Transcript GENERAL SURGERY FOR DENTAL STUDENTS

GENERAL SURGERY
FOR
DENTAL STUDENTS
BY
Dr. AHMAD K. SHAHWAN
PH.D. GENERAL SURGERY
Approach to the Surgical Patient:
The management of surgical disorders
requires not only the application of
technical skills and training in the basic
sciences to the problems of diagnosis and
treatment but also a sympathy and indeed
love for the patient. The surgeon must be a
doctor, an applied scientist, an engineer, an
artist. Because life or death often depends
upon the validity of surgical decisions, the
surgeon's judgment must be matched by
courage in action and by a high degree of
technical proficiency
Approach to the Surgical Patient:
1)
2)
3)
4)
5)
6)
7)
Historyphysical Examination InvestigationsPre-operative preparation operation post-operative treatmentmanagement of complications.
Approach to the Surgical Patient:

The History :
At their first contact, the surgeon must gain
the patient's confidence and convey the
assurance that help is available and will be
provided. The surgeon must demonstrate
concern for the patient as a person who
needs help and not just as a "case" to be
processed. This is not always easy to do,
and there are no rules of conduct except to
be gentle and considerate.
The History
I- The chief complaint :i.e. what the problem that
bring the patient to the doctor& its duration .
II- The present history: in full detail:
1-when the complaint start exactly ? (day , hour).
2-how it starts? (slowly ,abruptly )
3-its course ? (increasing , the same or decreasing ).
4- any associated symptoms? (pain vomiting ,fever
,drowsiness ,change in vision ,………..) .
5- the provoking factors: what increase the complaint?
6- the releasing factors;what decrease the complaint ?
7- relieved by medication or not ?
8- constant or intermittent ,its duration & for how long ?
The History
e.g. The pain:
1)
The site :
2)
The onset :gradual ,sudden or explosive
3)
The character: burning ,colicky, vague
,heaviness,…..
4)
The severity: mild ,moderate or sever .
5)
constant or intermittent .
6)
relieved by medication or not & what medication ?
7)
Factors increase it :movement ,eating, standing ,….
8)
Factors decrease it :movement ,eating, standing ,…
9)
Radiation to other site ?
10)
Associated symptoms: vomiting ,fever …..
The History
E.g.: vomiting :

What did the patient vomit? Food ,fluid
,……

How much?

How often?

What did the color of the vomitus ? yellow
,green, brown,….

Was vomiting projectile?

The taste of the vomitus ?acidic , bitter
,…..
The History
III- The past history;
1)
Any same complain before ? How it started
& how ended?
2)
Any other complain before? Related to the
complaint or not related ?
3)
Any other diseases? hypertension.
,diabetes mellitus , cardiac problem,…
IV –The drug history :aspirin ,anticoagulant
,contraceptive pills ,chemotherapy .
V- The surgical history :any operation before,
type of anesthesia ,any complication?
The History
VI- Nutritional history :dehydration . Loss
of electrolyte ,protein deficiency.
VII- Menstrual history :regularity ,duration ,
amount,..
VIII-Family history: known disease in the
family ,same disease in the family
,hereditary diseases? .
IX- Environmental history.
X- Habbit history :smoking, alcohol ,drug
abuse .
XI- Hypersensitivity history .
The physical examination:


All patients are sensitive and somewhat
embarrassed at being examined .
The examining room and table should be
comfortable ,worm, closed, and drapes
should be used if the patient is required to
strip for the examination. A female nurse
should be present if the patient is female.
Most patients will relax if they are allowed to
talk a bit during the examination, which is
another reason for taking the past history
while the examination is being done.
The physical examination:
I.
II.
III.
IV.
Inspection :any scar, pulsation,
swelling, redness, discharge,
asymmetry, hair distribution, ulcers,
wound ,….
Palpation :(superficial palpation for
masses, tenderness,….&deep palpation
for deep masses )
Percation :to differentiate between air &
solid surfaces.
Auscultation :by use stethoscope to
hear normal & abnormal sounds.
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1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
12)
E.g. if we find a lump (mass), we should know:
The site .
The size .
The shape .
The edge (cut or rounded).
Tenderness .
Pulsation .
Flactuality .
Consistency .
Mobility .
The surface.
Reducibility .
Regional draining lymph node .

1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
E.g. if we find an ulcer we should know:
The site .
The size .
The shape .
The edge .
The base (what you can feel) .
The floor (what you can see) .
The color .
The secretion .
The vascularity .
Regional draining lymph node .
Investigations
I- Simple blood investigations:
1)
C.B.C. (complete blood count) which
reveals hemoglobin, white blood cells, red
blood cells, platelets count,
2)
Blood group & Rh-factor.
3)
Blood sugar (fasting or random or post
brandial) .
4)
The kidney function tests (Blood urea
,serum creatinine) .
5)
Electrolyte: Na+ ,K+, Ca++,…..
6)
The liver function test (ALT, AST ,Serum
bilirubin ,Serum protein & albumin ) .
7)
P.T. & P.T.T.
Investigations
II- urine exam (general & culture).
III- Stool exam (general & culture).
IV- ultrasonography.
V- X-ray:
1- simple X-ray (without dye) e.g. chest X-ray
,abdominal X-ray ,K.U.B. ,skull X-ray ,panorama
X-ray, ….
2- X-ray with dye :e.g. barium meal ,barium
enema, I.V.P……
3- C.T. ( computerized tomography ) scan .
4- M.R.I. (magnetic resonance imaging) .
VI- E.C.G . (electro cardio graphy )
Investigations
Special Examinations:
such as cystoscopy, gastroscopy,
esophagoscopy, colonoscopy,
angiography, and bronchoscopy are
often required in the diagnosis of certain
surgical disorders. The surgeon must be
familiar with the indications and
limitations of these procedures and be
prepared to consult with colleagues in
medicine and other surgical specialties
as required.

Pre-operative preparation
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1)
2)
3)
4)
5)
6)
7)
8)
According to the type of operation, we should
do:
All the required investigations
Prepare blood .
Shaving the operation site.
The patient take a bath.
Examined by the anesthetist.
Prepare I.C.U. if the patient need.
Give him premedications like diazepam a night
before the operation.
Fasting 8 hours before the operation .
The patient should enter the operation
room in the optimum condition
Approach to the Surgical Patient:
--operation --post-operative treatment--management of complications.
(according to the type of
the operation.)
Postoperative Care:
The recovery from surgery can be divided into
three phases:
(1) an immediate, or post-anesthetic phase;
(2) an intermediate phase, ( the hospitalization
period);
(3) a convalescent phase.
During the first two phases, care is principally
directed at maintenance of homeostasis, treatment
of pain, and prevention and early detection of
complications. The convalescent phase is a
transition period from the time of hospital
discharge to full recovery.
The trend toward earlier postoperative discharge
after major surgery make the 3rd phase more
important.

1-The Immediate Postoperative Period

The major causes of early complications
and death following major surgery are
acute pulmonary, cardiovascular, and fluid
derangements. The post-anesthesia care
unit (PACU) is staffed by specially trained
personnel and provided with equipment for
early detection and treatment of these
problems. All patients should be monitored
in this specialized unit initially following
major procedures .
1-The Immediate Postoperative Period
The patient can be discharged from the recovery
room when cardiovascular, pulmonary, and
neurologic function have returned to baseline,
which usually occurs 1–3 hours following
operation.
Patients who require continuing ventilatory or
circulatory support or who have other conditions
that require frequent monitoring are transferred to
an intensive care unit (I.C.U.) . In this setting,
nursing personnel specially trained in the
management of respiratory and cardiovascular
emergencies are available.
Monitoring equipment is available to enable early
detection of cardio-respiratory derangements.
Postoperative Orders in The Immediate
Postoperative Period
The nursing team must be advised of the nature of
the operation and the patient's condition.
Postoperative orders should cover the following:
1- Monitoring the following:
A- Vital Signs : Blood pressure, pulse, and
respiration should be recorded frequently until
stable and then regularly until the patient is
discharged from the recovery room. The
frequency of vital sign measurements thereafter
depends upon the nature of the operation and
the course in the PACU. Continuous
electrocardiographic monitoring is indicated for
most patients in the PACU. Any major changes
in vital signs should be communicated to the
anesthesiologist and surgeon immediately.
B-Central Venous Pressure
Central venous pressure should be
recorded periodically in the early
postoperative period if the operation
has entailed large blood losses or fluid
shifts, and invasive monitoring is
available. A Swan-Ganz catheter for
measurement of pulmonary artery
wedge pressure is indicated under
these conditions if the patient has
borderline cardiac or respiratory
function.
C- Fluid Balance
The anesthetic record includes all fluid
administered as well as blood loss and urine
output during the operation. This record
should be continued in the postoperative
period and should also include fluid losses
from drains and stomas. This aids in
assessing hydration and helps to guide
intravenous fluid replacement. A bladder
catheter can be placed for frequent
measurement of urine output. In the absence
of a bladder catheter, the surgeon should be
notified if the patient is unable to void within
6–8 hours after operation.
D- Other Types of Monitoring
Depending on the nature of the operation
and the patient's pre-existing
conditions, other types of monitoring
may be necessary. Examples include
measurement of intracranial pressure
and level of consciousness following
cranial surgery and monitoring of distal
pulses following vascular surgery or in
patients with casts.
2- Respiratory Care
In the early postoperative period, the
patient may remain mechanically
ventilated or treated with supplemental
oxygen by mask or nasal prongs. These
orders should be specified. For intubated
patients, tracheal suctioning or other
forms of respiratory therapy must be
specified as required. Patients who are
not intubated should do deep breathing
exercises frequently to prevent
atelectasis.
3- Position in Bed and Mobilization
The postoperative orders should describe any
required special positioning of the patient.
Unless doing so is contraindicated, the patient
should be turned from side to side every 30
minutes until conscious and then hourly for
the first 8–12 hours to minimize atelectasis.
Early ambulation is encouraged to reduce
venous stasis; the upright position helps to
increase diaphragmatic function.
Venous stasis may also be minimized by
intermittent compression of the calf by
pneumatic stockings.
4- Diet
Patients at risk for emesis and pulmonary
aspiration should have nothing by mouth
until some gastrointestinal function has
returned (usually within 4 days). Most
patients can tolerate liquids by mouth shortly
after return to full consciousness.
5- Administration of Fluid and Electrolytes
Orders for postoperative intravenous fluids
should be based on maintenance needs and
the replacement of gastrointestinal losses
from drains, fistulas, or stomas.
6- Drainage Tubes
Drain care should be included in the postoperative orders.
Details such as type and pressure of suction, irrigation
fluid and frequency, and skin exit site care should be
specified. The surgeon should examine drains
frequently, since the character or quantity of drain
output may herald the development of postoperative
complications such as bleeding or fistulas.
7- Medications
Orders should be written for antibiotics, analgesics,
gastric acid suppression, deep vein thrombosis
prophylaxis, and sedatives. If appropriate, preoperative
medications should be reinstituted. Careful attention
should be paid to replacement of corticosteroids in
patients at risk, since postoperative adrenal
insufficiency may be life-threatening. Other medications
such as antipyretics, laxatives, and stool softeners
should be used selectively as indicated.
8- Laboratory Examinations and
Imaging
The use of postoperative laboratory and
radiographic examinations should be to
detect specific abnormalities in highrisk groups. The routine use of daily
chest radiographs, blood counts,
electrolytes, and renal or liver function
panels is not useful.
The Intermediate Postoperative Period

The intermediate phase starts with
complete recovery from anesthesia and
lasts for the rest of the hospital stay.
During this time, the patient recovers
most basic functions and becomes
self-sufficient and able to continue
convalescence at home.
1- Care of the Wound :
Within hours after a wound is closed, the wound
space fills with an inflammatory exudate.
Epidermal cells at the edges of the wound
begin to divide and migrate across the wound
surface. By 48 hours after closure, deeper
structures are completely sealed off from the
external environment. Sterile dressings
applied in the operating room provide
protection during this period. Dressings over
closed wounds should be removed on the
third or fourth postoperative day. If the wound
is dry, dressings need not be reapplied; this
simplifies periodic inspection. Dressings
should be removed earlier if they are wet,
because soaked dressings increase bacterial
contamination of the wound.
1- Care of the Wound:
Dressings should also be removed if the patient
has manifestations of infection (such as fever
or increasing wound pain). The wound should
then be inspected and the adjacent area gently
compressed. Any drainage from the wound
should be examined by culture and Gramstained smear. Removal of the dressing and
handling of the wound during the first 24
hours should be done with aseptic technique.
Medical personnel should wash their hands
before and after caring for any surgical wound.
Gloves should always be used when there is
contact with open wounds or fresh wounds.
1- Care of the Wound :
Generally, skin sutures or skin staples may be
removed by the fifth postoperative day and
replaced by tapes. Sutures should be left in
longer (eg, for 2 weeks) in incisions that
1- cross creases (eg, groin, popliteal area);
2-for incisions closed under tension;
3-for some incisions in the extremities (eg, the
hand);
4-with incisions of any kind in debilitated
patients.
Sutures should be removed if suture tracts
show signs of infection. If the incision is
healing normally, the patient may be allowed to
shower or bathe by the seventh postoperative
day.
1- Care of the Wound :
Fibroblasts proliferate in the wound space quickly, and
by the end of the first postoperative week, new
collagen is abundant in the wound. On palpation of
the wound, connective tissue can be felt as a
prominence (the healing ridge) and is evidence that
healing is normal. Tensile strength is minimal for the
first 5 days. It increases rapidly between the fifth and
twentieth postoperative days and more slowly
thereafter. Wounds continue to gain tensile strength
slowly for about 2 years. In otherwise healthy
patients, the wound should be subjected to only
minor stress for 6–8 weeks. When wound healing is
expected to be slower than normal (e.g., in elderly or
debilitated patients or those taking corticosteroids),
activity should be delayed even further
1- Care of the Wound :
When a wound has been contaminated with bacteria
during surgery, it is often best to leave the skin and
subcutaneous tissues open and either to perform
delayed primary closure or allow secondary closure to
occur. The wound is loosely packed with fine-mesh
gauze in the operating room and is left undisturbed for
4–5 days; the packing is then removed. If at this time
the wound contains only serous fluid or a small
amount of exudate, the skin edges can be
approximated with tapes. If drainage is considerable
or infection is present, the wound should be allowed
to close by secondary intention. In this case, the
wound should be packed with moist-to-dry dressings,
which are changed once or twice daily. The patient can
usually learn how to care for the wound and should be
discharged as soon as his or her general condition
permits. Most patients do not require visiting nurses
to assist with wound care at home.
1- Care of the Wound :
Wound healing is faster if the state of nutrition is normal
and there are no specific nutritional deficits. For
example, vitamin C deficiency interferes with collagen
synthesis and vitamin A deficiency decreases the rate
of epithelialization. Deficiencies of copper, magnesium,
and other trace metals decrease the rate of scar
formation. Supplemental vitamins and minerals should
be given postoperatively when deficiencies are
suspected, but wound healing cannot be accelerated
beyond the normal rate by nutritional supplements.
Wound problems should be anticipated in patients taking
corticosteroids, which inhibit the inflammatory
response, fibroblast proliferation, and protein synthesis
in the wound. Maturation of the scar and gain of tensile
strength occur more slowly. Extra precautions include
using non-absorbable suture materials for fascial
closure, delaying removal of skin stitches, and avoiding
stress in the wound for 3–6 months.
2-Management of Drains :
Drains are used either to prevent or to treat an unwanted
accumulation of fluid such as pus, blood, or serum.
Drains are also used to evacuate air from the pleural
cavity so that the lungs can reexpand. When used
prophylactically, drains are usually placed in a sterile
location. Strict precautions must be taken to prevent
bacteria from entering the body through the drainage
tract in these situations. The external portion of the
drain must be handled with aseptic technique, and the
drain must be removed as soon as it is no longer useful.
When drains have been placed in an infected area, there
is a smaller risk of retrograde infection of the peritoneal
cavity, since the infected area is usually walled off.
Drains should usually be brought out through a
separate incision, because drains through the operative
wound increase the risk of wound infection.
2-Management of Drains :

