanus

Hippocrates (right) was Hippocrates (right) was said to describe tetanus said to describe tetanus as far back as the 5as far back as the 5thth century B.C.century B.C.

Nicolaier first produced Nicolaier first produced tetanus in animal tetanus in animal specimens.specimens.

Kitasato isolated the Kitasato isolated the organism from a human organism from a human victim and neutralized victim and neutralized the toxin.the toxin.

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How Tetanus Was DiscoveredHow Tetanus Was Discovered

The bacterium The bacterium Clostridium tetaniClostridium tetani is is abundant in soil and abundant in soil and Tetanus was Tetanus was produced by injecting produced by injecting soil specimens in soil specimens in animals.animals.

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Less than 100 cases per year in the UKLess than 100 cases per year in the UKMore prevalent in developing countriesMore prevalent in developing countriesFollowing deep or penetrating wound in Following deep or penetrating wound in

relatively avascular areasrelatively avascular areas

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Causal organismCausal organism

Clostridium tetani Clostridium tetani Gram-positive rod with terminal spores Gram-positive rod with terminal spores

(drum stick appearance).(drum stick appearance).A strict anaerobe A strict anaerobe Produce powerful exotoxin.Produce powerful exotoxin.Exotoxin causes muscle spasms and Exotoxin causes muscle spasms and

rigidityrigidity

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PathogenesisPathogenesis

Spores of Spores of Clostridium tetani Clostridium tetani live in feces, soil, dust live in feces, soil, dust an on instrument.an on instrument.

The spores enter through tiniest breach in skin The spores enter through tiniest breach in skin and mucous membraneand mucous membrane

They may then germinate and produce exotoxin.They may then germinate and produce exotoxin. This travel up peripheral nerves and interferes This travel up peripheral nerves and interferes

with inhibitory synapse.with inhibitory synapse. Reduces the release of inhibitory Reduces the release of inhibitory

neurotransmittersneurotransmitters Excess activity of motor neurones produces Excess activity of motor neurones produces

muscle spasmmuscle spasm

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PathologyPathology

Clostridium tetani Clostridium tetani usually enters the body usually enters the body through a wound.through a wound.

The spores germinate, The spores germinate, and two toxins are and two toxins are produced:produced:

Tetanospasmin Tetanospasmin TetanolysinTetanolysin

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PathologyPathology The toxin starts out as a polypeptide, and changes into two The toxin starts out as a polypeptide, and changes into two

chains.chains. The heavy chain travels to the central nervous system, which The heavy chain travels to the central nervous system, which

activates the light chain.activates the light chain. The light chain releases an inhibitor which causes muscle The light chain releases an inhibitor which causes muscle

spasms to occur.spasms to occur.

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Clinical featuresClinical features

Incubation period ( time of injury to first Incubation period ( time of injury to first symptom)- 7-10 days, sometimes up to symptom)- 7-10 days, sometimes up to years.years.

Period of onset (first symptom to first Period of onset (first symptom to first reflex spasm) - 5-7 daysreflex spasm) - 5-7 days

Prodromal symptoms (fever, malaise, Prodromal symptoms (fever, malaise, headache)headache)

Trismus (patient can not open his mouth)Trismus (patient can not open his mouth)

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Risus sardonicus (a grin-like posture of Risus sardonicus (a grin-like posture of hypertonic facial muscles)hypertonic facial muscles)

Opisthotonus (arched body with Opisthotonus (arched body with hyperextended neck)hyperextended neck)

spasms (at first may be induced by spasms (at first may be induced by stimulus but later are spontaneous)stimulus but later are spontaneous)

Dysphagia and respiratory arrestDysphagia and respiratory arrestautonomic dysfunction (arrythmias, wide autonomic dysfunction (arrythmias, wide

fluctuation in BP)fluctuation in BP)

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Bad prognostic signsBad prognostic signs

Short incubation periodShort incubation periodRapid progression from trismus to spasms Rapid progression from trismus to spasms

(<48 hours)(<48 hours)Tetanus in neonates and old ageTetanus in neonates and old age

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SymptomsSymptoms

Begin about 8 days after infection.Begin about 8 days after infection. ““Lockjaw” or trismus occurs, which is Lockjaw” or trismus occurs, which is

muscle stiffness in the jaw.muscle stiffness in the jaw.Autonomic dysfunction. Autonomic dysfunction. Respiration difficulty.Respiration difficulty.

