Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 587 - файл
.pdf
Examination in Arterial Diseases
https://t.me/med1917
Fig. 5.37: Amputated 2nd toe (ray amputation) done for
toe gangrene—shows good healing. It was dry gangrene.
Causes for Raynaud’s phenomenon:
a. Raynaud’s disease: It is seen in females, usually
bilateral. It occurs in upper limb with normal
peripheral pulses. It is due to arteriolar spasm in
upper limb (hand) due to abnormal sensitivity to
cold. Patient develops blanching, cyanosis and later
flushing as Raynaud’s syndrome. Occasionally if
spasm persists gangrene may develop. Symptoms
can be precipitated and observed by placing hands
in cold water.
b. Working with vibrating tools: Like pneumatic road
drills, chain saws, wood cutting, and fishermen
traveling in machine boats—seen in males.
c. Collagen vascular diseases: Like Scleroderma,
Rheumatoid diseases causing vasculitis (all autoimmune diseases).
d. Other causes: Cervical rib, Buerger’s disease,
Scalene syndrome. It is often associated with
CREST syndrome (Calcinosis cutis, Raynaud’s
phenomenon, Esophageal defects, Sclerodactyly,
Telangiectasia).
T ypes of Raynaud’s phenomenon: V asospastic and
Obliterative. Coffman criteria for Raynaud’s
syndrome—episodic attacks of well demarcated
reversible self limiting colour changes for 1-20 minutes
(less than 320 minutes) on exposure to cold/emotional
stimuli. Raynaud’s can be—Primary Raynaud’ s is an
idiopathic vasospastic disorder without underlying
131
identifiable causes. Usually there is no significant pain
in primary type. Primary is probably due to increased
sensitivity of alpha 2 receptors to norepinephrine;
decreased nitric oxide and endothelin 1 in endothelial
cells; increased serotonin and thromboxane. It is
common in females and in younger age group. Usually
bilateral involving all digits. Secondary Raynaud’s is
vasospasm due to some underlying causes. Significant
pain will be present especially during rewarming stage.
There are positive autoantibodies; equal in both sexes;
occurs at any age group; need not be bilateral.
Subclavian Steal Syndrome
Following obstruction of the first part of subclavian
artery , vertebral artery provides collateral circulation
to the arm by reversing its blood flow. This causes
cerebral ischaemia with syncopal attacks, visual
disturbances, and diminished blood pressure in the
affected limb. Symptoms will be aggravated by arm
exercise (Fig. 5.38).
Fig. 5.38: Subclavian steal syndrome.
Takayasu’s Pulseless Arteritis (Takayasu,
1938-Ophthalmologist, Japan)
It is progressive, initially symptomless panarteritis
involving aortic arch and branches of aorta of unknown
aetiology, probably immunological. It is common in
young females (85%); common in Japan; commonly
involves subclavian artery; involves all layers of
132
https://t.me/med1917
arteries of upper limb and neck; often bilateral. It
remains unnoticed for long time. Fever, myalgia,
arthralgia, upper limb claudication; absence of pulses
in upper limb/limbs; neck; hypertension; fainting on
turning the neck or change in position; atrophy of face;
thrill/bruit along major arteries of upper limb and neck
are the features. Optic nerve atrophy without papilloedema; weakness and paraesthesia of upper limb;
cerebral softening, convulsions, hemiplegia can occur.
Occasionally it can be life threatening. Myocardial
infarction; embolism are other features.
SRB’s Clinical Surgery
perfusion pressure (30 mm Hg) causing impairment
of tissue perfusion. It is common in anterior compartment of leg and in front of forearm. Here because
of the closed compartment, pressure increases
following fracture, haematoma which compresses over
the vessel. It leads to blockade of vessel causing acute
ischaemia of the limb presenting with severe pain,
pallor, pulselessness. Measurement of intracompart-
mental pressure by placing a needle cannula directly
into the compartment and using pressure transducer
is ideal way to confirm the condition as Doppler still
may show strong signal of pulse.