Closed drains connected to suction devices
are preferable to open drains (such as
Penrose) that predispose to wound
contamination. The quantity and quality of
drainage should be recorded, and
contamination minimized. When drains are
no longer needed, they may be withdrawn
entirely at one time if there has been little or
no drainage or may be progressively
withdrawn over a period of a few days.
2-Management of Drains :

Sump drains (such as Davol drains) have an
airflow system that keeps the lumen of the drain
open when fluid is not passing through it, and
they must be attached to a suction device. Sump
drains are especially useful when the amount of
drainage is large or when drainage is likely to plug
other kinds of drains. Some sump drains have an
extra lumen through which saline solution can be
infused to aid in keeping the tube clear. After
infection has been controlled and the discharge is
no longer purulent, the large-bore catheter is
progressively replaced with smaller catheters, and
the cavity eventually closes.
3-Postoperative Pulmonary Care
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The changes in pulmonary function observed
following anesthesia and surgery are principally
the result of decreased vital capacity, functional
residual capacity (FRC), and pulmonary edema.
These changes are accentuated in patients who
are :
obese,
who smoke heavily, or
who have preexisting lung disease.
Elderly patients are particularly vulnerable
because they have decreased compliance,
increased closing volume, increased residual
volume, and increased dead space, all of which
enhance the risk of postoperative atelectasis.
3-Postoperative Pulmonary Care

Pain is thought to be one of the main causes
of shallow breathing postoperatively.
Complete abolition of pain, however, does
not completely restore pulmonary function .
The principal means of minimizing
atelectasis is deep inspiration. Early
mobilization, encouragement to take deep
breaths (especially when standing), and
good coaching by the nursing staff suffice
for most patients.
4-Postoperative Fluid & Electrolyte Management
Postoperative fluid replacement should be based on the
following considerations:
(1) maintenance requirements,
(2) extra needs resulting from systemic factors (e.g., fever,
burns),
(3) losses from drains, and
(4) requirements resulting from tissue edema and ileus (third
space losses).
Daily maintenance requirements for sensible and insensible
loss in the adult are about 1500–2500 mL depending on the
patient's age, gender, weight, and body surface area. A
rough estimate can be obtained by multiplying the patient's
weight in kilograms times 30 (e.g., 1800 mL/24 h in a 60-kg
patient). Maintenance requirements are increased by fever,
hyperventilation, and conditions that increase the catabolic
rate.
4-Postoperative Fluid & Electrolyte Management


For patients requiring intravenous fluid replacement
for a short period (most postoperative patients), it is
not necessary to measure serum electrolytes at any
time during the postoperative period, but
measurement is indicated in more complicated
patients (those with extra fluid losses, sepsis,
preexisting electrolyte abnormalities, or other
factors). Assessment of the status of fluid balance
requires accurate records of fluid intake and output
and is aided by weighing the patient daily.
As a rule, 2000–2500 mL of 5% dextrose &/or normal
saline & / or lactated Ringer's solution is given daily.
Potassium should usually not be added during the
first 24 hours after surgery, because increased
amounts of potassium enter the circulation during
this time as a result of operative trauma and
increased aldosterone activity.
Solution Glucos Na
e (g/l) (meq
/l)
Cl
Hco3 K
Osm
(meq/ (meq (meq/l) olari
l)
/l)
ty/l
5%
50
glucose
----
----
----
----
Iso=
300
0.9%
saline
----
154
154
----
----
Iso=
300
dextrose
4.3 % with
saline 0.18
%
43
31
31
----
----
Iso=
300
Ringer’s
lactate
solution
----
130
109
28
4
Iso=
300
5%
dextrose in
0.9%saline
50
154
154
----
----
Hyper
=600
4-Postoperative Fluid & Electrolyte Management
In most patients, fluid loss through a nasogastric
tube is less than 500 mL/d and can be replaced
by increasing the infusion used for maintenance
by a similar amount. About 20 meq of potassium
should be added to every liter of fluid used to
replace these losses. However, with the
exception of urine, body fluids are isosmolar and
if large volumes of gastric or intestinal juice are
replaced with normal saline solution, electrolyte
imbalance will eventually result. Whenever
external losses from any site amount to 1500
mL/d or more, electrolyte concentrations in the
fluid should be measured periodically, and the
amount of replacement fluids should be adjusted
to equal the amount lost.
5-Postoperative Care of the
Gastrointestinal Tract
In the immediate postoperative period, the stomach
may be decompressed with a nasogastric tube.
Nasogastric intubation was once used in almost
all patients undergoing laparotomy to avoid
gastric distention and vomiting, The nasogastric
tube should be connected to low intermittent
suction and irrigated frequently to ensure patency.
The tube should be left in place for 2–3 days or
until there is evidence that normal peristalsis has
returned (e.g., return of appetite, audible
peristalsis, or passage of flatus).
5-Postoperative Care of the
Gastrointestinal Tract
Once the nasogastric tube has been
withdrawn, fasting is usually continued for
another 24 hours, and the patient is then
started on a liquid diet. Opioids may
interfere with gastric motility and should be
stopped in patients who have evidence of
gastro-paresis beyond the first
postoperative week. After most operations
in areas other than the peritoneal cavity, the
patient may be allowed to resume a regular
diet as soon as the effects of anesthesia
have completely worn off.
6-Postoperative Pain
Severe pain is a common sequela of
intrathoracic, intra-abdominal, and major bone
or joint procedures. About 60% of such
patients perceive their pain to be severe, 25%
moderate, and 15% mild. In contrast, following
superficial operations on the head and neck,
limbs, or abdominal wall, less than 15% of
patients characterize their pain as severe. The
factors responsible for these differences
include duration of surgery, degree of
operative trauma, type of incision, and
magnitude of intraoperative retraction. Gentle
handling of tissues, expedient operations, and
good muscle relaxation help lessen the
severity of postoperative pain.
6-Postoperative Pain

While factors related to the nature of the
operation influence postoperative pain, it
is also true that the same operation
produces different amounts of pain in
different patients. This varies according
to individual physical, emotional, and
cultural characteristics. Much of the
emotional aspect of pain can be traced to
anxiety. Feelings such as helplessness,
fear, and uncertainty contribute to anxiety
and may heighten the patient's perception
of pain.
7-Physician-Patient Communication
Close attention to the patient's needs,
frequent reassurance, and genuine
concern help minimize
postoperative pain. Spending a few
minutes with the patient every day
in frank discussions of progress and
any complications does more to
relieve pain than many physicians
realize.
8-Parenteral Opioids
Opioids are the mainstay of therapy for
postoperative pain. Their analgesic effect is
via two mechanisms:
(1) a direct effect on opioid receptors and
(2) stimulation of a descending brain stem
system that contributes to pain inhibition.
Morphine ,pethidine & tramal are the most
widely used opioid for treatment of
postoperative pain. Morphine may be
administered intravenously, either
intermittently or continuously
Nonopioid Parenteral Analgesics
They are non-steroidal anti-inflammatory
drugs (NSAID) with potent analgesic and
moderate anti-inflammatory activities. It is
available in injectable form suitable for
postoperative use .
E.g. aspirin (acetyl salicylic acid ),diclofen
sodium ,piroxicam,….
Oral Analgesics
Within several days following most surgical
procedures, the severity of pain decreases to a
point where oral analgesics suffice. Aspirin should
be avoided as an analgesic postoperatively, since
it interferes with platelet function, prolongs
bleeding time, and interferes with the effects of
anticoagulants. For most patients, a combination
of acetaminophen with codeine (e.g., Tylenol) or
with propoxyphene (analgan) suffices.
As with all opioids, tolerance develops with longterm use.
 Continuous Epidural Analgesia
 Intercostal Block

Postoperative Complications:
Postoperative complications may result from
1- the primary disease,
2- the operation, or
3-unrelated factors.
Occasionally, one complication results from
another previous one (eg, myocardial
infarction following massive postoperative
bleeding). The clinical signs of disease are
often blurred in the postoperative period.
Early detection of postoperative
complications requires repeated evaluation
of the patient by the operating surgeon and
other team members .

Postoperative Complications:

Prevention of complications starts in the preoperative
period with evaluation of the patient's disease and risk
factors. Improving the health of the patient before surgery
is one goal of the preoperative evaluation. For example,
cessation of smoking for 6 weeks before surgery
decreases the incidence of postoperative pulmonary
complications from 50% to 10%. Correction of gross
obesity decreases intra-abdominal pressure and the risk of
wound and respiratory complications and improves
ventilation postoperatively.