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SymptomsSymptoms

Severe muscle spasms occur, bringing Severe muscle spasms occur, bringing many complications:many complications:Fracture of spine or long bonesFracture of spine or long bonesAbnormal heartbeatsAbnormal heartbeatsFlexion of arms and legsFlexion of arms and legsLaryngospamLaryngospam

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DiagnosisDiagnosis

History of injury or History of injury or presence of wound is presence of wound is used.used.

History of parental History of parental drug use or personal drug use or personal IV drug use IV drug use strengthens strengthens diagnosis.diagnosis.

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DiagnosisDiagnosis

Differential diagnosis includes:Differential diagnosis includes:Painful conditions of the lower jaw is includedPainful conditions of the lower jaw is includedAbnormalities in the peripheral nervous systemAbnormalities in the peripheral nervous systemMeningitisMeningitisBell’s palsy Bell’s palsy Stiffman’s syndromeStiffman’s syndrome

Appropriate history and physical examination Appropriate history and physical examination can differentiate most of these.can differentiate most of these.

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TreatmentTreatment

The treatment involves:The treatment involves:Neutralizing the toxinNeutralizing the toxinRemoving the source of the toxinRemoving the source of the toxinSupportive care for muscle spasms, Supportive care for muscle spasms,

respiration, and autonomic instabilityrespiration, and autonomic instabilityRecovered patients must receive a tetanus Recovered patients must receive a tetanus

immunization series, due to the fact that immunization series, due to the fact that survivors of tetanus have a greater risk of survivors of tetanus have a greater risk of getting it again.getting it again.

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TreatmentTreatment

Passive immunization Passive immunization with human immune with human immune globulin shortens the globulin shortens the course of tetanus and course of tetanus and may lesson severity.may lesson severity.

Penicillin and Penicillin and metronidazole are the metronidazole are the antibiotics commonly antibiotics commonly used.used.

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TreatmentTreatment

The spasms cause by tetanus can be The spasms cause by tetanus can be extremely harmful and cause many extremely harmful and cause many complications.complications.

Sedatives can be used to control spasms.Sedatives can be used to control spasms. Neuromuscular blocking agents are used to Neuromuscular blocking agents are used to

relax muscles.relax muscles. Metronidazole, diazepam, and Metronidazole, diazepam, and

benzodiazepine and most commonly used benzodiazepine and most commonly used to control spasms.to control spasms.

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ManagementManagementGeneral treatmentGeneral treatment

Hospitalised the patientHospitalised the patient Isolate the patient in quiet and comfortable Isolate the patient in quiet and comfortable

place with dim lighting.place with dim lighting.Change the position to prevent pressure Change the position to prevent pressure

soresore

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Clean wounds, debride as necessaryClean wounds, debride as necessaryUse i.v. penicillin or metronidazole for 7 Use i.v. penicillin or metronidazole for 7

days to destroy the bacteriadays to destroy the bacteriaHuman tetanus immune globulin (HTIG) Human tetanus immune globulin (HTIG)

500 U i.m. to neutralise free toxin500 U i.m. to neutralise free toxinAntitetanus toxoid to get active ammunityAntitetanus toxoid to get active ammunity

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Control feverControl feverAnalgesic for muscle painAnalgesic for muscle painFluid therapy for daily requirementFluid therapy for daily requirementCare and maintenance of airway during Care and maintenance of airway during

cyanotic convulsioncyanotic convulsion

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Specific treatment depends on Specific treatment depends on severity of diseaseseverity of disease

Stage 1. Mild case Stage 1. Mild case (Tonic rigidity alone)(Tonic rigidity alone) Initial sedation, relaxation by drugs Initial sedation, relaxation by drugs

promazine up to 200 mg. and a barbiturate or promazine up to 200 mg. and a barbiturate or diazepan.diazepan.

