Abdominal aortic aneurysm (AAA) is an enlargement of the aorta in the abdominal region. The most common cause is atherosclerosis. It can be asymptomatic and found incidentally or symptomatic with back pain, abdominal pain, or a pulsatile abdominal mass. Complications include rupture, infection, thrombosis, embolism, and erosion of nearby structures. Treatment involves surgical repair if the aneurysm reaches a certain size.

1. en love da Homoeopathy
ARTERIAL
DISEASES

2. en love da Homoeopathy
ANEURYSM

3. ANEURYSM

4. ANEURYSM
DEFINITION
• It is an abnormal permanent
dilatation of localised
segment of arterial system.
• Atherosclerosis whichis the
most common (90%)
facilitating cause of
aneurysmis due to
destruction and loss of
stability of tunica media.

5. TYPES
True aneurysm
• contains all three layers of
artery.
False aneurysm
• contains singlelayer of
fibrous tissue as wall of the
sac and it usuallyoccurs
after trauma

6. Fusiform
• uniformdilatation of entire
circumference of arterial wall ™
Saccular
• dilatation of part of
circumference of the arterial
wall
Dissecting
• througha tear in the intima
blood dissects between
inner and outer part of
tunica media of the artery

7. CAUSES
• Acquired:
• Degenerative:
Atherosclerosis
• mucoid degenerationof
intima and media
• Traumatic:
• Direct
• indirect
• likein poststenotic
dilatation by cervical
rib
• traumaticAV
aneurysmal sac
• aneurysmdue to
irradiation (due to
drynessand
destruction of vasa
vasorumcausing
weakening).

8. • Infective:
• Syphilis
• Mycotic
• tuberculosis (in lung);
• Arteritis
• acutesepsis
• Collagendiseases like
Marfan‘s syndrome
• polyarteritis nodosa
• EhlerDanos syndrome.
EhlerDanos syndrome

9. • Congenital:
• Berry aneurysm
• cirsoidaneurysm
• congenital AV fistula.
COMMONSITE
• Aorta.
• Femoral.
• Popliteal.
• Subclavian.
• Cerebral, mesenteric,
renal, splenic arteries.
• The most commonis true,
fusiform, atherosclerotic,
aortic aneurysms.
• Berry aneurysms are
multipleaneurysms
occurring in circle of
Willis.
Cirsoid aneurysm

10. CLINICALFEATURES
• Swelling at the site which is
pulsatile (expansile),
smooth, soft, warm,
compressible, withthrill on
palpation and bruit on
auscultation
• Swelling reduces in size
whenpressed proximally.
• Distal oedema due to
venous compression.
• Alteredsensationdue to
compressionof nerves.

11. • Erosionintobones, joints,
tracheaor oesophagus.
• Aneurysmwith
thrombosis can throwan
embolus causing gangrene
of toes, digits, extending
often proximallyalso.
INVESTIGATION
• Doppler study
• Duplex scan
• Angiogram
• DSA.
• Tests relevant for the cause,
likeblood sugar, lipid
profile, echocardiography.
Angiogram

12. TREATMENT
• Reconstruction of artery
using arterial grafts.
• Arterial
endoaneurysmorrhaphy
• Therapeuticembolisation.
• Clipping the vessel under
guidance

13. MYCOTICANEURYSM
CAUSES
• It is a misnomer.
• It is not due to fungus but
due to bacterialinfection
• Commonbacteria are
grampositive organisms
like Staphylococcus aureus
(most common) and
Streptococcus.
• Common aetiologyis
bacterial endocarditis but
could be any infective site

14. COMMONSITE
• Common vessels involved
are aorta, visceral, head
and neckand
intracranial.
• Commonlyit is saccular,
multilobed, with a narrow
neck.
CLINICALFEATURES
• Fever
• Toxaemia
• tender pulsatile mass if it
is in the periphery.
Mycotic aneurysm

15. INVESTIGATION
• Investigations: Leucocytosis.
• Positive blood culture
• MRI or CT angiogramare
relevant.
TREATMENT
• Broad-spectrumantibiotics
• Resectionof aneurysm;
debridement and drainage
of theinfectedaneurysm
with adequateblood
transfusions.
• Extra anatomicbypass
through uninfectedtissue
planes to avoid
contamination of the graft.
• Long termantibiotic
therapyis necessary

16. DISSECTINGANEURYSM
DEFINITION
• It is a misnomer.
• It is not an aneurysm,
only an aortic
dissection.
• It is the dissection of
media of the aorta after
splitting through
intima creating a
channel in the media of
thevessel wall.
DISSECTING
ANEURYSM

17. CAUSES
• Hypertension (It is
associatedin 80% of
dissecting aneurysms).
• Cysticmedial necrosis.
• Marfan’s syndrome and
collagen diseases.
• Trauma.
• Weakening of the elastic
layersof the media due to
shear forces.