The surgeon should explain the operation and the
expected postoperative course to the patient and family.
The preoperative hospital stay, if one is necessary, should
be as short as possible both to reduce costs and to
minimize exposure to antibiotic-resistant microorganisms.
Adequate training in respiratory exercises planned for the
postoperative period substantially decreases the incidence
of postoperative pulmonary complications.
Postoperative Complications:
Early mobilization, proper respiratory care, and
careful attention to fluid and electrolyte needs are
important. On the evening after surgery the patient
should be encouraged to sit up, cough, breathe
deeply, and walk, if possible. The upright position
permits expansion of basilar lung segments, and
walking increases the circulation of the lower
extremities and lessens the danger of venous
thromboembolism.
In severely ill patients, continuous monitoring of
systemic blood pressure and cardiac performance
enables identification and correction of mild
derangements before they become severe.
I- Wound Complications
2- Seroma :
A seroma is a fluid collection in the wound other than pus or
blood. Seromas often follow operations that involve
elevation of skin flaps and transection of numerous
lymphatic channels (eg, mastectomy, operations in the
groin). Seromas delay healing and increase the risk of
wound infection. Those located under skin flaps can
usually be evacuated by needle aspiration. Compression
dressings should then be applied to seal lymphatic leaks
and prevent reaccumulation. Small seromas that recur may
be treated by repeated evacuation. Seromas of the groin,
which are common after vascular operations, are best left
to resorb without aspiration, since the risks of introducing
a needle (infection, disruption of vascular structures, etc)
are greater than the risk associated with the seroma itself.
If seromas persist—or if they start leaking through the
wound—the wound should be explored in the operating
room and the lymphatics ligated.
I- Wound Complications
1- Hematoma :
Wound hematoma, a collection of blood and clot in the wound, is
one of the most common wound complications and is almost
always caused by imperfect hemostasis. Patients receiving
aspirin or low-dose heparin have a slightly higher risk of
developing this complication. The risk is much higher in
patients who have been given systemically effective doses of
anticoagulants and those with preexisting coagulopathies.
Vigorous coughing or marked arterial hypertension immediately
after surgery may contribute to the formation of a wound
hematoma.
Hematomas produce elevation and discoloration of the wound
edges, discomfort, and swelling. Blood sometimes leaks
through skin sutures. Neck hematomas following operations on
the thyroid, parathyroid, or carotid artery are particularly
dangerous, because they may expand rapidly and compromise
the airway. Small hematomas may resorb, but they increase the
incidence of wound infection. Treatment in most cases consists
of evacuation of the clot under sterile conditions, ligation of
bleeding vessels, and reclosure of the wound.
I- Wound Complications
3- Wound Dehiscence:
Wound dehiscence is partial or total disruption of any or
all layers of the operative wound. Rupture of all layers
of the abdominal wall and extrusion of abdominal
viscera is evisceration. Wound dehiscence occurs in
1–3% of abdominal surgical procedures. Systemic and
local factors contribute to the development of this
complication.
3-1-- Systemic Risk Factors :
Dehiscence is rare in patients under age 30 but affects
about 5% of patients over age 60 having laparotomy. It
is more common in patients with diabetes mellitus,
uremia, immunosuppression, jaundice, sepsis,
hypoalbuminemia, and cancer; in obese patients; and
in those receiving corticosteroids.
3-2- Local Risk Factors:
The three most important local factors predisposing to wound
dehiscence are inadequate closure, increased intra-abdominal
pressure, and deficient wound healing. Dehiscence often results
from a combination of these factors rather than from a single
one. The type of incision (transverse, midline, etc) does not
influence the incidence of dehiscence.
E.g. Adequacy of Closure:
This is the single most important factor. The fascial layers give
strength to a closure, and when fascia disrupts, the wound
separates. Accurate approximation of anatomic layers is
essential for adequate wound closure. Most wounds that
dehisce do so because the sutures tear through the fascia.
Prevention of this problem includes performing a neat incision,
avoiding devitalization of the fascial edges by careful handling
of tissues during the operation, placing and tying sutures
correctly, and selecting the proper suture material. Sutures must
be placed 2–3 cm from the wound edge and about 1 cm apart.
Dehiscence is often the result of using too few stitches and
placing them too close to the edge of the fascia. Ostomies and
drains should be brought out through separate incisions to
reduce the rate of wound infection and disruption.
II- Respiratory Complications
Respiratory complications are the most common single
cause of morbidity after major surgical procedures and the
second most common cause of postoperative deaths in
patients older than 60 years.
Patients undergoing chest and upper abdominal operations
are particularly prone to pulmonary complications. The
incidence is lower after pelvic surgery and even lower after
extremity or head and neck procedures.
Pulmonary complications are more common after emergency
operations.
Special hazards are posed by preexisting chronic obstructive
pulmonary disease (chronic bronchitis, emphysema,
asthma, pulmonary fibrosis). Elderly patients are at much
higher risk because they have decreased compliance,
increased residual volumes, and increased dead space, all
of which predispose to atelectasis.
II- Respiratory Complications
1- Atelectasis
Atelectasis, the most common pulmonary
complication, affects 25% of patients who
have abdominal surgery. It is more common
in patients who are elderly or overweight
and in those who smoke or have symptoms
of respiratory disease. It appears most
frequently in the first 48 hours after
operation and is responsible for over 90% of
febrile episodes during that period. In most
cases, the course is self-limited and
recovery uneventful.
Atelectasis is usually manifested by fever (pathogenesis
unknown), tachypnea, and tachycardia. Physical
examination may show elevation of the diaphragm and
decreased breath sounds.
Postoperative atelectasis can be largely prevented by early
mobilization, frequent changes in position, encouragement
to cough, and physiotherapy. Preoperative teaching of
respiratory exercises and postoperative execution of these
exercises prevents atelectasis in patients without
preexisting lung disease.
Treatment consists of clearing the airway by chest
percussion, coughing, or nasotracheal suction.
Bronchodilators and mucolytic agents given by nebulizer
may help in patients with severe chronic obstructive
pulmonary disease. Atelectasis from obstruction of a major
airway may require intrabronchial suction through an
endoscope, a procedure that can usually be performed at
the bedside with mild sedation
2- Pulmonary Aspiration
Aspiration of oropharyngeal and gastric contents is
normally prevented by the gastroesophageal and
pharyngoesophageal sphincters. Insertion of
nasogastric and endotracheal tubes and depression of
the central nervous system by drugs interfere with
these defenses and predispose to aspiration. Other
factors, such as gastroesophageal reflux, food in the
stomach, or position of the patient, may play a role.
Trauma victims are particularly likely to aspirate
regurgitated gastric contents when consciousness is
depressed. Patients with intestinal obstruction and
pregnant women—who have increased intra-abdominal
pressure and decreased gastric motility—are also at
high risk of aspiration. Two-thirds of cases of aspiration
follow thoracic or abdominal surgery, and of these, onehalf result in pneumonia. The death rate for grossly
evident aspiration and subsequent pneumonia is about
50%.
The magnitude of pulmonary injury produced by
aspiration of fluid, usually from gastric contents, is
determined by the volume aspirated, its pH, and the
frequency of the event. If the aspirate has a pH of 2.5
or less, it causes immediate chemical pneumonitis,
which results in local edema and inflammation,
changes that increase the risk of secondary infection.
Aspiration of solid matter can produce airway
obstruction. Obstruction of distal bronchi, though well
tolerated initially, can lead to atelectasis and
pulmonary abscess formation. The basal segments
are affected most often. Tachypnea, fever, and hypoxia
are usually present within hours; less frequently,
cyanosis, wheezing, and apnea may appear. In
patients with massive aspiration, hypovolemia caused
by excessive fluid and colloid loss into the injured
lung may lead to hypotension and shock.
Aspiration can be prevented by preoperative
fasting, proper positioning of the patient, and
careful intubation. A single dose of cimetidine
before induction of anesthesia may be of value
in situations where the risk of aspiration is
high.
Treatment of aspiration involves reestablishing
patency of the airway and preventing further
damage to the lung. Endotracheal suction
should be performed immediately, as this
procedure confirms the diagnosis and
stimulates coughing, which helps to clear the
airway. Bronchoscopy may be required to
remove solid matter. Fluid resuscitation should
be undertaken concomitantly. Antibiotics are
used initially when the aspirate is heavily
contaminated; they are used later to treat
pneumonia.
3- Postoperative Pneumonia



Pneumonia is the most common pulmonary
complication among patients who die after
surgery. It is directly responsible for death in
more than half of these patients. Patients who’s
requiring prolonged ventilatory support are at
highest risk for developing postoperative
pneumonia.
Atelectasis, aspiration, and copious secretions
are important predisposing factors.
The clinical manifestations of postoperative
pneumonia are fever, tachypnea, increased
secretions, and physical changes suggestive of
pulmonary consolidation. A chest x-ray usually
shows localized parenchymal consolidation.
3- Postoperative Pneumonia


Maintaining the airway clear of secretions
is of paramount concern in the prevention
of postoperative pneumonia. Respiratory
exercises, deep breathing, and coughing
help prevent atelectasis, which is a
precursor of pneumonia.
Treatment consists of measures to aid the
clearing of secretions and administration
of antibiotics. Sputum obtained directly
from the trachea, usually by endotracheal
suctioning, is required for specific
identification of the infecting organism.
III-Fat Embolism


Fat embolism is relatively common but only
rarely causes symptoms. Fat particles can be
found in the pulmonary vascular bed in 90% of
patients who have had fractures of long bones or
joint replacements. Fat embolism can also be
caused by exogenous sources of fat, such as
blood transfusions, intravenous fat emulsion, or
bone marrow transplantation. Fat embolism
symptoms consist of neurologic dysfunction,
respiratory insufficiency, and petechiae of the
axillae, chest, and proximal arms.
Fat embolism characteristically begins 12–72
hours after injury but may be delayed for several
days. The diagnosis is clinical. The finding of fat
droplets in sputum and urine is common after
trauma.
IV- Cardiac Complications


Cardiac complications following surgery may be
life-threatening. Their incidence is reduced by
appropriate preoperative preparation.
Dysrhythmias, unstable angina, heart failure, or
severe hypertension should be corrected before
surgery whenever possible. Valvular disease—
especially aortic stenosis—limits the ability of the
heart to respond to increased demand during
operation or in the immediate postoperative
period. When aortic stenosis is recognized
preoperatively , the incidence of major
perioperative complications is small. Thus,
patients with preexisting heart disease should be
evaluated by a cardiologist preoperatively.
IV- Cardiac Complications





General anesthesia depresses the myocardium, and
some anesthetic agents predispose to dysrhythmias.
Monitoring of cardiac activity and blood pressure
during the operation detects dysrhythmias and
hypotension early.
In patients with a high cardiac risk, regional
anesthesia may be safer than general anesthesia for
procedures below the umbilicus.
Non-cardiac complications may affect the
development of cardiac complications by increasing
cardiac demands in patients with a limited reserve.
E.g. Postoperative sepsis and hypoxemia. Fluid
overload can produce acute left ventricular failure.
Patients with coronary artery disease, dysrhythmias,
or low cardiac output should be monitored
postoperatively in an intensive care unit.
V- Complications of Intravenous
Therapy & Hemodynamic Monitoring
1- Air Embolism
Air embolism may occur during or after insertion of a venous
catheter or as a result of accidental introduction of air into
the line. Intravenous air lodges in the right atrium,
preventing adequate filling of the right heart. This is
manifested by hypotension, jugular venous distention, and
tachycardia.
This complication can be avoided by placing the patient in
the Trendelenburg position when a central venous line is
inserted.
Emergency treatment consists of aspiration of the air with a
syringe. If this is unsuccessful, the patient should be
positioned right side up and head down, which will help
dislodge the air from the right atrium and return circulatory
dynamics to normal.
V- Complications of Intravenous
Therapy & Hemodynamic Monitoring
2- Phlebitis
A needle or a catheter inserted into a vein and left in
place will in time cause inflammation at the entry
site. When this process involves the vein, it is
called phlebitis. Factors determining the degree of
inflammation are the nature of the cannula, the
solution infused, bacterial infection, and venous
thrombosis. Phlebitis is one of the most common
causes of fever after the third postoperative day.
The symptomatic triad of induration, edema, and
tenderness is characteristic. Prevention of
phlebitis is best accomplished by observance of
aseptic techniques during insertion of venous
catheters, frequent change of tubing (ie, every 48–
72 hours),
VI-Postoperative Fever
Fever occurs in about 40% of patients after major
surgery. In most patients the temperature elevation
resolves without specific treatment. However,
postoperative fever may herald a serious infection,
and it is therefore important to evaluate the patient
clinically.
Normal body tempreture is 36.7—37.3’c
Fever within 48 hours after surgery is usually caused by
1- atelectasis: Re-expansion of the lung causes body
temperature to return to normal.
2- reactions to drugs ,anesthesia ,blood transfusion ,
absorption of haematoma ,
VI-Postoperative Fever



fever appears in the third postoperative day,
atelectasis is a less likely explanation. The
differential diagnosis of fever at this time includes
catheter-related phlebitis, pneumonia, and urinary
tract infection. A directed history and physical
examination complemented by focused laboratory
and radiologic studies usually determine the
cause.
Patients without infection are rarely febrile after
the fifth postoperative day.
Fever in the fifth postoperative day suggests
wound infection or, less often, anastomotic
breakdown and intra-abdominal abscesses.
VI-Postoperative Fever

Fever after the 7th postoperative day (in
the 2nd week ) suggests deep venous
thrombosis in the calf muscles .
Special Medical Problems in Surgical
Patients
Diabetes Mellitus :
Diabetic patients undergo more surgical
procedures than do non-diabetics, and
management of the diabetic patient before, during,
and after surgery is an important responsibility of
the surgeon. Fortunately, because close control of
fluids, electrolytes, glucose, and insulin is now
possible in the operating room, control of blood
glucose levels during the peri-operative period is
usually relatively simple. Marked hyperglycemia
should be avoided during surgery; the greater
danger, however, is from severe unrecognized
hypoglycemia.
Diabetes Mellitus :

Preoperative Workup :

Blood glucose concentrations may
be elevated in diabetic patients
during the preoperative period.
Physical trauma, if present,
combined with the emotional and
physiologic stress of the illness may
cause epinephrine and cortisol levels
to rise, in each case resulting in
increased blood glucose levels.
Diabetes Mellitus :
The preoperative workup of patients with diabetes
mellitus includes
1. A thorough physical examination, with special care to
discover occult infections;
2. An ECG to rule out myocardial infarction;
3. A chest x-ray to identify hidden pneumonia or
pulmonary edema.
4. A complete urinalysis can rule out urinary tract
infection and proteinuria, the earliest signs of
diabetic renal disease.
5. Serum potassium levels are measured to check for
hypokalemia or hyperkalemia .
6. Serum creatinine levels are used to assess renal
function.
The serum glucose concentration should ideally be
between 100 and 200 mg/dL,

Preoperative & Intraoperative
Management of Diabetic Patients

Type 2 (Non-Insulin-Dependent) Diabetes
Mellitus
Approximately 85% of diabetics over age 50 years have only
a moderately decreased ability to produce and secrete
insulin, and when at home they can usually be controlled
by diet or by oral hypoglycemic drugs. If the serum
glucose level is below 200 mg/dL on the morning of
surgery, oral hypoglycemic drugs should be withheld; and
5% glucose solution should be administered intravenously
at a rate of about 100 mL/h. This means that over a 10-hour
period, only 50 g of glucose would be given; by contrast,
during an average day, a diabetic on a normal diet would
consume four to five times as much carbohydrate (ie, 200–
250 g).
If the operation is lengthy, blood glucose levels should be
measured every 3–4 hours during surgery to ensure
adequate glucose control. The goal is to maintain
glucose levels between 100 and 200 mg/dL,

Type 1 (Insulin-Dependent) Diabetes Mellitus
Type 1 patients require insulin during surgery. It can be
administered by any of the following methods:
(1) subcutaneous administration of short-acting insulin;
(2) constant infusion of a mixture of glucose and insulin; or
(3) separate infusions of glucose and insulin.
blood glucose levels should be monitored at least every 2
hours during the procedure to avoid hypoglycemia below
60 mg/dL and hyperglycemia above 200 mg/dL.
Blood glucose levels can be measured rapidly during surgery
with a portable electronic glucose analyzer.
Postoperative Care

Hypoglycemia, the most common postoperative
complication, most often follows the use of longacting insulin given subcutaneously before surgery.
Although hypoglycemia may also occur if the
intravenous insulin infusion is excessive in relation to
that of the glucose, an infusion of 1.5 units or less of
insulin per hour, when given with 5% glucose, rarely
results in hypoglycemia. Blood glucose levels should
be measured every 2–4 hours and the patient
monitored for signs and symptoms of hypoglycemia
(eg, anxiety, tremulousness, profuse sweating without
fever). When hypoglycemia is detected, the amount of
glucose infused should be promptly increased and the
insulin decreased.
Postoperative Care

In the intermediate
phase ;we do blood
sugar every 6 hours
& give soluble
insulin
subcutaneously
according to the
following table :
Less than
200 mg/dl
200-250
Nothing
250-300
10 units
300-350
15 units
5 units
Above 350 20 units



This is continue till the patient can drink &/0r eat
then the patient return to his old medical treatment
& do blood sugar twice daily to be sure that its
level below 180 mg/dl.
A marked increase in glucose and insulin
requirements postoperatively suggests the
presence of occult infection (eg, wound infection,
cellulitis at the intravenous site, urinary tract
infection, or unrecognized aspiration pneumonia).
Adjustments in the rate of glucose or insulin
administration must be based on blood glucose
levels.
Hypertension


Patients with uncomplicated and
controlled hypertension usually tolerate
surgery well. The patient advised to took
his medication till the day of surgery & at
the morning of surgery & continue after
the surgery if possible or replace it with
parentral drugs.
The patient should stop aspirin a week
before surgery & an internist should
consulted before the operation.
Respiratory Disease

Acute Upper Respiratory Tract Infections :
Both anesthesia and surgery provide opportunities for the spread
of infection because respiratory defense mechanisms are
compromised and instrumentation of the airway may be
required. Therefore, the presence of a cold, pharyngitis, or
tonsillitis is a relative contraindication to elective surgery,
since viral infections decrease defense mechanisms against
bacterial infections.
If surgery is necessary, the appropriate antibiotic should be
administered and manipulation of the infected area avoided
when possible.