Erythromelalgia/Erythralgia
It is severe burning pain and redness in the feet.
Sensation of heat is so severe that patient keeps the
feet in cold water to reduce it. It presents as episodic
attack. There will be flushing in feet; prominent veins;
warmness in the skin; severe hyperaesthesia is typical;
even touching can be painful. It can be primary or
secondary. Secondary, which is not uncommon is
observed in arterial obliterative conditions, erythrocyanosis frigida, polycythaemia, gout and frostbite.
Primary is due to unknown etiology; it is very rare.
Acute Arterial Occlusion
Causes: 1.Trauma; 2. Embolism.
Traumatic Acute Arterial Occlusion
Causes: (1) Thrombus due to trauma; (2) Subintimal
haematoma; (3) Acute compartment syndrome; (4)
During femoral or brachial arterial catheterisation,
either for diagnostic or therapeutic procedures.
Pathophysiology: Brain tolerates ischaemia only for
4 minutes; heart for 20 minutes; limbs for 6 hours in
profound acute ischaemia. Skin and bone are relatively
resistant to ischaemia compared to nerves. Nervous
system is most sensitive for ischaemia. When
peripheral nerve is affected by ischaemia, it causes pain,
paraesthesia and paralysis. Muscles play a major role
in limb ischaemia as muscle accounts for the 75% of
limb weight.
Clinical features: History of trauma; pain, swelling
at the site, pallor, pulselessness, cold limb (pallor).
Acute compartment syndrome: There is sudden
increase in compartment pressure more than capillary
Treatment: Immediate decompression by longitudinal
fasciotomy, is the treatment of choice, wherein deep
fascia is cut adequately to relieve the compression.
Otherwise limb may go for severe ischaemia, gangrene
and may end with amputation. Associated fractures,
haematoma, vessel tear has to be managed accordingly.
Embolism: It is due to a solid material which is floating
and traveling in the bloodstream, eventually blocking
the vessel on its pathway.
Arterial emboli: Cardiac source (80%)—due to mural
thrombus following mitral stenosis and atrial
fibrillation (50%); myocardial infarction (25%); others
(5%). Noncardiac (10%)—aneurysms (5%); others
(4%); paradoxical (1%). Idiopathic is 10%. Cervical
rib causing poststenotic dilatation of subclavian artery
can cause emboli. Venous emboli are due to DVT
causing pulmonary embolism. Fat and air embolism
are other types.
Effects of arterial embolism: Brain—Blockage at
middle cerebral artery causes hemiplegia, transient
ischaemic attacks (TIA), visual disturbances; Blockage
at central retinal artery causes amaurosis fugax, or
permanent blindness; Blockage at mesenteric vessels
causes intestinal gangrene; Blockage at renal artery
leads to haematuria, loin pain; Blockage at limb vessels
causes pain, pallor, pulseless, paraesthesia, paresis,
ulceration, gangrene. Complete sudden embolic block
causes cool, waxy-white pallor whereas a partial
occlusion causes pallor on elevation and rubor on
dependency (Fig. 5.39). Commonest site of arterial
emboli is common femoral artery (40%).Aortic
bifurcation, cerebral vessel, iliac vessels account for
15% each. Upper limb and popliteal vessels are 10%
each. V isceral/mesenteric is 5%.
Examination in Arterial Diseases
https://t.me/med1917
Fig. 5.39: Fogarty catheter. It is 80 cm in length with 4 to 7
French size. It is used for embolectomy. Note the inflated
balloon at the tip.
133
Fig. 5.40: Saddle embolus blocking the bifurcation of
abdominal aorta.
Saddle embolus: It is an embolus blocking at bifurcation of aorta.
Causes: Mural thrombus after myocardial infarction
and mitral stenosis with atrial fibrillation; aortic
aneurysm. The embolus which blocks at aortic
bifurcation is usually large (Fig. 5.40).