18. SITES
• thoracicaorta- ascending
aorta
• other parts of aorta or other
vessels.
• aortic arch or thoracic
descending aorta.
PATHOLOGY
• This dissected aortic
channel gets linedby
endothelium, often reopens
distally into the aorta
causing double-barrelled
aorta which, in fact,
prevents complications

19. CLINICALFEATURES
• Painin the chest, back
whichis excruciating.
• Features of ischaemia due
to blockageof different
vessels
INVESTIGATION
• Chest X-ray shows
mediastinal widening
• Arterial Doppler
• Angiogram
Doppler – dissecting
aneurysm

20. COMPLICATION
• Acute: Rupture into the
pericardiumor pleura—
dangeroustype
• Chronic: Blockage of
coronary vessels and major
vessels like carotidand
subclavianarteries with
aortic insufficiency
TREATMENT
• Antihypertensives.
• Surgery: Using Dacron
graft reconstruction of
aorta has to be done with
cardiopulmonary bypass.

21. CIRSOIDANEURYSM
DEFINITION
• It is actuallya rare
arteriovenous fistula /
malformationof the scalp
usually of congenital origin
but occasionallycan be
traumatic.
• It is a rare variant of
capillary haemangioma
occurring in skin, beneath
whichabnormal artery
communicates with the
distendedveins.
CIRSOID
ANEURYSM

22. • 90%occur in relation to
superficial temporal artery
but few occur additionally
also in relationto occipital
arteries.
• It should be differentiated
fromthe true aneurysmof
the superficial temporal
artery.
• Cirsoidmeans varix.

23. COMMONSITE
• Commonly seenin
superficial temporal
arteryand its branches.
• Oftenthe underlying
bone gets thinned out
due to pressure.
• Occasionally extends
into the cranial cavity.
• Ulcerationis the
eventual problemwhich
will lead to
uncontrollable
haemorrhage.

24. CLINICALFEATURES
• Pulsatile swelling in
relationto superficial
temporal artery, whichis
warm, compressible,
witharteria lisationof
adjacentveins and with
bone thinning (due to
erosion).
• It feels likea ‘pulsating
bag of worms’
Bag of worms

25. INVESTIGATION
• Doppler study
• CT scan.
• Angiogram
• X-rayof the part.
X-ray

26. TREATMENT
• Ligation of feeding artery
and excision of lesion, often
requires preliminary
ligation of external carotid
artery.
• Intracranial extension
requires formal neuro
surgical approach.
• Endovascular therapy is
also useful

27. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

28. en love da Homoeopathy
ABDOMINAL
AORTIC
ANEURYSM

29. ABDOMINAL
AORTIC
ANEURYSM

30. ABDOMINALAORTIC
ANEURYSM(AAA)
DEFINITION
An enlargement of the aorta, the
mainblood vessel that delivers
blood to the body , at the level of
abdomen
CAUSES
• Atherosclerosis (as
degenerative process)
• Familial aorticaneurysm -
more females
• Cysticmedial necrosis
• associationwith
Chlamydiapneumoniae

31. • Others:
• Syphilis
• Dissection
• Trauma
• collagen diseases
• Infection
• Arteritis
CLASSIFICATON
• ClassificationI
• Infrarenal—most
common
• Suprarenal—5%.
(associatedwiththoracic
and or infrarenal types. )
• Isolated

32. • ClassificationII
• Asymptomatic.
• Symptomatic.
• Symptomaticruptured
ASYMPTAMATICTYPE
• It is foundincidentally either
on clinical examinationor
on angiography or on
ultrasound.
• Repair is requiredif
diameter is over 5.5 cm on
ultrasound.
• It is identifiedduring routine
abdominal palpation or while
assessing or operating for
some other abdominal
conditions.

33. SYMPTAMATIC
• Backpain,
• Abdominal pain
• Mass abdomenwhichis
smooth, soft, nonmobile,
• not moving withrespiration,
• vertically placed abovethe
umbilical level,
• pulsatile both in supine as
well as kneeelbowposition
with
• same intensity
• Resonant on percussion.