Acute Lower Respiratory Tract Infections
(Tracheitis, Bronchitis, Pneumonia) :
These infections are absolute contraindications to
elective surgery. For emergency surgery, therapy
includes humidification of inhaled gases, removal of
lung secretions, and continued administration of
bronchodilators and antibiotics.

Bronchial Asthma :
patients with bronchial asthma who are undergoing
surgery are at increased risk of pulmonary
complications. Preoperative management includes
adjustment of bronchodilator medication, cessation
of smoking, and treatment of infection.
Intraoperative bronchoconstriction from mechanical
stimulation of the airway must be prevented so that
appropriate anesthetics can be given in adequate
concentrations. Since intraoperative use of
bronchodilators may be necessary, adverse
interactions between anesthetic agents and
bronchodilators must be avoided. Many patients with
bronchial asthma have been treated with
corticosteroids and require corticosteroid therapy in
the perioperative period
aneamia



Surgical patients with anemia should undergo a thorough
workup to identify and treat the underlying cause before
elective procedures are undertaken. A detailed history
should be obtained to identify any symptoms of blood loss
from the genitourinary and gastrointestinal tracts. A history
of renal, hepatic, hematologic, or endocrinologic disorders
and a medication history should be elicited. A history
suggestive of hemolytic episodes or a family history of
anemia may offer clues to the diagnosis. Signs of pallor,
jaundice, lymphadenopathy, and organomegaly should be
sought on physical examination.
A complete laboratory evaluation including CBC,
reticulocyte count, peripheral smear, and stool test for
occult blood should be done.
Correctable causes of anemia, like deficiencies of iron,
folate, and vitamin B12 , should be treated.
Preoperative red blood cell (RBC) transfusions are not
routinely recommended, and the decision to transfuse
should be based on the need to improve tissue
oxygenation.
pregnancy
The Pregnancy may alter or mask the signs and symptoms of
the particular presentation or course of disease, so that
diagnosis is made more difficult. Furthermore, the fetus
and changes in maternal physiology and anatomy must be
considered in the use of diagnostic tests, medical therapy,
and the planning of surgical procedures.
Any major operation represents a risk not only to the mother
but to the fetus as well. An increase in both preterm
delivery and growth restriction in infants that resulted from
pregnancies that involved a surgical procedure.
Although there is no evidence that congenital anomalies are
induced in the developing fetus by anesthesia,
semielective procedures should be deferred until the
second trimester of pregnancy, exercising the greatest
precautions to prevent hypoxia and hypotension.
Emergent surgical procedures should proceed as necessary;
however, changes in maternal physiology—particularly in
cardiac output and maternal blood volume—as well as of
the size of the gravid uterus must be considered.
Normal values
:
Blood urea
25-40mg/dl
Serum creatinine
0.7-1.2 mg/dl
Fasting blood sugar
Post brandial B.S.
80 -120 mg/dl
120-180 mg/dl
Random B.S.
120 -140 mg/dl
Serum sodium
135 -145 meq /l
Serum potassium
3.5 – 4.5 meq /l
Serum calcium
9 -11 mg/dl
WBC
4000-10000 cell/dl
RBC
4 -10 *10^6 cell/dl
Heamoglobin
12-16 gm /dl
Fluid & Electrolyte Management
Fluid intake (input ) is derived from two sources:
(1) exogenous;
and
(2) endogenous.
Exogenous water: is either drunk or ingested in solid food.
The quantities vary within wide limits, but average 2—3
litres per 24 hours, of which nearly half is contained in
solid food.
The water requirements of infants and children are relatively
greater than those of adults because of:
(1) the larger surface area per unit of body weight;
(2) the greater metabolic activity due to growth; (3) the
comparatively poor concentrating ability of the immature
kidney.
Endogenous water: is released during the oxidation of
ingested food; the amount is normally less than 500 ml /
24 hours. However, during starvation, this amount is
supplemented by water released from the breakdown of
body tissues.
Fluid output
Water is lost from the body by four routes.
1 • By the lungs. About 400 ml of water is lost in expired air each 24
hours. In a dry atmosphere, and when the respiratory rate is
increased, the loss is correspondingly greater .
2•By the skin. When the body becomes overheated, there is visible
perspiration, but throughout life invisible perspiration is always
occurring. The cutaneous fluid loss varies with the atmospheric
temperature and humidity, muscular activity and body temperature.
In a temperate climate the average loss is between 600 and 1000 ml
/ 24 hours.
3• Faeces. Between 60 and 150 ml of water are lost by this route daily.
In diarrhoea this amount is greatly multiplied.
4• Urine. The output of urine is under the control of multiple
influences, such as blood volume, hormonal and nervous
influences, among which the antidiuretic hormone acts by
stimulating the reabsorption of water from the renal tubules. The
normal urinary output is approximately 1500 ml / 24 hours, and
provided that the kidneys are healthy, the specific gravity of the
urine bears a direct relationship to the volume. A minimum urinary
output of approximately 400 ml / 24 hours is required to excrete the
end products of protein metabolism.
Water depletion :
Pure water depletion is usually due to diminished
intake. This may be due to lack of availability,
difficulty or inability to swallow because of painful
conditions of the mouth and pharynx, or
obstruction in the oesophagus. Pure water
depletion may also follow the increased loss from
the lungs after tracheostomy. This loss may be as
much as 500 ml in excess of the normal insensible
loss. After tracheostomy, humidification of the
inspired air is an important preventive measure.
Clinical features :
The main symptoms are weakness and intense
thirst. The urinary output is diminished and its
specific gravity increased.
Treatment by drinking water &/or give 5%glucose
water solution.



Water intoxication
This can occur when excessive amounts
of water, low sodium or hypotonic
solutions are taken or given by any route.
The commonest cause on surgical wards
is the over-prescribing of intravenous 5%
glucose solutions to postoperative
patients.
Similarly, water intoxication can occur if
the body retains water in excess to
plasma solutes. This can be seen in the
syndrome of inappropriate antidiuretic
hormone (SIADH) secretion which is
most commonly associated with lung
conditions such as lobar pneumonia,
empyema and oat-cell carcinoma of
bronchus, as well as head injury.

Clinical features:
These include drowsiness, weakness, sometimes
convulsions and coma. Nausea and vomiting of clear fluid
are common, and, with the exception of the SIADH, usually
the patient passes a considerable amount of dilute urine.
Laboratory investigations may show a falling haematocrit,
serum sodium and other electrolyte concentrations.

Treatment :
The intake of water having been stopped, the best course is
water restriction. If the patient fails to improve, transfer to
an intensive care unit will be necessary for more invasive
monitoring and controlled manipulation of fluids and
electrolytes. The administration of diuretics or hypertonic
saline should not be undertaken lightly as rapid changes in
serum sodium concentration may result in neuronal
demyelination and a fatal outcome.
Haemorrhage
The types of haemorrhage :
1- Arterial haemorrhage :
Arterial haemorrhage is recognised as bright red blood,
spurting as a jet which rises and falls in time with the
pulse.
2- Venous haemorrhage :
Venous haemorrhage is a darker red, a steady and copious
flow. The colour darkens still further from excessive
oxygen desaturation when blood loss is severe. Blood loss
is particularly rapid when large veins are opened, e.g.
common femoral or jugular.
Venous bleeding can be under increased pressure as in
asphyxia, or from ruptured varicose veins. Pulmonary
artery haemorrhage is dark red (venous blood) , whereas
bleeding from the pulmonary veins is bright red
(oxygenated).
3- Capillary haemorrhage :
It is a bright red, often rapid, ooze. If continuing for
many hours, blood loss can become serious, as in
haemophilia.
4- Primary haemorrhage :
It occurs at the time of injury or operation.
5- Reactionary haemorrhage :
It may follow primary haemorrhage within 24 hours
(usually 4—6 hours) and is mainly due to rolling
(‘slipping’) of a ligature, dislodgement of a clot or
cessation of reflex vasospasm. The precipitating
circumstances are:
(1) The rise in blood pressure and the refilling of the
venous system on recovery from shock;
(2) Restlessness, coughing and vomiting which raise the
venous pressure (e.g. reactionary venous
haemorrhage within a few hours of thyroidectomy).
6- Secondary haemorrhage :
Secondary haemorrhage occurs after 7—14 days,
and is due to infection and sloughing of part of the
wall of an artery. Predisposing factors are
pressure of a drainage tube, a fragment of bone, a
ligature in an infected area or cancer. It is also a
complication of arterial surgery and amputations.
It is heralded by ‘warning’ haemorrhages, which
are bright red stains on the dressing, followed by
a sudden severe haemorrhage which may be fatal.
In advanced cancer, the erosion of a main vessel
(e.g. carotid or uterine) by a locally ulcerating
growth becomes the way of merciful termination
to the patient’s suffering. Secondary haemorrhage
is prone to occur with anorectal wounds, for
example after haemorrhoidectomy.
7- External haemorrhage :
External haemorrhage is visible, revealed
haemorrhage.
8- Internal haemorrhage :
Internal haemorrhage is invisible, concealed
haemorrhage. Internal bleeding may be
concealed as in ruptured spleen or liver,
fractured femur, ruptured ectopic gestation or in
cerebral haemorrhage.
Concealed haemorrhage may become revealed as
in haematemesis or melaena from a bleeding
peptic ulcer, as in haematuria from a ruptured
kidney, or via the vagina in accidental uterine
haemorrhage of pregnancy.
Measurement of acute blood loss:
Assessment and management of blood loss must
be related to the pre-existing circulating blood
volume, which can be derived from the patient’s
weight:
• infant 80—85 ml/kg;
• adult 65—75 ml/kg.

Measuring blood loss :
1- Blood clot : The size of a clenched fist is
roughly equal to 500 ml.
2- Swelling in closed fractures : Moderate swelling
in closed fracture of the tibia equals 500—1500
ml blood loss. Moderate swelling in a fractured
shaft of femur equals 500—2000 ml blood loss.
3- Swab weighing : In the operating theatre, blood
loss can be measured by weighing the swabs
after use and subtracting the dry weight. The
resulting total obtained (1 g = 1 ml) is added to
the volume of blood collected in the suction or
drainage bottles. Blood, plasma and water are
also lost from the vascular system because of
evaporation from open wounds, sweating and
expired water via the lungs.
4- Haemoglobin level : This is estimated in g/100
ml (g/dl), normal values being 12—16 g/100 ml
(12—16 g/dl). There is no immediate change in
haemorrhage, but after some hours the level
falls by influx of interstitial fluid into the
vascular compartment in order to restore the
blood volume.
5- Measurement of central venous pressure .
The treatment of haemorrhage
1-
Pressure and packing
The first-aid treatment of haemorrhage from a wound is a
pressure dressing made from anything handy which is
soft and clean. The dressing or pack should be bound on
tightly.
Other examples of pressure used to control haemorrhage
include digital pressure, for example the use of forefinger
and thumb for epistaxis.
Packing by means of rolls of wide gauze is an important
standby in operative surgery. If several rolls are used, the
ends must be tied together to ensure complete removal
later.
N.B. If on removal of pressure or packing, bleeding appears
to have ceased completely, one should not assume that
all is well, especially when dealing with deep wounds
involving large veins. Continued close observation is
required and rapid operative action may be called for .
2- Position
and rest
Elevation of limbs (e.g. in ruptured varicose veins) employs
gravity to reduce bleeding. Elevation also causes helpful
vasoconstriction. A bed elevator is often used to raise the
foot of the bed, and thus increasing venous return to the
heart also augmenting cardiac output. Gravity is also
used in certain operations, as in thyroidectomy when the
patient is tilted feet downwards (reverse Trendelenburg
position) or as in stripping of varicose veins when a headdown tilt is used (Trendelenburg position ).
3- operative
techniques
Artery forceps (haemostats) and clips are mechanical
means of controlling bleeding by pressure. The clamped
vessel can be ligated or it can be coagulated with
diathermy.
Suturing may be employed. The vessel can be underrun or
transfixed by needle and suture, and then ligated, while if
the continuity of a main vessel is to be restored ;very thin
thread is used on atraumatic needle.
4- Other topical applications for
oozing include gauze or sponge, which is
absorbed by the body. ‘Oxycel’ or gelatin
sponge provides a network upon which
fibrin and platelets can be deposited.
Gauze soaked in adrenalin (1:1000) can be
applied. Bone wax is used for oozing
bone.
The whole or part of a bleeding viscus may
have to be excised (e.g. splenectomy ) . A
ruptured kidney is treated conservatively
if possible .
Natural blood volume and red cell
recovery :
The recovery of blood volume begins
immediately by the withdrawal of fluid
from the tissues into the circulation.
There is haemodilution. Plasma
proteins are replaced by the liver. Red
cell recovery takes some 5—6 weeks.
The iron content will be less than
normal if stores are depleted or
absorption is impaired, for example
after gastrectomy.
Transfusion of blood and blood products
The indications for transfusion in surgical practice are as
follows :
1• Following traumatic incidents where there has been severe
blood loss, or haemorrhage from pathological lesions, for
example from the gastrointestinal tract.
2• During major operative procedures where a certain amount
of blood loss is inevitable, for example above knee
amputation or cardiovascular surgery.
3• Following severe burns where, despite initial fluid and
protein replacement, there may be associated haemolysis.
4• Postoperatively in a patient who has become severely
anaemic.
5• Preoperatively, usually in the form of packed cells given
slowly in cases of chronic anaemia where surgery is
indicated urgently, i.e. where there is inadequate time for
effective iron or other replacement therapy, or where the
anaemia is unresponsive to therapy, for example aplastic
anaemia.
Preparation of blood products for transfusion