Clinical features: Features of ischaemia and gangrene
in both lower limbs often with neurogenic ischaemic
injury.
Features of embolism
Earlier history of claudication is absent but history
suggestive of disease for source of emboli will be present
Sudden, dramatic, rapid development of pain with
numbness
Limb becomes rapidly cold and mottled with blebs
Loss of sensation and movements
Absence of distal pulses but forcible, expansile, prominent
proximal pulse. Example – prominent femoral artery
pulsation with embolic bock at popliteal level
Toxic features
Fat Embolism
It is commonly seen after fracture femur, tibia, or
multiple fractures and occasionally following electro-
convulsive therapy , usually occurs in 24-72 hours. It
is due to aggregation of chylomicrons, derived from
bone marrow , causing fat embolism. It is often a fatal
condition.
Features: Cerebral: Drowsy, restless, disoriented,
constricted pupils, pyrexia, and coma. Pulmonary:
Cyanosis, tachypnoea, right heart failure, froth in mouth
and nostrils, fat droplets in sputum, eventually respiratory failure. Cutaneous: Petechial haemorrhages
in the skin. Retinal artery emboli is the earliest sign
to appear, causing striae haemorrhages, fluffy exudates confirmed on fundoscopic examination. Kidney:
Blockage of renal arterioles results in fat droplets in
urine.
Air embolism: Causes: Through venous access like
IV cannula; during artificial pneumothorax; during
surgeries of neck and axilla; traumatic opening of major
veins sucking air inside causing embolism; during
fallopian tube insufflation; during illegal abortion.
Amount of air required to cause air embolism is
50 ml. When the air enters the right atrium, it gets
churned up forming foam which enters the right
ventricle and blocks the pulmonary artery.
Therapeutic embolisation: Indications: Haemangio-
mas; AV fistulas; Malignancies like renal cell carcinoma, hepatoma; craniovascular problems; to arrest
haemorrhage from GIT , urinary and respiratory tract.
In bleeding duodenal ulcer or gastric ulcer, embolisation is used to occlude gastroduodenal artery or left
gastric artery respectively . It is also useful in bleeding
oesophageal varices, secondaries in liver (mainly due
to carcinoids), hepatoma. Materials used are—blood
clot; human dura; gel foam; plastic microspheres;
balloons; ethyl alcohol; quick setting plastics; wool;
stainless steel coils.
134
https://t.me/med1917
Aneurysms
SRB’s Clinical Surgery
It is dilatations of localised segment of arterial system.
It is due to weakening of the wall of artery. True
aneurysm contains all three layers of artery. False
aneurysm contains single layer of fibrous tissue as
wall of the sac and it usually occurs after trauma (Fig.
5.41).
Fig. 5.41: True and false aneurysms. In true type, all layers
are intact. In false type all layers breached with haematoma
having a false capsule.
Causes: Acquired: 1. Degenerative – Atherosclerosis
(commonest cause); mucoid degeneration of intima
and media (in South African young Negroes). 2.
Traumatic—direct; indirect like in poststenotic
dilatation by cervical rib; traumatic AV aneurysmal
sac; aneurysm due to irradiation (due to dryness and
destruction of vasa vasorum causing weakening of
the wall). 3. Infective—Syphilis; mycotic; tuberculosis
(in lung); arteritis; polyarteritis nodosa; acute sepsis.
Congenital: Berry aneurysm; cirsoid aneurysm;
congenital A V fistula; Collagen diseases like Marfan’s
syndrome, Ehlers-Danlos syndrome.
Sites: Aorta (Fig. 5.43); femoral; popliteal; subclavian;
cerebral, mesenteric, renal, splenic arteries.
Commonest is true, fusiform, atherosclerotic, aortic
aneurysms. Berry’ s aneurysms are multiple aneurysms
occurring in circle of Willis.