Feeding orally +/- IV fluidFeeding orally +/- IV fluid

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Stage 2. A seriously ill patientStage 2. A seriously ill patient

Dysphagia and reflex spasm.Dysphagia and reflex spasm.SedationSedationFeeding by nasogastric tube or total Feeding by nasogastric tube or total

parenteral nutritionparenteral nutritionTracheostomy should be considered if the Tracheostomy should be considered if the

patients has any difficulty in breathing.patients has any difficulty in breathing.

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Stage 3. Dangerously ill patientsStage 3. Dangerously ill patients

A major cyanotic convulsion A major cyanotic convulsion curarisation to maintain relaxation.curarisation to maintain relaxation. Intermittent positive-pressure ventilation Intermittent positive-pressure ventilation

should be provided.should be provided. Increasing sedationIncreasing sedationFeeding - total parenteral nutrition, IV fluidFeeding - total parenteral nutrition, IV fluid

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Intensive nursing careIntensive nursing care2 hourly position change to prevent bedsore2 hourly position change to prevent bedsore Indwelling urinary catheter changeIndwelling urinary catheter changeMouth attendanceMouth attendanceCare of tracheostomy, parenteral feeding and Care of tracheostomy, parenteral feeding and

feeding linefeeding line If recovery takes place, the patient can be If recovery takes place, the patient can be

weaned from ventilator.weaned from ventilator.

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PreventionPreventionPrevention of high risk groupPrevention of high risk group

Pregnant mother ( ATT - first dose at 28 Pregnant mother ( ATT - first dose at 28 weeks, second dose-6weeks later, third weeks, second dose-6weeks later, third dose-6 weeks after delivery)dose-6 weeks after delivery)

Infant - ATT 3 doses during infancy and Infant - ATT 3 doses during infancy and booster dose at 5 years.booster dose at 5 years.

Farmers, labourers - ATT - 3 doses( 6 Farmers, labourers - ATT - 3 doses( 6 weeks after first and 6 months after weeks after first and 6 months after second) . Booster dose for ever 5 years or second) . Booster dose for ever 5 years or at the time of injury.at the time of injury.

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Prevention at the time of injuryPrevention at the time of injury

Thorough wound debridementThorough wound debridementPenicillin to kill the Penicillin to kill the Cl. tetaniCl. tetaniPatient with adequate immunisation Patient with adequate immunisation

booster dose of ATTbooster dose of ATT

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Patient with inadequate or no Patient with inadequate or no immunisationimmunisationsmall risk wound - ATTsmall risk wound - ATTHigh risk wound - ATT plus human High risk wound - ATT plus human

antitetanus globulinantitetanus globulinfollowed by second and third dose of followed by second and third dose of

ATT at 6 weeks and 6 months intervalATT at 6 weeks and 6 months interval

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PrognosisPrognosis

The death rate is high in children and the The death rate is high in children and the elderly.elderly.

The worldwide mortality rate is 50%, and it The worldwide mortality rate is 50%, and it is 30% in the United States.is 30% in the United States.

Drug users have a high rate of death Drug users have a high rate of death because of complications due to the drug.because of complications due to the drug.

Untreated tetanus is usually fatal within a Untreated tetanus is usually fatal within a few weeks.few weeks.

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PrognosisPrognosis

The four types of tetanus all have different The four types of tetanus all have different mortality rates.mortality rates.Generalized tetanus has a 50% mortality rate.Generalized tetanus has a 50% mortality rate.Local tetanus has a 1% mortality rate.Local tetanus has a 1% mortality rate.Neonatal tetanus has a 70% mortality rate.Neonatal tetanus has a 70% mortality rate.Cepahic tetanus has a 15-30% mortality rate.Cepahic tetanus has a 15-30% mortality rate.

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PrognosisPrognosis

The amount of tetanus bound to the nerves The amount of tetanus bound to the nerves affects prognosis, and the more toxin, the poorer affects prognosis, and the more toxin, the poorer the prognosis. the prognosis.

Surgical removal of damaged tissue and medical Surgical removal of damaged tissue and medical treatment improve prognosis.treatment improve prognosis.

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