34. • Common in males
• commonin smokers.
• GIT
• urinary, venous symptoms
can also occur
• Hypertension
• Diabetes
• Cardiac problems
• In infrarenal type upper
border is clearlyfelt.
• Lower limb ischaemia
• embolicepisodes can occur.

35. • Being a retroperitoneal
mass back painis common
- due to retroperitoneal
stretching, nerve irritation
or vertebral erosion.
• inflammatoryaneurysm
adherent to ureters
• Aortocaval fistula-
presenting as GI bleed,
malaena, shock.
• highoutput cardiacfailure
withcontinuous bruitin
abdomen
• severe lower limb ischaemia
• (steal phenomenon).

36. INVESTIGATION
• Blood urea,
• serumCeratinine
• CT angiogram
• MR angiogram.
• Blood sugar
• lipid profile
• other
• ECG
• Echocardiography
• Cardiac and pulmonary
assessment

37. COMPLICATION
• Rupture
• infection
• Thrombosis
• embolism
• Distal ischaemia/gangrene
• Aortocaval fistula formation
• Aortoenteric fistula
• Erosion of vertebra
• Spinal cord ischaemia when
thrombosis develops

38. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

39. en love da Homoeopathy
ARTERIAL
OCCLUSION

40. ARTERIAL
OCCLUSION

41. ARTERIAL OCCLUSION
DEFINITION
• It is a condition of acutelack
of tissue perfusion due to
sudden cessation of
circulation.
• Mainaxial artery of thelimb
is blockedpresenting within
minutes to hour after
occlusion.
COMMONSITES
• It is common in lower limb
• upper limb
• Also occur in mesenteric,
cerebral, coronaryarteries.

42. CAUSES
• Embolismis the most
commoncausein developing
country.
• Trauma.
• Thrombosis of an artery
• polycythaemia rubra vera
• thrombocytosis.
• It is commonly observedin
external iliac artery,
profunda femoris arteryand
popliteal artery.

43. PATHOPHYSIOLOGY
• Distal ischaemia
↓
begins immediatelyafteracute
obstruction.
↓
Most sensitive peripheral nerves
are first involved
↓
and thenmuscles, subcutaneous
tissue and skin are affected in
order.
↓
Irreversible ischaemiaoccurs in 6
hours.
↓
Golden period is 1–6 hours.
↓
Ischaemia may get aggravatedby
↓
propagationof thrombus below
and abovethe block
↓
occluding the orifices of
collaterals
↓

44. fragmentationof embolus,
associatedthrombosis, acute
compartment syndrome.
• Acute ischaemia causes
endothelial injuryof
↓
capillaries, arterioles and venules
with luminal obliteration.
↓
Raisedcapillarypermeability
causes fluid leakageinto
extravascular space
↓
forming massive tissue
oedema deepto deepfascia
↓
whichby raising the
intracompartmental
pressure
↓
further reduces the
perfusionleading intoacute
compartment syndrome.

45. CLINICALFEATURES
• Painwhich is continuous,
severe, steady, bursting.
• Pallor of the distal part
withextreme coldlimb.
• Pulselessness—sudden
loss of earlier palpable
pulse.
• Paraesthesia—sensory
disturbances liketingling,
numbness or complete loss
of sensation.
PATHOLOGY

46. • Paresis—damage to motor
nerve and muscle leading
into paralysis as a late grave
feature.
• Poikilothermia—changein
thetemperature (cold).
• Pain, paraesthesia, paresis
are due to ischaemia of
peripheral nerves which are
sensitive to hypoxia.

47. DUETO
TRAUMA/TRAUMATIC
ACUTEARTERIAL
OCCLUSION
CAUSES
• Thrombus due to trauma.
• Subintimal haematoma.
• Acute compartment
syndrome.
• During femoral or brachial
arterial catheterisationfor
either diagnosticor
therapeutic procedures.