Types: Fusiform—uniform dilatation of entire circum-
ference of arterial wall; Saccular—dilatation of part
of circumference of the arterial wall; Dissecting –
through a tear in the intima blood dissects between
inner and outer part of tunica media of the artery (Fig.
5.42).
Fig. 5.42: Fusiform and saccular types of aneurysms.
Fig. 5.43: Thoracic aortic aneurysm.
Clinical Features of Aneurysm
1. Asymptomatic. 2. Symptoms: Swelling which is
pulsatile; pain may be dull aching / severe acute type
due to sudden stretching of artery / bursting type when
it ruptures or forms a haematoma; referred pain due
to pressing over adjacent nerves may be seen; features
of ischaemia of the distal limb; painful, cyanotic distal
oedema due to venous compression. 3. On palpation:
Swelling at the site is pulsatile (expansile), smooth,
soft, warm, compressible, with thrill on palpation and
bruit on auscultation. Swelling reduces in size when
Examination in Arterial Diseases
https://t.me/med1917
pressed proximally; moves sideward but not along
the line of artery . There is often altered sensation due
to compression of nerves; erosion into bones, joints,
trachea or oesophagus; aneurysm with thrombosis can
throw an embolus causing gangrene of toes, digits,
often extending proximally also.
Differential diagnosis: 1. Pyogenic abscess: Abscess
has to be always confirmed by aspiration; especially
in axilla, popliteal region, and groin. 2. Vascular
tumours. 3. Pulsating tumours: Sarcomas, pulsating
secondaries. 4. Pseudocyst of pancreas mimics aortic
aneurysm. 5. A-V fistula.
Abdominal Aneurysms
Abdominal aortic aneurysm is the commonest aortic
aneurysm. It has got 2% incidence.
Causes: Atherosclerosis: 95%. Others: Syphilis,
dissecting, traumatic, collagen diseases.
Classification I: 1. Infrarenal—Commonest 95%. 2.
Suprarenal 5%. Classification II: (1) Asymptomatic:
Found incidentally either on clinical examination or
on angiography or on ultrasound. Repair is required
if diameter is more than 5.5 cm on ultrasound. (2)
Symptomatic without rupture: Present as back pain,
abdominal pain, mass abdomen which is smooth, soft,
nonmobile, not moving with respiration, vertically
placed above the umbilical level, pulsatile both in
supine as well as in knee—elbow position with same
intensity , resonant on percussion. GIT, urinary , venous
symptoms can also occur. Hypertension, diabetes,
cardiac problems should be looked for and dealt with.
If aneurysm is more than 5.5 cm then surgery is the
choice. (3) Symptomatic ruptured aortic aneurysm:
Risk of rupture is 1%, if diameter is within 5.5 cm
in size. Risk increases to 20% once the diameter
≥7 cm. It may be anterior rupture (20%) into the free
peritoneal cavity causing severe shock and very early
death; or posterior rupture (80%) with formation of
retr operitoneal haematoma of large size causing severe
back pain, hypotension, and shock, absence of femoral
pulses and with palpable mass in the abdomen (Figs
5.44 and 5.45). Emergency management is needed.
Effects of aneurysm: Thrombosis and emboli forma-
tion; peripheral ischaemia; rupture; erosion into adja-
135
Fig. 5.44; Chest X-ray showing aortic aneurysm.
Fig. 5.45: Abdominal aortic aneurysm ultrasound picture.
cent structures like bone, bowel, pressure on organs
like oesophagus (causing dysphagia); sexual dysfunction; aortoduodenal fistula; aortovenacaval fistula;
spinal cord ischaemia; infection.
Peripheral Aneurysms
Popliteal aneurysm is the commonest (70%) peripheral aneurysm. It is 65% bilateral. 25% cases are
associated with abdominal aortic aneurysm. 75%
causes complications in 5 years. Presentations are—
136
https://t.me/med1917
SRB’s Clinical Surgery
swelling in popliteal region which is smooth, soft,
pulsatile, well localised, warm, and compressible, often
with thrill and bruit. It may mimic a pyogenic abscess.