It is important that blood donors should be fit and with no
evidence of infection, in particular hepatitis and human
immunodeficiency virus (HIV) infection{ acquired immunodeficiency syndrome (AIDS)}, which are transmitted in donor
blood.
Blood is collected into a sterile commercially prepared plastic
bag with needle and plastic tube attached in a complete, closed
sterile unit.
With the donor lying on a couch, a sphygmomanometer cuff is
applied to the upper arm and inflated to a pressure of 70 mmHg .
After introducing 0.5 ml of local anaesthetic, a big needle is
introduced into the median cubital vein and 410 ml of blood
allowed to run into the bag containing 75 ml of anticoagulant
solution (CPD — citrate potassium dextrose).
During collection, the blood is constantly mixed with the
anticoagulant to prevent clotting, and at the end of the
procedure the tube is clamped and the needle removed.
Specimens for use in blood grouping and cross-matching
procedures may be obtained by clamping off small sections of
the plastic tubing containing the donor blood.
Blood storage :
All blood for transfusion must be stored in special blood bank
refrigerators controlled at 4’C ± 2’C. Blood allowed to stand
at higher temperatures for more than 2 hours is in danger of
transmitting infection.
CPD blood has a shelf-life of 3 weeks (CPDA of 5 weeks).
The red blood cells : or erythrocytes, suffer a temporary
reduction (24—72 hours) in their ability to release oxygen to
the tissues of the recipient, so if a patient requires an urgent
and massive transfusion it is wise to give 1 or 2 units of
blood which are less than 7 days old.
White blood cells : White blood cells are rapidly destroyed in
stored blood.
Platelets: At 4 ‘C the survival of platelets is considerably
reduced, and few are functionally useful after 24 hours.
Platelets which are separated show good survival even after
72 hours.
Clotting factors : Like platelets, clotting factors VIII and V are
labile and their levels fall quickly
Blood fractions :
Whole blood may be divided into various fractions. This is
not only more economical of blood donors, but certain
fractions are more appropriate than whole blood
transfusion for certain clinical conditions. Fractionation
procedures are relatively safe and simple, using sealed
sterile plastic bag units.
Packed red cells :
Packed red cells are especially advisable in patients with
chronic anaemia, in the elderly, in small children and in
patients in whom introduction of large volumes of fluid
may cause cardiac failure. Packed red cells are suitable
for most forms of transfusion therapy, including major
surgery. Good packing can be obtained by letting the
blood sediment and removing the plasma, or by
centrifugation of whole blood at 2000—2300g for 15—20
minutes.
Platelet-rich plasma :
Platelet-rich plasma is suitable for transfusions to patients
with thrombocytopenia who are either bleeding or require
surgery. It is prepared by centrifugation of freshly donated
blood at 150—200 g for 15—20 minutes.
Platelet concentrate :
Platelet concentrate for transfusion to patients with
thrombocytopenia is prepared by centrifugation of platelet
rich plasma at 1200—1500 g for 15—20 minutes.
Plasma :
This is removed after centrifugation of whole blood at 2000—
2300 g for 15—20 minutes and it may be further processed
or fractionated in various ways.
Human albumin 4.5 % : Repeated fractionation of plasma by
organic liquids followed by heat treatment results in this
plasma fraction, which is rich in protein but free from the
danger of transmission of serum hepatitis. This may be
stored for several months in liquid form at 4’C and is
suitable for replacement of protein, for example following
severe burns.
Fresh frozen plasma: Plasma removed from fresh blood
obtained within 4 hours is rapidly frozen by immersing in a
solid carbon dioxide and ethyl alcohol mixture. This is
stored at - 40’C and is a good source of all the coagulation
factors. It is the treatment of choice when considering
surgery in patients with abnormal coagulation due to
severe liver failure. It may also be given in any of the
congenital clotting factor deficiency diseases in their
milder forms, especially Christmas disease (Factor IX
deficiency) or haemophilia (Factor VIII deficiency).
Cryoprecipitate: When fresh frozen plasma is allowed to
thaw at 4’C a white glutinous precipitate remains and, if the
supernatant plasma is removed, this cryoprecipitate is a
very rich source of Factor VIII. It is stored at - 40’C and is
immediately available for treatment of patients with
haemophilia (Factor VIII deficiency). The advantage of
cryoprecipitate treatment in haemophilia is the simplicity of
administering large quantities of Factor VIII in relatively
small volumes by intravenous injection. It is also a rich
source of fibrinogen, of value in hypofibrinogenaemic
states.
Blood grouping and cross-matching
There are two groups of antigens
on the cell surface of human red
cells :
1- antigens of the ABO blood
groups
2- antigens of the rhesus (Rh)
blood groups.
Antigens of the ABO blood
groups :
These are strongly antigenic found
on the RBC cell membrane and
are associated with naturally
occurring antibodies in the
serum. Individuals show four
different ABO cell groups : A , B
, AB & O
Antigen
Antibody
A
Anti B
B
Anti A
AB
Nothing
O
Anti A &
anti B
Antigens of the rhesus blood
groups :
The antigen of major
importance in this group is
Rh(D), which is strongly
antigenic . Antibodies to the
D antigen are not naturally
present , but their formation
may be stimulated by the
transfusion of Rh-positive
red cells to Rh.negative
patient . Such acquired
antibodies are capable,
during pregnancy, of
crossing the placenta and, if
present in a Rh-negative
mother, may cause severe
haemolytic anaemia and
even death (hydrops fetalis)
in a Rh-positive fetus in
utero.
Blood
group Rh
positive
Blood
group Rh
negative
A+,B+
AB+,
O+
A-,B-,
ABO-
Blood group
Give to :
Take from :
A+
A-
A+,AB+
A+,A-,O+,OA+,A-,AB+,AB- A-,O-
B+
B-
B+,AB+
B+,B-,O+,OB+,B-,AB+,AB- B- ,O-
AB+ AB+
ABO+
O-
A+,A-,B+,B,AB+,AB,O+,O-(all
blood groups)
AB+, ABA-,B-,AB-,OA+,B+,AB+,O+ O+,OAll blood
Ogroups
Incompatibility
If antibodies present in the recipient’s serum are incompatible with
the donor’s cells, a: transfusion reaction will result. This is the
result of agglutination and haemolysis of the donated cells
leading in severe cases to acute renal tubular necrosis and renal
failure. For this reason, therefore, it is essential that all
transfusion should be preceded by:
1• ABO and rhesus grouping of the recipient’s and donor’s cells
so that only ABO and Rh(D) compatible blood is given;
2•direct matching of the recipient’s serum with the donor’s cells to
confirm ABO compatibility and to test for rhesus and any other
blood group antibody present in the serum of the recipient.
Blood grouping and cross-matching require full laboratory
procedures and take 1 hour. In emergencies it may be necessary
to reduce this time. In such emergencies, it may be advisable to
restore the patient’s blood volume by saline, gelatin (e.g.
Haemaccel), dextran or human albumin 4.5 % until blood has
been made available. Alternatively, donor blood, group 0negative, which is compatible with the majority of individuals,
should be given and this should always be available in acute
emergency situations.
Giving blood :
Blood transfusion is commenced by:
1 • selection and preparation of the site;
2 • careful checking of the donor blood: this should bear a
compatibility label stating the patient’s name, hospital reference
number, ward and blood group;
3 • insertion of the needle or cannula — the latter may be valuable if
intravenous therapy is required for any length of time;
4 • giving detailed written instructions as to the rate of flow, for
example 40 drops/m allows one 540 ml unit of blood to be
transfused in 4 hours.
In acute emergencies, it may be necessary to increase the rate of flow
and it is possible to give 1—2 units in 30 minutes using a pressure
cuff around a plastic bag of blood.
Warming blood : the blood must be warmed before reaching the
patient by passing it through a carefully temperature-regulated
blood warming unit, thus reducing the risk of cardiac arrest from
large volumes of cold blood direct from the refrigerator.
Filtering blood : A filter with an absolute filtration rating of 40
micron will filter off platelet aggregates and leucocytes
membranes in stored blood.
Auto-transfusion
This is an old, well-tried method of immediately
restoring a patient’s blood volume, by transfusion
with his or her own blood. In an emergency, for
example, in a case of ruptured ectopic gestation, the
blood is collected from the peritoneal cavity and put
into a sterile container suitable for connecting to
transfusion tubing. The classical method of filtration
of this blood to prevent the transfusion of any small
clots is to place a piece of sterile gauze within the
container. Nowadays, special autotransfusion
apparatus is being marketed.
For major elective procedures, the patient may
‘donate’ his or her own blood, withdrawal and
storage taking place up to 3 weeks before it is
required. Natural blood volume and most of the red
cell recovery will have taken place in that time.
Complications of blood transfusion :
1-Congestive cardiac failure
This is especially liable to occur in the
elderly or where there is cardiovascular
insufficiency, and may result from too
rapid infusion of large volumes of blood. It
is advisable in the individual with chronic
anaemia to give packed red cells and, at
the same time, give diuretic drugs. The
transfusion should be given slowly, i.e. I
unit over 4—6 hours and, if necessary, on
two separate occasions.
2- Transfusion reactions :
These may be the result of the following problems:
2-1 • Incompatibility. This should be avoided if the correct
procedures of grouping and cross-matching have been
adopted but, in fact, it is nearly always due to human error in
the collection, labelling or checking of the specimens and
donor bags. The patient develops a rigor, temperature and
pain in the loins, and may become extremely alarmed. The
transfusion should be stopped immediately, and a fresh
specimen of venous blood and urine from the patient sent
together with the residue of all the used units of donor blood
to the laboratory for checking.
A close watch should be kept on the patient’s pulse, blood
pressure and urinary output. Frusemide 80—120 mg i.v.
should be given to provoke a diuresis, and repeated if the
urine output falls below 30 ml/hour. Dialysis may be
necessary.
2-2 • Simple pyrexial reactions in which the patient develops
pyrexia, rigor and some increase in pulse rate. These are the
result of ‘pyrogens’ in the donor apparatus and are largely
avoided by the use of plastic disposable giving sets.
2-3 • Allergic reactions in which the patient develops mild
tachycardia and an urticarial rash; This is the result of
allergic reaction to plasma products in the donor blood. The
reaction is treated by stopping the transfusion and giving an
antihistamine drug (chlorpheniramine 10 mg or
diphenhydrazine 25 mg).
2-4 • Sensitisation to leucocytes and platelets. This is not
uncommon in those patients who have received many
transfusions in the past, for example for thalassaemia,
refractory anaemia or aplastic anaemia. The individual
develops antibodies to donated white cells or platelets,
which cause reactions with each transfusion. They may be
minimised by giving packed red cells from which plasma is
removed . Aspirin, antihistamines or steroids may also be
given to the recipient if necessary.
2-5 • Immunological sensitisation. Only the same ABO and
Rh(D) groups are considered for blood transfusion. Immune
antibodies may be stimulated by transfusion, and may give
rise to difficulties with compatibility tests or to haemolytic
transfusion reactions.
3-Infections
There are four main reasons for blood transfusion causing infection in
the recipient.
3-1 • Serum hepatitis virus may be transmitted from the donor and is
usually a severe hepatitis arising approximately 3 months after the
transfusion. It should be avoided by adequate good screening of the
blood donor and by testing for the presence of the hepatitis
associated antigen in the blood prior to transfusion.
3-2 • HIV infection can be transmitted by blood and blood products. All
donors must be screened . Haemophiliacs are at special risk because
of their more frequent requirements for blood products.
3-3 • Bacterial infection may result faulty storage. This arises most
commonly from the donor blood being left in a warm room for some
hours before the transfusion is commenced. This allows proliferation
of any bacteria, and transfusion of such infected blood may result in
severe septicaemia in the recipient and rapid death.
3-4 • Malaria can be transmitted by blood transfusion in areas where the
disease is endemic. Whenever possible, donors should be screened
and the disease eradicated (by treatment of the donors who are
positive) before blood is obtained or given. If the need for transfused
blood is so urgent that precautions are impossible before
transfusion, then the patient should be given prophylactic
antimalarial drugs.
4- Thrombo phlebitis
5- Air embolism
6- Coagulation failure
Coagulation failure is due to:
6-1 • Dilution of clotting factors/platelets due to
large volumes of stored blood being used to
replace losses as stored blood is low in platelets,
Factor VIII and Factor V;
6-2 • Disseminated intravascular coagulation (DIC)
following an incompatible blood transfusion,
particularly ABO incompatibility. The further
haemorrhage may be treated by replacement of
the deficient factors (usually fibrinogen, Factors
VIII, V and II, and platelets), with fresh frozen
plasma, cryoprecipitate and platelet
concentrates. Paradoxically, heparin may be used
sometimes for the treatment of DIC.
E.g. of haemorrhagic diseases :
1- Haemophilia :
Haemophilia (haemophilia A) is a haemorrhagic diathesis
caused by the congenital deficiency in the blood of
Factor VIII [ antihaemophilic globulin (AHG) ]. It is a sexlinked characteristic, transmitted by the asymptomatic
female carriers, and manifest only in males.
The levels of Factor VIII in the blood of severe
haemophiliacs may be less than 1 % of the average
normal level. In the case of spontaneous haemorrhage
(e.g. into joints) treatment should aim at raising the level
to at least 20 %. Should surgery be anticipated in the
haemophiliac, the level should be raised to 50-100 %.
2- Christmas disease :
Christmas disease (haemophilia B) is a congenital disease
resulting from the deficiency of Factor IX (Christmas
factor). Clinically, the manifestations of the disease are
similar to haemophilia. Factor IX is replaced by the
transfusion of fresh frozen plasma,
3- Von Willebrand’s disease:
is a type of haemorrhagic disease, with low
plasma levels of both Factor VIII
complement and Factor VIII related
antigen, and platelet abnormalities.
Blood substitutes — albumin, dextran, (colloid solution)
One of the most urgent requirements in a patient
suffering from acute blood loss is the re-establishment
of a normal blood volume. This may be achieved
satisfactorily with a number of plasma substitutes.
1- Human albumin 4.5 % was used whilst cross-matching
is being performed. Two to three units (1.2 litres) are
given intravenously over 30 minutes. It is valuable in
patients with burns where there has been severe loss
of protein. There is no risk of transmitting hepatitis.
2- Dextrans are polysaccharide polymers of varying
molecular weight producing an osmotic pressure
similar to that of plasma. They have the disadvantage
of inducing rouleaux of the red cells and this interferes
with blood-grouping and cross-matching procedures,
hence the need for a blood sample beforehand.
Dextrans interfere with platelet function and may be
associated with abnormal bleeding, and for this reason
it is recommended that the total volume of dextran
should not exceed 1000 ml.
Parenteral fluid therapy (crystelloid solution )
1• dextrose 5 % is an isotonic solution that supplies calories without
electrolytes. It is useful in the postoperative period when sodium
excretion is reduced. It is also valuable when the salt requirements
of a patient needing much fluid have been satisfied on a particular
day. Prolonged administration of 5 % dextrose solution alone is
liable to result in hyponatraemia, and may cause thrombosis of the
vein used;
2• isotonic (0.9 % ) saline solution is required to replace the normal
sodium requirement (500 ml isotonic saline/day) and additional
volume is required when a large amount of sodium has been lost by
vomiting, or by gastric, duodenal or intestinal aspiration, or
excessive sweating.
3• dextrose 4.3 % with saline 0.18 % (one-fifth isotonic saline) — this
solution is isotonic. Usually it is referred to as dextrose—saline. It
must not be confused with 5% dextrose in saline, which is
hypertonic;
4• Ringer’s lactate solution contains sodium, potassium and chloride
in almost the same concentrations as they are in the plasma. It also
contains some calcium and some lactate. This solution can be used
in hypovolaemic shock while awaiting blood. It is also suitable for
replacing lost intestinal secretions.
Solution Glucos Na
e (g/l) (meq
/l)
Osmol
Cl
Hco3 K
arity
(meq/ (meq (meq/l) meq/l
l)
/l)
5%
50
glucose
----
----
----
----
Iso=
300
0.9%
saline
----
150
150
----
----
Iso=
300
dextrose
4.3 % with
saline 0.18
%
43
31
31
----
----
Iso=
300
Ringer’s
lactate
solution
----
130
109
28
4 + Ca Iso=
+lactate 300
5%
dextrose in
0.9%saline
50
150
150
----
----
Hyper
=600
Shock
Shock is a life-threatening situation. It is due to poor tissue
perfusion with impaired cellular metabolism, manifested in turn
by serious pathophysiological abnormalities.
Types of shock :
1- Vasovagal shock :
Vasovagal shock is brought about by pooling of blood in larger vascular
reservoirs (limb muscles), and by dilatation of the splanchnic arteriolar
bed, causing reduced venous return to the heart, low cardiac output
and reflex bradycardia due to over stimulation of vagus N.
Consequently, the reduced cerebral perfusion causes cerebral hypoxia
and unconsciousness, but this leads to reflex vasoconstriction & then
increases the venous return and cardiac output as to restore cerebral
perfusion and consciousness. It must be remembered that if the
patient is maintained in an upright or a sitting position (e.g. in a dental
chair) permanent cerebral damage will occur.
2- Psychogenic shock :
Psychogenic shock immediately follows a sudden fright (e.g.
bad news) or accompanies severe pain (e.g. a blow to the
testes) ,also due to over stimulation of vagus N.
3- Neurogenic shock :
Neurogenic shock is caused by traumatic or
pharmacological blockade of the sympathetic nervous
system, producing dilatation of resistance arterioles and
capacitance veins leading to relative hypovolaemia and
hypotension. There is a low blood pressure, a normal or
decreased cardiac output, a normal pulse rate and a warm
dry skin. This may be corrected by putting the patient in
the Trendelenburg position, the rapid administration of
fluids and or a vasopressor drug.
4- Hypovolaemic shock :
Hypovolaemic shock is due to loss of intravascular volume
by haemorrhage, dehydration, vomiting and diarrhoea
(e.g. cholera, acute enterocolitis). Until 10—15 % blood
volume is lost, the blood pressure is maintained by
tachycardia and vasoconstriction. Fluid moves into the
intravascular space from the interstitial space . In
addition, the venous capacitance vessels constrict,
pushing blood into the arterial system and therefore
compensating for the volume deficit.
E.g. of Hypovolaemic shock :
4-1- Traumatic shock:
Traumatic shock is due primarily to hypovolaemia from
bleeding externally (open wounds), from bleeding
internally (torn vessels in the mediastinal or peritoneal
cavities, ruptured organs such as liver and spleen or
fractured bones) or by fluid loss into contused tissue or
into distended bowel. Traumatic contusion to the heart
itself may cause pump failure and shock, while damage to