48. CLINICALFEATURES
• Historyof trauma
• Pain
• Swelling at the site
• Pallor
• Pulselessness
• Cold limb.
INVESTIGATION
• Duplex scan
• Angiogram
TREATMENT
• Wound is exploredand tear
in the artery is identified.
• Proper antibiotics and
heparin are required to
prevent thrombosis of the
vesseL
ASSOCIAEDFEATURES
• Immediate decompression
by longitudinal fasciotomy
• Haematoma
• Vessel tear has to be
managed accordingly

49. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

50. en love da Homoeopathy
ARTERIOVENOUS
FISTULA

51. ARTERIOVENOUS
FISTULA

52. ARTERIOVENOUS FISTULA
(AVF)
DEFINITION
• It is an abnormal
communication betweenan
arteryand vein.
TYPES
• 1. Congenital—is
arteriovenous malformation.
2. Acquired (Trauma is
commoncause).

53. SITE
• Limbs, either part or
whole of the limb is
involved.
• It may be localisedto toes
or fingers.
• Lungs.
• Brain—incircle of Willis.
• Other organs likebowel,
liver.

54. CLINICALFEATURES
• Structural changes in the
limb:
↓
Limbis lengtheneddue to
increasein blood flow
↓
since developmental period.
↓
Limb girthis also increased.
↓
Limb is warm.
↓
Continuous thrill & continuous
machinerymurmur all over the
lesion.
↓
Dilatedarterialised varicose
veins
↓
due to increasedblood flow &
valvular incompetence.
↓
bone erosionor extensionof
AVF into the bone as such.

55. • Physiological changes
↓
Because of the hyperdynamic
circulation
↓
there is increasedcardiacoutput
↓
congestive cardiac failure
COMPLICATION
• Haemorrhage
• Thrombosis
• Cardiac failure (CCF)

56. INVESTIGATION
• Angiogram—MR
angiogramis ideal.
• Doppler study.
• X-rayof the part.
• ECG
• Echocardiography
TREATMENT
• Conservative
• Sclerotherapy
• Compression
• avoiding injury.
INDICATIONS FOR
INNERVATION
• Absolute: Haemorrhage,
ischaemia, CCF.
• Relative: Pain, functional
disability, cosmesis, limb
asymmetry.
• Emergency: Torrential
bleeding usuallyafter
trauma (example—road
traffic accidents

57. ACQUIREDARTERIOVENOUS
FISTULA
CAUSES
• Trauma in (most common
cause): Femoral region.
Popliteal region. Brachial
region. Wrist. Aorta—
vena caval. Abdomen.
• After surgical intervention
of major vessels.
• Therapeutic: For renal
dialysis, AVF is created
(Cimino fistula) to achieve
arterialisation of veins and
also to have hyperdynamic
circulation.
• It is done to have easy and
adequatevenous accessfor
long time haemodialysis.
• Common sites
• Wrist
• Brachial
• Femoral region

58. PATHOPHYSIOLGY
Physiological changes:
• Cardiac failure due to
hyperdynamiccirculation.
Structural changes:
• Changes at theLevel of
Fistula
↓
Blood flows fromhighpressure
arteryto low pressurevein
↓
causing diversion of most of the
blood.
↓
Between the artery and vein, at
the site of fistula

59. ↓
dilatation develops with
formation of fibrous sac called
as Aneurysmal sac.
↓
This presents as warm, pulsatile,
smooth, soft, compressible
swelling at the site
↓
with continuous thrill and
continuous machinerymurmur

60. • Changes Belowthe Level of
the Fistula
↓
Because of diversionof arterial
blood distal part
↓
becomes ischaemic
↓
Because of highpressure
arterialisationof veins
↓
& valvular incompetence occurs
causing varicoseveins.

61. • Changes Proximal to the
Fistula
↓
Hyperdynamiccirculation
causes cardiac failure.
↓
Cardiac failure may be very
severe in traumaticAVF
↓
If pressure is appliedto the
arteryproximal to the fistula,
↓
swelling will reduce in size
↓
thrill and bruit will disappear,
pulserate and pulsepressure
becomes normal.
↓
This is calledas Nicoladoni’s
signor Branham’s sign.

62. INVESTIGATION
• Doppler
• Angiogram.
• ECG
• Echocardiography.
TREATMENT
• Excision of fistula and
reconstructionof artery
and vein with graft.
• Done in early stages—
larger vessels.
• Venous or Dacrongraft is
used.

63. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgery by Das
3. A Concise textbookof
Surgery by Das

64. en love da Homoeopathy
ARTHROSCLEROSIS

65. ARTHROSCLEROSIS
It is also calledas
Arteriosclerotic Vascular
Diseases(AVD)

66. ARTHROSCLEROSIS
Definition
• It is a chronic, complex
inflammatorycondition of
elasticand muscular
arteries, involving as
systemicand segmental. It
begins in childhood as fatty
streaks.