Thrombosis and emboli from popliteal aneurysm can
cause distal gangrene which may spread proximally
and may lead to amputation. Rupture may cause
torrential haemorrhage.
Dissecting Aneurysm
It is the dissection of media of the aorta after splitting
through intima creating a channel in the media of the
vessel wall.
Causes: Hypertension (It is associated in 80% of
dissecting aneurysms); cystic medial necrosis;
Marfan’s syndrome and collagen diseases; trauma;
weakening of the elastic layers of the media due to
shear forces. It is always seen in thoracic aorta, common
in ascending aorta (70%). It is uncommon in other
parts of aorta or other vessels. It can occur in aortic
arch or thoracic descending aorta. This dissected aortic
channel gets lined by endothelium, often re-opens
distally into the aorta causing double-barreled aorta
which in fact prevents complications. It is commonly
associated with aortic insufficiency. Dissecting
aneurysm is a misnomer. It is only aortic dissection.
Atherosclerosis is not a usual cause for dissecting
aneurysm.
Classification (DeBakey’s): Type I: Dissection begins
in ascending aorta extends into descending thoracic
aorta (70%). Type II: Dissection origins and extends
only up to the origin of the major vessels. It is safer
type with fewer complications. Type III: Dissection
begins in the descending thoracic aorta beyond the
origin of the left subclavian artery. Dissecting aneurysm
can be acute, chronic, healed dissecting aneurysm
which communicates distally again to aorta as double
barreled aorta.
Complications: Acute: Rupture into the pericardium
or pleura—dangerous type. Chronic: Blockage of
coronary vessels, major vessels like carotid, subclavian
arteries with aortic insufficiency.
Clinical features: Pain in the chest, back which is
excruciating. Features of ischaemia develop due to
blockage of different vessels (Fig. 5.46).
Fig. 5.46: Dissecting aneurysm.
Mycotic Aneurysm
It is a misnomer. It is not due to fungus but due to
bacterial (commonly Staphylococcus, Str eptococcus)
infection. Origin of bacteria may be from any site of
infection in the body. Common aetiology is bacterial
endocarditis but could be any infective site. Common
vessels involved are aorta, visceral, head and neck
and intracranial. Commonly it is saccular, multilobed,
with a narrow neck. Patient presents with fever, toxaemia and tender pulsatile mass if it is in the periphery.
Acrocyanosis (Crurum Puellarum Frigidum)
It is persistent, painless cyanosis seen in fingers and
often in legs with paraesthesia and chilblains affecting
young females. It is chronic persistent arteriolar
constriction with slow rate of blood flow. Trophic
changes, ulcerations are not seen. Cyanosis which is
persisting may aggravate on exposure to cold. It may
be associated with endocrine dysfunction. Vasodilators, and cervical sympathectomy may be effective.
Gangrene
It is macroscopic death of tissue in situ (in continuity
with adjacent viable tissue) with or without putrefaction. It can occur in—limbs, appendix, bowel, testes,
gallbladder.
Examination in Arterial Diseases
https://t.me/med1917
Types of Gangrene
Dry gangrene is due to slow gradual loss of blood
supply to the part causing dry, desiccated, wrinkled,
mummified part with proper line of demarcation (Fig.
5.47). Wet gangr ene is due to infection with putrefac-
tion, causing oedematous, swollen, discolouration,
spreading proximally , with vague line of demarcation
137
A
B
Figs 5.48A and B: Gangrene both in lower and
upper limbs. Note all features of gangrene.
Fig. 5.47: Dry gangrene of leg. Patient needed above
knee amputation.