the nervous system or to the respiratory system results in
hypoxia.
4-2-Burns shock :
Burns shock occurs as a result of rapid plasma loss from
the damaged tissues, causing hypovolaemia. When 25 %
or more of the body surface area is burnt, a generalised
capillary leakage may result in gross hypovolaemia in the
first 24 hours. Endotoxaemia due to infection makes
matters worse and large volumes of fluids are required for
resuscitation.
5- Cardiogenic shock :
Cardiogenic shock occurs when more than 50 % of the
wall of the left ventricle is damaged by infarction. Fluid
overload, particularly when using colloids, can lead to
over-distension of the left ventricle, with pump failure.
The resultant high filling pressures exerted by the right
ventricle make fluid leak out of the pulmonary
capillaries, thereby causing pulmonary oedema and
hypoxia. If an arrhythmia occurs this will reduce the
pumping efficiency of the heart, while hypovolaemia
from excess sweating, vomiting and diarrhoea will
further diminish cardiac output.
Acute massive pulmonary embolism from a thrombus
originating in a deep vein or an air embolus (more than
50 ml), if obstructing more than 50 % of the pulmonary
vasculature, will cause acute right ventricular failure.
This greatly reduces venous return to the left ventricle,
and cardiac output falls catastrophically causing
sudden death or severe shock.
6- Septic (endotoxic) shock :
6-1- Hyperdynamic (warm) septic shock: This occurs in
serious Gram-negative infections , for example from strangulated
intestine, peritonitis, leaking oesophageal or intestinal
anastomoses, or suppurative biliary conditions. At first, the patient
has abnormal or increased cardiac output with tachycardia and a
warm, dry skin, but the blood is shunted past the tissue cells,
which become damaged by anaerobic metabolism (lactic acidosis).
The capillary membranes start to leak and endotoxin is absorbed
into the bloodstream, leading to a generalised systemic
inflammatory state. The immediate and ready treatment of the
cause, including the drainage of pus, is vital to the recovery of the
patient at this stage (in strangulated hernia ‘the danger is in the
delay, not in the operation’ ).
6-2- Hypovolaemic hypodynamic (cold) septic shock : This
follows if severe sepsis or endotoxaemia is allowed to persist.
Generalised capillary leakage and other fluid losses lead to severe
hypovolaemia with reduced cardiac output, tachycardia and
vasoconstriction. The systemic infection induces cardiac
depression, pulmonary hypertension, pulmonary oedema and
hypoxia which, in turn, reduce cardiac output still further. The
patient becomes cold, clammy, drowsy and tachypnoeic, but still
can be converted to hyperdynamic (warm) shock by the
administration of several litres of plasma or other colloidal solution.
7- Anaphylactic shock :
Penicillin administration is amongst the common
causes of anaphylaxis. Other causes include
anaesthetics, dextrans, serum injections, stings
and the consumption of shellfish. The antigen
combines with immunoglobin E (IgE) on the
mast cells and basophils, releasing large
amounts of histamine and SRS-A (slow-release
substance-anaphylaxis). These compounds
cause bronchospasm, laryngeal oedema and
respiratory distress with hypoxia, massive
vasodilatation, hypotension and shock. The
mortality is around 10 %.
Clinical monitoring
In summary, patient monitoring in shock should include:
1• pulse;
2• blood pressure (recording systolic and diastolic
pressure, the pulse pressure, using an intraarterial line if necessary);
3• heart rate and rhythm (cardioscope);
4• respiratory rate and depth;
5• CVP;
6• PCWP (pulmonary capillary wedge pressure ) in
severe shock when the diagnosis is in doubt;
7• urine output;
8• serial blood gases and serum electrolyte
measurements.
Treatment of shock
The management of all types of shock should be vigorous
and quick . The objectives are to increase the cardiac
output and to improve tissue perfusion, especially in
the coronary, cerebral, renal and mesenteric vascular
beds. The plan of action should be based on:
(1) Treat the primary problem —arrest of haemorrhage,
draining pus, etc.
(2) Improving ventricular filling by giving adequate fluid
replacement, for example human albumin solution or
fresh frozen plasma, in sepsis and burns;
(3) Improving myocardial contractility with inotropic
agents — dopamine, dobutamine, adrenaline infusions;
(4) Correcting acid—base disturbances, using molar
sodium bicarbonate when the pH of arterial blood is
less than 7.2, and electrolyte abnormalities, especially
potassium and calcium levels.
(5) In endotoxic shock, once the haemodynamic
status has been improved, full doses of the
appropriate antibiotics are given to treat the
causal infection. Usually we use tripple
antibiotics (amoxicillin for gram positive
infection , gentamycin for gram negative
infection & metroniadazole for anaerobic
infection ).
Diabetic patients in endotoxic shock are in a
precarious position. Careful monitoring and
control of their nutrition and insulin
requirements are necessary under the
instruction of a clinician with a special interest
in diabetes.
(6) Vasodilators(hydralazine, phentolamine, glyceryl
trinitrate infusions and chlorpromazine boluses) may be
given provided the blood volume has been corrected and
cardiac depression treated such that the systolic blood
pressure is 90 mmHg or more. The indication is persistent
vasoconstriction with oliguria, high CVP or PCWP and
pulmonary oedema. Such therapy will improve cardiac
output and tissue perfusion, and reduce the work done by
the heart.
It must be emphasised that vasodilators can only
be used with extreme caution and full
haemodynamic monitoring, because the sudden
production of vasodilation in a hypovolaemic or
dehydrated patient can be followed by a
catastrophic fall in arterial blood pressure.
These drugs should be given only in small intravenous
doses or infusions and only until the extremities become
warm and pink, and the veins are dilated and well filled.
Sterilisation
Sterilisation by steam :
Instruments can be sterilised by steam under pressure
using autoclaves. Vegetative bacteria, including
tuberculosis, and viruses such as hepatitis B, hepatitis C
and human immunodeficiency virus (HIV) and heatresistant spores, including Clostridium tetani and
Clostridium perfringens, are killed. The combination of
pressure, temperature and time with the moist heat is
important:
• 134’C (30 lb/in.2) for a hold time of 3 minutes;
• 121’C (15 lb/in.2) for a hold time of 15 minutes;
• prepacked materials and instruments are processed
through a porous load autoclave which incorporates a
pre-vacuum cycle necessary to extract air. If this is not
achieved then the dried saturated steam cannot penetrate
efficiently. Unwrapped instruments can be sterilised in a
small autoclave within the theatre , which is convenient
when instruments are dropped.
Monitoring :
All autoclaves must be regularly maintained according to
the manufacturer’s instructions, and a record should be
kept of the cycle time, the pre-vacuum phase, the
pressure and temperature. In addition, the steam
penetration test (Bowie—Dick test) and chemical
indicators, for example Brownes tubes or impregnated
tapes, are used to ensure that such errors as poor
packing do not interfere with the efficiency of the
process. Biological indicators are not appropriate.
Sterilisation by ethylene oxide gas :
Ethylene oxide is a highly penetrative non-corrosive gas
which has a broad-spectrum cidal action. It is utilised for
heat-sensitive materials including electrical equipment. It
is not recommended for ventilator ,respiratory equipment
or soiled instruments because organic debris, including
serum, has a marked adverse effect.
Sterilisation by hot air :
This is inefficient compared with moist steam sterilisation,
but it has the advantage in the ability to treat solid nonaqueous liquids grease/ointments and to process closed
(airtight) containers. Lack of corrosion may be important,
particularly with instruments with fine cutting edges such
as ophthalmic instruments. It cannot be used for
substances such as rubber, plastics and intravenous fluids
which are denatured.
Sterilisation by low-temperature steam and formaldehyde :
This uses a combination of dried saturated steam and
formaldehyde, with the main advantage being that
sterilisation is achieved at a low temperature (73’C) and the
method is therefore suitable for heat-sensitive materials
and equipment with integral plastic components. It is not
recommended for sealed, oily items or those with retained
air. Some plastics and fabrics absorb formaldehyde,
releasing this in a delayed manner which may cause
hypersensitivity to the users.
Sterilisation by irradiation :
This technique employs gamma rays or accelerated
electrons. It is an industrial process and is
particularly appropriate to the sterilisation of
large batches of similar products, such as
syringes, catheters and intravenous cannulas.
The delivery of an irradiation dose in excess of
25 kGy is accepted as providing adequate
sterility assurance.
Disinfection
Cleaning of items is essential before
disinfection is undertaken and the
efficiency also depends on:
1. the nature of microorganisms;
2. the load of microorganisms;
3. the duration of exposure to the agent;
4. the temperature.
Disinfection with low-temperature steam :
Typical conditions include exposure to dry
saturated steam at a temperature of 73’C for a
period of 20 minutes at a pressure below
atmospheric. This is a useful process for
dealing with dirty returns from the operating
theatre or clinics which may be contaminated
with protein from bodily secretions and
microorganisms. Following this method of
disinfection the instruments must be cleaned.
Disinfection with boiling water :
This utilises soft water at 100’C at normal
pressure for 5minutes. Instruments must be
thoroughly cleaned before being utilised.
Disinfection with formaldehyde :
Formaldehyde gas is a broad-spectrum
antimicrobial agent. This process utilises a
cabinet which is airtight and circulates gaseous
formaldehyde up to 50’C.
Disinfection with glutaraldehyde :
A 2 per cent solution of glutataldehyde is effective
against most bacterial viruses, including
hepatitis B and C and HIV, and is particularly
useful for the decontamination of flexible
endoscopes.
• Thorough cleansing is essential.
• The degree of decontamination is proportional to
the time of immersion.
• It is a toxic substance and causes irritant, allergic
reactions to the staff, particularly skin reactions,
which limits its use.
Safeguards for equipment during sterilisation :
Safeguards during sterilisation must include:
1 • thorough cleaning;
2 • appropriate packing for the sterilisation of disinfection
process in order to avoid reduced penetration of the
active agent. This is particularly important in the packing
in the autoclave;
3 • arrangements of articles so that all surfaces are directly
exposed to the agent. This includes opening or unlocking
jointed instruments and disassembling instruments;
4 • the use of chemical indicators routinely;
5 • the interval monitoring of sterilisation process with
chemical, thermal and, sometimes, biological indicators;
6 • the utilisation of flash sterilisation, where a temperature
of 147’C is used at a pressure of 40 lb/in.2, is now rare
and should only be considered in an emergency situation;
7 • a careful maintenance plan for all sterilisation
processes.
Conclusion :
Antibiotics, both prophylactic and
therapeutic, have not reduced the
essential role of asepsis and sterile
precautions. Protocols with regard to
instrument sterilisation, equipment
maintenance, air filtration and
ventilation, and staff behavior are
essential. Regular staff education is
imperative.
Tumours :
A tumour is a new growth of tissue (a mass) which can refer to
an inflammatory swelling such as inflammatory tumour or
to a neoplastic growth. A neoplastic tumour is an
uncontrolled proliferation of a clone of cells without useful
function.
Causation :
Cancer is a disease of genes. The cell is the basic unit of
organisation and control. The genetic code is contained
within the deoxyribonucleic acid (DNA) molecule present
within the cell nucleus. Genes make proteins which govern
the function and structure of a cell. There are around
100 000 genes (human genome) representing approximately
10 % of the DNA; each cell expresses 5—150000 genes.
Since all genes are present in each cell nucleus, any gene
may be expressed if the gene promoter is switched on, as
occurs in neoplasia. Cancer is caused by disease of genes
which control production of daughter cells from stem cells,
cell proliferation, terminal differentiation and programmed
cell death (apoptosis)= from the Greek — shedding of
autumn leaves. There are three important classes of genes
involved in cancer:
1- tumour suppressor genes, which control the cell cycle by
slowing down the cycle or triggering apoptosis (TP53, P16,
APC, RB1);
2- oncogenes, which promote cell proliferation by increasing
signalling activity from the cell surface to the transcription
apparatus on gene promoters (KRAS, ERBB2, C-MYC);
3- growth factors and their receptors which are switched on
by oncogenes or switched off by tumour suppressor genes
(EGF, TGFa, IGF, FGF).
A benign tumour grows by expansion without invasion of the
extra-cellular matrix. A malignant tumour (cancer) grows by
invasion into the extracellular matrix; most solid tumours
also invade the basement membrane of endothelium and
metastasise. The unit of cancer is the altered malignant cell
which proliferates (clone). Different clones usually arise
with different characteristics, such as the ability to
metastasise via blood vessels or lymphatics. Cancer is a
disease of genes which may be inherited or acquired .
Inherited cancers are caused by a specific DNA mutation of
a tumour suppresser gene inherited in all cells.
In cells of the organ affected, the (second) homologous gene
is lost, initiating a sequence of genetic mutations
culminating in cancer. Chemical carcinogens probably
account for the majority of sporadic (acquired) cancers.
Natives of Kashmir are prone to cancer of the skin of the
thighs and lower abdomen. This is due to their habit of
keeping warm by squatting and hugging earthenware pots
containing glowing charcoal [the pot being termed a fangri
], with the result that the adjacent skin is irritated by heat
and fumes. ‘Chimney-sweep’s’ cancer’ , ‘countryman’s lip’,
and ‘tar workers’ cancer’ are other examples of carcinoma
due to chemical carcinogens. DNA strand breaks are
induced by ultraviolet and ionising radiation which, if not
repaired, lead to cancer. Cellular instability from ageing of
stem cell-lines (many common cancers) or chronic
inflammation leads to increased cell proliferation and
reduced apoptosis. This results in malignant
transformation. Squamous cell carcinoma occasionally
occurs in a chronic ulcer or in a scar ‘Marjolin’s ulcer’). A
fibrosarcoma also may arise in a scar. At least 20 % of
cancers world-wide are caused by oncogenic viruses.
Environmental cofactors are also important.
Helicobacter pylori is linked to the development
of gastric cancer by an unknown mechanism. A
diet high in calories and rich in saturated fats
(from red meat) is implicated in many cancers
including those of the colorectum and pancreas.
In viral carcinogenesis there are specific
cofactors for different cancers: malaria
(Burkitt’s lymphoma), immunosuppression
(post-transport lymphomatous proliferative
disease — PTLPD), human immunodeficiency
virus (Kaposi’s sarcoma ), smoking (cervical
cancer) and aflatoxins (liver cancer).
Definitions :
• Hypertrophy :is an increase in the size of an organ without an
increase in cell numbers.
• Hyperplasia : is an increase in the size of an organ due to an
increase in cell numbers.
• Metaplasia : The epithelium from which the tumour grows has
already changed its characteristics: bladder transitional
epithelium to squamous epithelium, gallbladder columnar to
squamous epithelium, bronchial columnar to squamous
epithelium, gastric columnar epithelial pattern to intestinal
epithelial pattern and oesophageal squamous to columnar
epithelium (Barrett’s oesophagus).
• Dysplasia :This represents the earliest changes of neoplastic
transformation than can be detected at the microstructural level
(e.g. by light microscopy). In fact, genetic mutations are
detectable at an earlier stage. Alterations in intracellular
organisation, the individual size and shape of the nucleus,
cellular size and shape and intercellular three-dimensional
organisation indicate dysplasia. These changes may be
classified as mild, moderate or severe dysplasia. Any grade of
dysplasia may revert to normal due to elimination of the
neoplastic clone, but is least likely with severe dysplasia.
Carcinoma in situ : Severe dysplasia may progress to
carcinoma in situ: the cellular, nuclear and threedimensional architecture resemble cancer but without
invasion into the extracellular matrix.
• Genotype : This is the molecular structure of any cell. A
malignant genotype will have losses and mutations of
tumour suppresser genes and the presence of
oncogenes.
• Phenotype : This is the appearance of a cell at a
microstructural level (microscopic phenotype) and its
functional state (biological phenotype). A changed
genotype will always precede a particular phenotype: for
a time the cell may appear to be normal even though it
has already acquired a malignant genotype.
• Differentiation : Depending on the degree to which the
cells and organisation (morphology) of tumours resemble
the parent tissue they are divided into well-differentiated,
moderately differentiated and poorly differentiated forms.
o
Anaplasia : Tumours are usually composed of
cells which resemble those of the tissue from
which they arise. Complete loss of
differentiation (anaplasia) is associated with
an aggressive cancer.
• Teratomas : arise from embryonic stem cells
containing representative cells from all three
embryonic layers: ectoderm, endoderm,
mesoderrn . Teratomatous dermoids contain
hair and teeth, muscle and gland tissue. An
unusual type is the sacrococcygeal teratoma
,which can be considered as foetus in foeto
(an ‘included’ foetus).
• Blastomas : develop from ‘unipotent’ cells, and
arise from any one of the three embryonic
layers (e.g. neuroblastoma).
o
cysts : ‘Dermoid’ is a loose term given to cysts
lined by squamous epithelium occurring in various parts
of the body. Sebaceous cysts are lined by superficial
squamous cells and should more accurately be called
‘epidermoid’.
---Teratomatous dermoids (see above) are found in the
ovary, testis retroperitoneum, superior mediastinurn and
the presacral area. Malignant change (carcinomatous or
sarcomatous) can occur.
— Sequestration dermoids are not new growths, but are
formed by the inclusion of epithelial ‘nests’ beneath the
surface at places where lines of developing skin meet
and join: midline, external angular process, branchial
cysts .
— Implantation dermoids may follow puncture wounds,
commonly of the fingers, when living epithelial cells are
implanted beneath the surface.
• Dermoid
Benign tumour :
A benign tumour is usually encapsulated, and does not
disseminate or recur after complete removal. Symptoms and
effects, which can be harmful, are due to its size, position, and
pressure. Certain adenomas secrete a hormone which may
affect bodily functions. Benign tumours are often multiple.
Malignant tumour :
The characteristics of malignancy are:
— invasion of surrounding tissues;
— pleomorphism (variable shapes) of cells and nuclei;
— rapid growth;
— the tendency to spread to other parts of the body (metastasis)
by the lymphatics, the bloodstream, along nerve sheaths and
across body cavities;
— general weight loss (cachexia in advanced disease).
At an early stage, evidence of invasion is the most important sign
of malignancy. Many cells of a malignant tumour have an
abnormal number of chromosomes which is not a multiple of the
usual haploid number (= ‘aneuploidy’).