67. RISKFACTORS
• Definitive
Hypercholesterolaemia,
• hyperlipidaemia
• Cigarette smoking
• Hypertension
• Diabetes mellitus,
• Sedentarylife
• obesity
• Family history.

68. PATHOGENESIS
• It develops as a chronic
inflammatoryresponse of
the arterial wall to
endothelial injury
• Interactions of modified
lipoproteins
↓
monocycte –derived
macrophages ,T-lymphocyctes
& normal consituents of the
arterial wall
↓
Lesion progression
• It is expressedby the
Response to – injury
Hypothesis

69. 1. Chronicendothelial injury
2. Accumulationof
lipoproteins
3. Monocyte Adhesionto the
endothelium
4. Platelet Adhesion
5. Factor release
6. SMC proliferation &ECM
production
7.LipidAccumulation
Response To-Injury
Hypothesis
1.Chronic endothelial injury
• Causes increased
permeability
• leucocyte adhesion&
thrombosis

70. 2.Accumulation of lipoproteins
MainlyLDL
Endothelial injuryis Oxidized
by free radicals
↓
it comes into contact with an
arterywall
↓
series of reactions occurs for
repair mechanism
↓
cholesterol can be transported
only by lipoproteins

71. 3. Monocyte adhesionto the
endothelium
Body’s immune system
responds to the damaged
arterial wall
↓
by sending specializedwhite
blood cells(macrophages & T-
lymphocytes) to absorb the
oxidizedLDL forming
specialised Foamcells
↓
they growmore & then
ruptures
↓
depositing cholestrol in the
arterial wall
↓
continuing the cycle

72. 4. Platelet adhesion
5.Factor release Fromactivated
plaelet, Macrophages , Vascular
wall cells
6.SMCproliferations &ECM
production
Cholesterol plague causes the
smoothmuscle cellsto enlarge
↓
forma hardcover over affected
area
↓
it causes the narrowing of the
artery
↓
reduces the blood flow
increases the blood pressure

73. 7.LipidAccumulation
Accumulationof the lipid
↓
containing macrophages in the
intima
↓
give rise to fatty streaks
↓
and fibro fattyatheroma
(consisting of proliferated SMC,
Foamcells )
↓
Extracellular lipids &ECMis
formed

74. CONTAINS
• smoothmuscle cells,
connective tissue matrix,
macrophages and lipid
• Ulcerationand calcification
occurs in these plaques
↓
highlythrombogeniccausing
thrombosis
↓
block the vessel
↓
ischaemiaand infarction
INVOVLEDARTERIES
• abdominal aorta
• coronary arteries
• iliofemoral vessels,
• popliteal arteries.

75. FEATURES
• Smoking
• Hypertension
• Diabetes
• raised cholesterol
• Thrill and bruit over
femoral, renal, carotid
arteries may be felt/heard
• Signs of a pulsating
bulge(aneurysm)- in
abdomenor behindknee
• localised stenosis
• Absence/ feeble pulses

76. INVESTIGATION
• Blood sugar
• Doppler ultrasound
• Ankle-brachial index-
detectatherosclerosis in the
arteries in legs & feet
• Angiogram
• Electrocardiogram
• fasting lipid profile
• ECG
Ankle-brachial index

77. COMPLICATION™
• Narrowing of the arteries:
• Coronary
• Cerebral
• renal,
• Ischaemia
• ulcerations,
• gangrene can occur.
Aneurysmformation
• Carotidarterydiseases
• Peripheral arterydiseases
• Aneurysms

78. TREATMENT
• Avoid smoking
• control of hypertension
• Diabetes
• Hypercholesterolaemia
• Percutaneous
transluminal angioplasty
(PTA)

79. Surgeries
• Thrombectomy
• Endarterectomy
• profundaplasty.
• By pass graft
• Iliofemoral
• Aortofemoral
• iliopopliteal,
• femorofemoral
grafts.

80. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgery by Das
3. A Concise textbookof
Surgery by Das

81. en love da Homoeopathy
BUERGER’S
DISEASES

82. BUERGER’S
DISEASES
It is also calledas
Thrombophlebitis
obliterans (TAO)

83. DEFINITION
• It is a segmental,
progressive, occlusive,
inflammatorydiseases of
small & mediumsized
vessels with superficial
thrombophlebitis oftenmay
present as Raynaud’s
Phenomenonwithmicro
abscess, along with
neutrophil & giant cell
infiltrationwithSkiplesion

84. • commonly seenin young
and middle aged males
• smokers and tobaccousers
AFFECTIONS
• starts in lower limb one
side and later on the other
side.
• Upper limb involvement
occurs only afterlower limb
is diseased. More common in lower limb

85. CAUSES
• It is common in Jewish
people
• Hormonal influence
• familial nature,
• hypersensitivity to
cigarette,
• alteredautonomic
functions
• Lower socioeconomic
group,
• poor hygiene are other
factors.

86. PATHOGENESIS
• PANARTERITIS.
• due to smoking
↓
produce-vasospasms and
Hyperplasia of Intima in Artery
↓ Foll.by-
Thrombosis and obliteration of
vessels (mostlyMediumsize
vessels involved.)
produce- PANARTERITIS.
• Nerve involvementcause
REST PAINISCHAEMIA

87. • Once blockageoccurs,
collaterals blood supply is
maintained called as
Compensatory Peripheral
Vascular Diseases
CRITICAL LIMP ISCHAEMIA
CLASSIFICATION
Type I: Upper limbTAO—
rare.
Type II: Involving leg/s and
feet—crural/infrapopliteal.
Type III: Femoropopliteal.
Type IV: Aortoiliofemoral.
Type V: Generalised.
PANARTERITIS

88. CLINICALFEATURES
• Intermittent claudication
in foot
• Recurrent migratory
superficial
thrombophlebitis.
• May presentas Raynaud’s
phenomenon.

89. Complication
• Embolisation
• Ulcer formation
• Amputation
• Muscle weaknessatrophy
• Sensory& motor
impairment

90. INVESTIGATION
• Transbrachial angiogram
• Ultrasoundabdomento see
abdominal aortafor block/
aneurysm.
• Vein, artery, nerve biopsy.
Angiogram in arterial
diseases

91. TREATMENT
• Analgesics
• Stop smoking.
“Opt for either cigaretteor
limb, but not both.”
Surgical
• Sympathectomy
• Enarterotomy
• Amputation
• PTCA
• PABG

92. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

93. en love da Homoeopathy
BED
SORES

94. BED SORE

95. BEDSORE
DEFINITION
• Bedsore is a trophic ulcer
with bone as the base. It is
nonmobile, deep, punched
out ulcer.
COMMON
• Old age
• Bedridden
• Tetanus
• Patients with orthopaedic
and head injuries
• Diabetic
• Paraplegic
• Comatose

96. SITES
• Sites of bedsore are occiput
• Heel
• Sacrum
• Ischium
• Scapula
FACTORS
• Malnutrition
• Pressure
• Anaemia
• sensory loss
• moisture
TREATMENT
• Changeof positions is
alwaysencouraged.
• Use of waterbed, ripple
bed is advised.
• Moisture has to be
avoided.
• Soaking by urine, sweat,
pus, and faeces has to be
takencare off.
• Good nursing, regular
dressing, good nutrition
are necessary.

97. • Antibiotics, blood
transfusions are very
essential.
• Excision of dead tissue
followedby skin grafting or
local rotation flaps may have
to be done.
• Rehabilitation.
Water bed

98. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

99. en love da Homoeopathy
FROSTBITE

100. FROSTBITE

101. FROSTBITE
DEFINITION
• It is due to exposure to cold
windor highaltitude.
• It is common in old age
during cold spells.
CLINICALFEATURES
• Damage to vessel wall
occurs causing oedema
• Blistering
• Gangrene formation
• Part is painlessand waxy.

102. • Cells get frozen at – 5°C.
Initially rednessand
oedema
• 1st degree - blister
formation
• 2nd degree - skin necrosis
• 3rd degree - gangrene
• 4thdegree - develops
gradually.
Gangrenous Frost bite

105. TREATMENT
• Gradual warming is
done.
• Part shouldbe wrapped
with cottonwool and
rested.
• Warming is gradually
done with44°C in 30
minutes withwarm
water.
• Limb elevation is done to
reduce oedema.
• Intraarterial vasodilators
may help.

106. • Warmdrinks, analgesics,
paravertebral injections to
sympathetic chain,
hyperbaricoxygen are
effective.
• If gangrene develops,
amputation is needed.
REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

107. A
Special Thanks
To A Very
Special Doctor