Causes
1. Secondary to arterial obstruction like atherosclerosis, emboli, diabetes, T AO, Raynaud’ s disease,
ergots etc. 2. Infective: Boil, carbuncle, gas gangrene,
Fournier’s gangrene, cancrum oris. 3. Traumatic:
Direct/indirect. 4. Physical: Burns, scalds, frostbite,
chemicals, irradiation, electrical. 5. V enous gangrene.
Clinical Features
Colour changes: Pallor, grayish, purple, brownish
black discolouration due to disintegration of haemoglobin to sulphide; Absence of pulse; Loss of sensation;
Loss of function; Loss of temperature; Line of
demarcation between viable and dead tissue by a band
of hyperaemia and hyperaesthesia with development
of a layer of granulation tissue. In dry gangrene
separation occurs by aseptic ulceration with minimum
infection and gangrene is dry, and mummified. In
moist gangrene separation takes place by septic
ulceration. Often demarcation is vague with skin lesions
more proximally and so ends up with higher level of
amputations. Even after amputation skin flap may show
die back process, leading to failure of taking up of
amputation flap and so requires still higher level of
amputation. Proximal ischaemic features may be
present with rest pain, colour changes, hyperaesthesia
– pregangrene (Figs 5.48A and B and 5.49).
Diabetic Foot and Diabetic Gangrene
Foot is a complex structure with many layers of
muscles, ligaments, joints, arches, fat, thick plantar
fascia, vascular arches, neurological system which
maintains weight bearing, gravity, normal walk (swing,
and stance phases).
Problems in diabetic foot: Callosities; ulceration;
abscess and cellulitis of foot; osteomyelitis of different
bones of foot like metatarsals; cuneiforms; calcaneum;
Fig. 5.49: Below knee amputation stump which is also
ischaemic. Patient underwent below knee amputation.
138
https://t.me/med1917
SRB’s Clinical Surgery
diabetic gangrene; arthritis of the joints. Meggitt’s
classification of diabetic foot: Grade 0: Foot symptoms
like pain, only . Grade 1: Superficial ulcers. Grade 2:
Deep ulcers. Grade 3: Ulcer with bone involvement.
Grade 4: Forefoot gangrene. Grade 5: Full foot
gangrene.
Pathogenesis of diabetic foot/ gangrene: High
glucose level in tissues is a good culture media for
bacteria. So infection is common. Diabetic micro-
angiopathy causes blockade of microcirculation
leading to hypoxia. Diabetic neuropathy: Due to
sensory neuropathy, minor injuries are not noticed and
so infection occurs. Due to motor neuropathy,
dysfunction of muscles, arches of foot and joints, and
loss of reflexes of foot occurs causing more prone
for trauma, abscess, etc. Due to autonomic neuropathy,
skin will be dry, causing defective skin barrier and
so more prone for infection. Diabetic atheroscler osis
itself reduces the blood supply and causes gangrene.
Thrombosis can be precipitated by infection causing
infective gangrene. Blockage occurs at plantar, tibial
and dorsalis pedis vessels. Increased glycosylated
haemoglobin in blood causes defective oxygen
dissociation leading to more hypoxia. At tissue level
there will be increased glycosylated tissue proteins,
which prevents proper oxygen utilisation and so
aggravates hypoxia.
Clinical features: Pain in the foot; ulceration; absence
of sensation; absence of pulsations in the foot (posterior
tibial and dorsalis pedis arteries); loss of joint movements; abscess formation; change in temperature and
colour when gangrene sets in (Fig. 5.50).
Fig. 5.50: Diabetic leg severely infected with necrosis
Infective Gangrene
which needs amputation.
It is development of gangrene due to infection commonly bacterial occasionally by specific organisms.
Cancrum oris; gas gangrene; carbuncle; Fournier’s
gangrene are the examples. It is due to infective
thrombosis of local end arteries causing gangrene of
the tissues and skin of that particular area.