It has been suggested that the division of
tumours into these two major groups
imposes a concept which is too rigid .
A third group of intermediate tumors exists
which includes some carcinoid tumours,
adenoma of the bronchus, ‘mixed’ salivary
tumours and basal-cell carcinoma. These
intermediate types invade locally, but are
much less inclined to lymphatic or
especially vascular dissemination.
Benign tumours
Adenoma
Adenomas arise in secretory glands, and
resemble the structure from which they
arise. They are encapsulated, and
sometimes they secrete hormones which
profoundly influence metabolism, as in the
case of the thyroid, parathyroid and
pancreas. Occasionaliy an adenoma
contains a large proportion of fibrous
tissue, e.g. the hard fibroadenoma in the
breast, while in other situations, notably
the pancreas and thyroid gland, cystic
degeneration is common. Those arising
from superficial glands of mucous
membrane are liable to pedunculation, as
in the case of a rectal ‘polyp,.


Papilloma
A papilloma consists of a central axis of connective
tissue, blood vessels and lymphatics; the surface
is covered by epithelium, either squamous,
transitional, cuboidal or columnar, according to
the site of the tumour. The surface may be
merely roughened, or composed of innumerable
delicate villous processes, as in the case of
those occurring in the kidney, bladder and
rectum. In these situations, papillomas resemble
malignant tumours, as secondary growths arise
by implantation and, sooner or later, the tumour
becomes frankly malignant . Other common sites
for papillomas are the skin, the colon, the
tongue and lip, vocal cords and the walls of cysts
(particularly those the breast and ovary).
Fibroma
A true fibroma (containing only fibrous connective tissue) is
rare. Most fibromas are combined with other mesoderm
tissues such as muscle (fibromyoma), fat (fibrolipoma) ,a
nerve sheaths (neurofibroma). Multiple tumours are not
uncommon as, for example, in neurofibrornatosis (von Recklinghausen’s disease,
Fibromas are either hard or soft, depending on the
proportion of fibrous to the other cellular tissue. Soft
fibromas a common in the subcutaneous tissue of the
face, and appear soft, brown swellings.
Desmoid ;This unusual type of flbroma occurs in the
abdominal wall . An intraperitoneal form is associated
with familial adenomato polyposis .
Keloid :This overgrowth of fibrous tissue commonly occurs
in scars, especially black people.