Cancrum oris (Noma) is an infective gangrene, a
severe form of Vincent’s acute ulcerative gingivitis
and stomatitis. It is seen in poorly nourished, ill child
due to Borrelia vincentii and Fusiformis fusiformis
bacteria. It starts in gums, spreads into cheek, bone,
soft tissues and skin causing extensive tissue loss;
destruction of mucous membrane, soft tissues, bone
and skin with severe toxaemia. There will be other
secondary infection also. Fetid odour, excessive
salivary secretion is usual. Phagedena is destructive
ulceration with gangrene seen in cancrum oris and
chancroid. In phagedena there is destruction without
proliferation whereas in malignancy there is destruction
with proliferation. Condition has high mortality.
Gas Gangrene
It is an infective gangrene caused by clostridial
organisms involving mainly skeletal muscles. Earlier
it was called as malignant oedema. Organisms—
Clostridium welchii (Perfringens) a gram negative,
central spore bearing, nonmotile,capsulated organism;
Clostridium oedematiens; Clostridium septicum;
Clostridium histolyticum. Clostridium welchii produce
toxins—Alpha (Commonest); Beta; Epsilon; Iota.
Various strains include—A, B, C, D, E. ‘A’ strain is
commonest. Exotoxins: Lecithinase is important toxin
which is haemolytic, membranolytic and necrotic
causing extensive myositis. Haemolysin causes
extensive haemolysis. Hyaluronidase helps in rapid
spread of gas gangrene. Proteinase causes breaking
down of proteins in an infected tissue. Spores enter
through the devitalised tissues commonly following
road traffic accidents and crush injury, etc. Spores
germinate → Released bacteria will multiply →
Exotoxins are released → cause their effects.
Effects: Extensive necrosis of muscle with production
of gas H2S which stains brown or black → usually
muscle gets involved from origin to insertion → Often
may extend into thoracic and abdominal muscles →
When it effects the liver it causes necrosis with frothy
blood → foaming liver, is characteristic.
Examination in Arterial Diseases
https://t.me/med1917
Clinical features: Incubation period is 1-2 days.
Features of toxaemia, fever, tachycardia, pallor are
common. Wound is under tension with foul smelling
discharge and Khaki brown coloured skin due to
haemolysis. Exposed muscle is typically brick red/
green/black coloured. Crepitus can be felt. Jaundice
may be ominous sign and also oliguria signifies renal
failure.
Clinical types: Fulminant type causes rapid progress
and often death due to toxaemia, renal failure or liver
failure or MODS. Massive type involves whole of one
limb containing fully dark coloured gas filled areas.
Group type: Infection of one group of muscles like
extensors of thigh, flexors of leg. Single muscle type
will be affecting one single muscle. Subcutaneous type
of gas gangrene involves only subcutaneous tissue (i.e.
superficial involvement). X-ray will show gas in
muscle plane or under the skin. Once a ward or
operation theatre is been used for a patient with gas
gangrene, then it should be fumigated properly for
48 hours to prevent the risk of spread of infection
to other patients (Fig. 5.51).
139
Ainhum
A fissure develops at the interphalangeal joint of the
toe which becomes a fibrous band that encircles the
digit causing necrosis and gangrene of toe. It is common
in males but can occur in females. History of barefoot
walk during childhood is common. It is common in
blacks; common in Negroes; it is often bilateral;
common in 5th toe; can occur in other toes also. Dry
gangrene with a constriction band / groove leading
into autoamputation is common (Figs 5.52A and B).
Fig. 5.51: Gas gangrene.
Frostbite
It is due to exposure to cold wind or high altitude
(below freezing point). It is common in old age during
cold spells. There is arteriolar spasm; protein denaturation; cell destruction. Damage to vessel wall causes
oedema, blistering, deep ulcer and gangrene formation. Part is painless and waxy.
Treatment: Gradual warming is done. Part should
be wrapped with cottonwool and rested. W arm drinks,
analgesics, paravertebral injections to sympathetic
chain, hyperbaric oxygen are effective.
Chilblains also called as perniosis is due to exposure
to intense cold causing cutaneous arteriolar constriction
with superficial ulcers.
Figs 5.52A and B: Typical Ainhum. Note it is bilateral. Note
the constriction ring in the little toe. It may go for autoamputation. It needs Z plasty. It is common in blacks and Negroes.
Morvan’s Disease
It is painless whitlow seen in fingers in syringomyelia.
It is neuropathic ulceration / gangrene. Olivier d’Anger
described syringomyelia in 1824 wherein there is
formation of cavity in spinal cord along with fourth
ventricle with thinning of neural tissue component.
It causes sensory disturbances in upperlimb; weakness
of hands; loss of pain and temperature sensation in
hands; progressive kyphoscoliosis. Hindbrain herniation may lead into ataxia, spasticity, headache,
lower cranial nerve palsy. It may be associated with
Type I Arnold-Chiari malformation.
140
https://t.me/med1917
Reperfusion Injury
SRB’s Clinical Surgery
It occurs after reestablishment of arterial flow to an
ischaemic tissue bed which further leads to tissue death.
It is due to sudden release of oxygen free radicals which
blocks the microcirculation, with release of high levels
of potassium and myoglobin. Haemodynamically
patient becomes unstable with lactic acidosis, intracellular changes, interstitial oedema and cardiac
dysfunction. Severe ischaemia causes oedema in the
muscular compartment with raise in compartment
pressure more than the essential capillary perfusion
pressure causing acute compartment syndrome. It is
common in the anterior compartment of the leg.
Acidosis, acute renal failure and cardiac arrhythmias
set in and becomes life threatening. Features are –
toxaemia; oliguria; persistent pain and oedema in the
leg with muscular tenderness; raised blood urea and
serum creatinine with features of acute ischaemia in the
limb.
Treatment—Mannitol to prevent renal failure; fluid
therapy; fasciotomy to reduce raised compartment
pressure; antibiotics. Condition may be life threatening.
Upper limb ischaemia
Trauma / cervical rib are the common causes
Opposite limb, lower limbs should be examined
Cardiovascular system should be examined
Neck should be examined
Wasting / girth should be checked
All relevant clinical methods are equally significant
Auscultation over neck / axilla / carotids for bruit are
important
Doppler; angiogram; nerve conduction studies; CT neck
and thorax are essential investigations
Arterial repair; therapy for cervical rib; scalenotomy;
cervical sympathectomy are the different modalities of
treatment (Figs 5.53A and B and 5.54)
Digital amputation may be required
Upper Limb Ischaemia
It is a rare entity compared to lower limb ischaemia
but important because of its difficulty in managing.
Higher-level amputations are rare in upper limb
ischaemia.
Causes—Thoracic outlet syndrome; Raynaud’s
disease and phenomenon; embolism due to causes like
atrial fibrillation and endocarditis; trauma; T AO upper
limb (along with lower limb TAO); atherosclerosis
of upper limb vessels; T akayasu’s arteritis; Polyarteritis
nodosa; Scleroderma.
Features—Upper limb claudication and ischaemic rest
pain; ischaemic features; ulcers and gangrene
commonly in fingers; wasting of hand and forearm
muscles; mass in the neck, bruit in the neck in
supraclavicular region; Adson test, hyperabduction
test, Roos test, Allen’s tests are important.
Investigations—Arterial Doppler; subclavian angiogram; investigations to confirm vasculitis; blood sugar;
lipid profile; cardiac evaluation.
A
B
Fig. 5.53: Cervical sympathectomy scar (done for upper
limb ischaemia) in the neck/ patient has developed Horner’s
syndrome. Healed ulcer area over tip of index finger on left
side is seen. Patient is asymptomatic after sympathectomy.
Ptosis—typical look in another patient.
Arteriovenous Fistula (AVF)
It is an abnormal communication between an artery
and vein. It can be congenital (arteriovenous malfor-
Соседние файлы в папке @xirurgi_2025