Lipoma :
A lipoma is a slowly growing tumour composed of fat cells adult type.
Lipomas may be encapsulated or diffuse. It occur anywhere in the
body where fat is found and earn the titles of the ‘universal tumour’.
The head and neck area, abdominal wall and thighs are particularly
favoured sites.
Encapsulated lipomas are among the commonest of tumours. The
characteristic features are the presence of a definite edge and
lobulation. A sense of fluctuation may be obtained. As would be
expected, a lipoma deeply situated is liable to be mistaken for other
swellings. Most lipomas are painless, but some give rise to an aching
sensation which may radiate.
Multiple lipomas are not uncommon. The tumours remain small or
moderate in size, and are sometimes painful, in which case the
condition is probably one of neurolipomatosis.
Dercum ‘s disease characterised by tender deposits of fat, especially on
the trunk.
Should the lipoma contain an excessive amount of fibrous tissue, it is
termed a fibrolipoma. In other cases, considerable vascularity is
present, often with telangiectasis of the overlying skin, in which case
the tumour is a naevo-lipoma. Large lipomas of the thigh , the shoulder
and the retroperitoneum occasionally undergo sarcomatous changes.
Myxomatous degeneration, saponification and calcification sometimes
occur in lipomas of long duration.
Clinically, circumscribed lipomas are classified according to their
Situation.
• Subcutaneous lipoma : Commonly found on the shoulders
or the back, although no part of the body is immune. A
lipoma may be present over the site of a spina bifida.
Subcutaneous lipomas occasionally become
pedunculated.
• Sub- fascial lipoma : Occurring under the palmar or plantar
fascia, they are liable to be mistaken for tuberculous
tenosynovitis, as the tough, overlying fascia masks the
definite edge and lobulation of the tumour. Difficulty is
encountered in complete removal as pressure encourages
the tumour to ramify. Subfascial lipomas also occur in the
areolar layer under the epicranial aponeurosis and, if of
long duration, they erode the underlying bone, so that a
depression is palpable on pushing the tumour to one side.
• Sub-synovial lipoma : From the fatty padding around joints,
especially the knee. In the knee, they are mistaken from
Baker’s cysts but are easily distinguished as, in distinction
to a cyst or bursa, their consistency is constant whether
the joint is in extension or flexion.
• Intermuscular lipoma : Mainly in the thigh or around the shoulder.
Owing to transmitted pressure, the tumour becomes firmer when the
adjacent muscles are contracted. Weakness or aching results, owing
to mechanical interference with muscular action. The condition is
often difficult to distinguish from a fibrosarcoma.
• Peri-osteal lipoma : occasionally occur under the periosteum of a
bone.
• Subserous lipoma : is sometimes found beneath the pleura, where
they constitute one variety of innocent thoracic tumour.
• Submucous lipoma : occur under the mucous membrane of the
respiratory or alimentary tracts. Rarely a submucous Iipoma in the
larynx causes respiratory obstruction. A submucous lipoma can
occur in the tongue. One situated in the intestine is likely to cause an
intussusception, which may be the first indication of its presence.
• Central nervous system Lipomas : may occur anywhere within the
extradural spaces, the spinal cord and brain; they usually arise from
the pia mater, within the central subarachnoid spaces; a lipoma of the
corpus callosum may be accompanied by calcification .
• Intraglandular Lipomas : have been found occasionally in the
pancreas, under the renal capsule and in the breast .
• Retropenitoneal lipoma :. Large lipomas are seen not infrequently in
the retroperitoneal tissues. Some of them turn out to be
liposarcomas.
Treatment of lipoma :
If a lipoma is causing trouble on account of its
site, size, appearance or the presence of pain,
removal is indicated.
During operation, any finger-like projections of the
tumour into the surrounding tissue should also
be removed. Although the tumour is relatively
avascular, care is needed to obtain complete
haemostasis in the resulting cavity otherwise a
haematoma is common, which may be followed
by infection and delay in wound healing;
drainage is often necessary.
Diffuse lipoma occasionally occurs in the
subcutaneous tissue of the neck, from which it
spreads on to the preauricular region of the face.
The tumour is not obviously encapsulated, and
gives rise to no trouble, beyond being unsightly.
Neuroma :
True neuromas are rare tumours, and occur in connection
with the sympathetic system. They comprise the following
types:
• Ganglioneuroma : which consist of ganglion cells and nerve
fibres. It arises in connection with the sympathetic ganglia,
and therefore is found in the retroperitoneal tissue, or in
the neck or thorax.
• Neuroblastoma ; which is less differentiated than the
ganglioneuroma, the cells being of an embryonic type. The
tumour somewhat resembles a round-celled sarcoma, and
disseminates by the bloodstream. It occurs in infants and
young children. It may occasionally undergo spontaneous
remission.
• Myelinic neuroma : is very rare, being composed only of
nerve fibres, as the ganglion cells are absent. They arise in
connection with the spinal cord or pia mater.
Neurilemmoma (syn. Schwannoma)
These lobulated and encapsulated tumours arise from the
neurilemmal cells. They are soft and whitish in appearance.
They displace the nerve from which they arise and can be
removed .
Neurofibroma
Neurofibroma arise from the connective tissue of
the nerve sheath. The following varieties are
described.
A single neurofibroma is usually found in the
subcutaneous tissue = The ‘painful subcutaneous
nodule’ forms a smooth firm swelling which may
be moved in a lateral direction, but is otherwise
fixed by the nerve from which it arises.
Paraesthesia or pain is likely to occur from the
pressure of the tumour on the nerve fibres which
are spread over its surface. Cystic degeneration
or sarcomatous changes occur occasionally.
Neurofibromas may also grow from the sheath of a
peripheral nerve or a cranial nerve, e.g. the
acoustic tumour . As the nerve fibres are ‘part
and parcel’ of the tumour they are difficult to
remove without removal of the nerve itself. In
major nerves recurrence is a problem, as is
malignant (sarcomatous) change.
Generalised neurofibromatosis =
(syn.
von Rechlinghausen’s disease of nerves) :
In this inherited (autosomal-dominant) disease, any
cranial, spinal or peripheral nerve may be diffusely or
modularly thickened . The overgrowth occurs in
connection with the endoneurium. Associated
pigmentation (cafe au lait) of the skin is common, and
sarcomatous changes may occur.
Plexiform neurofibromatosis :
This rare condition usually occurs in connection with
branches of the fifth cranial nerve , although it may
occur in the extremities . The affected nerves become
enormously thickened as a result of myxofibromatous
degeneration of the endoneurium.
False neuroma :
Arises from the connective tissue of the nerve sheath
after injury to a nerve (lacerations or amputation).
These swellings consist of fibrous tissue and coiled
nerve fibres.
Haemangiomas :
They are represented in various forms, capillary, cavernous
and plexiform being common.
Glomangioma (syn. glomus tumour) :
These tumours arise from a cutaneous glomus composed of
a tortuous arteriole which communicates directly with a
venule, the vessels being surrounded with a network of
small nerves. These specialised organs regulate the
temperature of the skin, and are found in the limbs,
especially the nail beds. The tumour is compressible. The
associated pain is out of all proportion to the size of the
tumour, which may be only a few millimetres in diameter.
The pain is burning in nature and radiates peripherally, and
is more often noticeable when the limb is exposed to
sudden changes in temperature.
Cutaneous glomus tumours grow very slowly, and do not
become malignant. They should be excised.
Hamartoma :
The term hamartoma is roughly translated from
the Greek as a ‘fault’, and its original
meaning was ‘missing the mark in spear
throwing’.
It is a developmental malformation consisting
of overgrowth of tissue or tissues proper to
the part. The possible range therefore is very
wide and the lesions are often multiple.
Common lesions that are hamartomas are
benign pigmented moles, and the majority of
angiomas and neurofibromas. On rare
occasions a malignant change occurs in a
hamartoma, but for practical purposes the
lesion is benign .
Malignant tumours
Carcinomas arise from cells which are ectodermal or
endodermal in origin, and they are classified squamous,
basal-celled or glandular (adenocarcinomas).
Sarcomas occur in connection with structures of mesoblastic
origin, hence fibrosarcoma, osteosarcoma.
Germ cell tumours arise from germ cells (teratoma,
seminoma, thecoma). Ovarian cancer is an
adenocarcinoma: it does not arise from oocytes.
Carcinoma
Squamous cancer arises from surfaces covered by
squamous epithelium, particularly as a result of ultraviolet
or ionising radiation and chronic irritation. Chronic
irritation of transitional cells (e.g. by a stone in the renal
pelvis) or columnar cells (e.g. the gall bladder) will cause a
change in these cells to a squamous type (squamous
metaplasia), which may lead on to carcinoma. The regional
lymph nodes are likely to be invaded, and may also be
infected from the sepsis attendant upon the primary
growth. Blood-borne metastases occur, but uncommonly
from skin squamous cell carcinoma.
Methods of spread :
1- Direct spread (local extension) : Invasion takes place readily along
connective tissue planes, but no structures are resistant. Veins are
invaded commonly. Arteries are rarely invaded. Muscle is less
susceptible to invasion or metastatic deposits than other tissues.
Fascia also limits direct extension,
2- Lymphatics : by invasion and by embolism.
• Invasion. The malignant cells grow along the lymphatic vessels from
the primary growth (permeation). This may even occur in a
retrograde direction. The cancer cells stimulate perilymphatic
fibrosis, but this does not stop the advance of the disease. In some
instances, groups of cells may so overcome the surrounding
fibrosis that they give rise to intermediate deposits between the
primary growth and the lymph nodes.
• Embolism. Cancer cells which invade a lymphatic vessel can break
away and are carried by the lymph circulation to a regional node, so
that nodes comparatively distant from the tumour may be involved
in the early stages.
3- Blood stream : Cancer cells may be detected in the venous blood
draining an organ involved in carcinoma. A carcinoma of the kidney
may invade the renal vein and grow inside the lumen into the vena
cava. Malignant emboli may be arrested in the lungs, liver and bone
marrow (secondary deposits — metastases). Thyroid, breast and
bronchial cancers also commonly disseminate via the blood stream.
4- Implantation : Implantation of carcinoma has been
observed in situations where skin or mucous membrane
is in close contact with a primary growth. Examples of
this is carcinoma of the lower lip affecting the upper lip .
Recurrence after operation is occasionally due to
implantation of malignant cells in the wound. Examples of
this is nodules of carcinoma in the scar of the incision
after mastectomy for a carcinoma of the breast. When a
cavity is involved, free-floating cells from a carcinoma
may spread like snowflakes all over its serous surface.
For the abdomen, transcoelomic spread is specially
notable when cells from a colloid carcinoma of the
stomach gravitate on to an active ovary and give rise to
malignant ovarian tumours (Krukenberg’s tumour )
intracavitary dissemination can also take place within the
pleura and cerebrospinal spaces.
5- Nerve sheaths ; Adenocarcinomas, especially pancreas,
may disseminate along nerve sheaths.
Grading and staging :
Grading and staging are used to assess the degree of malignancy
of the tumour as an indication of the prognosis, and may be
used as a guide to determine the type and the extent of the
treatment which is required. Advanced staging and grading may
indicate the need for adjuvant methods of treatment, e.g. by
chemotherapy or irradiation.
Grading : Grading predicts the aggressiveness of a malignant
neoplasm by characterising its microscopic appearance taking
into account the degree of differentiation, nuclear and cellular
appearance, architectural integrity and the proportion of active
mitoses.
• Grade 1: well differentiated;
• Grade 2: moderately well differentiated;
• Grade 3: poorly differentiated.
Staging : (i) TNM classification. This has been adopted by the
International Union against Cancer (UICC) and has been
extended to many sites of cancer. This is a detailed clinical
staging which is arrived at simply by the clinician ascertaining
the following points. What is the extent of the primary Tumour?
Are any lymph Nodes affected? Are there any Metastases? The
information so obtained is scored, e.g. ii carcinoma of the
breast, as follows:
Tumour
T1 2 cm or less.
No skin fixation
Nodes
N0 No nodes
T2 More than 2 cm,
but less than 5 cm.
Skin tethered or
dimpled. No
pectoral fixation
N1 Axillary nodes
movable (a) not
significant,
(b) significant
T3 More than 5 cm,
but less than 10 cm.
Skin infiltrated or
ulcerated. Pectoral
fixation
N2 Axillary
nodes fixed
T4More than 10 cm.
Skin involved but
not beyond breast,
Chest-wall fixation
N3 Supraclavicular
nodes. Oedema
of arm
Metastasis
M0 No metastasis
M1 Metastases are
present including
involvement of skin
beyond breast, and
contralateral nodes
(i) Thus, for example, one patient may
have an early carcinoma which is
T1N0M0, while in another late case the
extent of the disease may be T2N2M1.
(ii) Manchester staging. This is a method
of staging clinical spread of carcinoma
of the breast .
(iii) Dukes’ staging. This is a method of
classifying the spread of carcinoma of
the rectum and colon .
Wounds

Wounds and their management are
fundamental to the practice of surgery.
Any elective surgical intervention will
result in a wound in order to gain
access to and deal with the underlying
pathology. In the surgery of trauma the
wound is the primary pathology.In both
situations the surgeon’s task is to
minimise the adverse effects of the
wound, remove or repair damaged
structures and harness the processes
of wound healing to restore function.
Wound Healing
PHASES OF WOUND HEALING ;
The wound healing process follows a predictable
pattern that can be divided into :
1- hemostasis and inflammation,
2- proliferation
3- maturation
4- remodeling.
This sequence of events is fluid and overlapping.
All wounds need to progress through this series
of cellular and biochemical events that
characterizes the phases of healing to
successfully re-establish tissue integrity.
1- Hemostasis and Inflammation ;
Hemostasis precedes and initiates inflammation with the
ensuing release of chemotactic factors from the wound
site. Wounding disrupts tissue integrity, Leading to
division of blood vessels and direct exposure of
extracellular matrix to platelets. Exposure of
subendothelial collagen to platelets results in platelet
aggregation, degranulation, and activation of the coagulation
cascade resulting In a fibrin clot. Platelet granules release
a number of wound-active substances such as plateletderived growth factor (PDGF), platelet-activating factor
(PAF), fibronectin, and serotonin. In addition to achieving
hemostasis, the fibrin clot serves as scaffolding for the
migration into the wound of inflammatory cells such as
polymorphonuclear leukocytes (PMNs,neutrophils) and
monocytes.
Cellular infiltration after injury follows a
characteristic, predetermined sequence.PMNs are
the first infiltrating cells to enter the wound site,
peaking at 24-48h. Increased vascular
permeability, local prostaglandin release, and the
Presence of chemotactic substances such as
complement factors, interleukin-1 (IL-1), tumor
necrosis factor-? (TNF-?), platelet factor 4, or
bacterial products all stimulate neutrophil
migration.
The second population of inflammatory cells that
invades the wound consists of macrophages.
Derived from circulating monocytes, macrophages
achieve significant numbers in the wound by 48–
96 h post-injury and remain present until wound
healing is complete
Macrophages,like neutrophils ,participate in wound
d´ebridement via phagocytosis and contribute to microbial
stasis via oxygen radical and nitric oxide synthesis. The
macrophage’s most pivotal function is activation and
recruitment of other cells via mediators such as cytokines
and growth factors. By releasing such mediators as TGF?,
vascular endothelial growth factor (VEGF), insulin-like
growth factor (IGF), epithelial growth factor (EGF), and
lactate, macrophages regulate cell proliferation, matrix
synthesis, and angiogenesis.
Macrophages also play a significant role in regulating
angiogenesis and matrix deposition and remodeling.
T-lymphocytes comprise an other population of inflammatory
/ immune cells that routinely invades the wound. Less
numerous than macrophages, T- Lymphocyte numbers
peak at about 1 week post-injury and bridge the transition
From the inflammatory to the proliferative phase of healing.
2- Proliferation :
The proliferative phase roughly spans days 4 through 12.
During this phase, Tissue continuity is re-established.
Fibroblasts and endothelial cells are the last Cell
populations to infiltrate the healing wound, and the
strongest chemotactic factor for fibroblasts is plateletderived growth factor (PDGF), On entering the wound
environment, recruited fibroblasts first need to proliferate,
and then become activated, to carry out their primary
function of matrix synthesis and remodeling.
This activation is mediated mainly by the cytokines and
growth factors released from wound macrophages.
Endothelial cells also proliferate extensively during this
phase of healing.
These cells participate in the formation of new capillaries
(angiogenesis). Endothelial cells migrate from intact
venules close to the wound. Their migration, replication,
and new capillary tubule formation are under the
influence of such cytokines and growth factors as TNF-a,
TGF-?, and VEGF.
Matrix Synthesis :
Biochemistry of Collagen :
Collagen is the most abundant protein in the body.
Type I collagen is the major component of
extracellular matrix in skin. Type III, which also
normally is present in skin, becomes more
prominent and important during the repair process.
Biochemically, each chain of collagen is composed of
a glycine residue in every third position. These
changes in the triplet is made up of proline or lysine
during the translation process. The polypeptide
chain that is translated from mRNA is called
protocollagen. Release of protocollagen into the
endo- plasmic reticulum results in the hydroxylation
of proline to hydroxyproline and of lysine to
hydroxylysine by specific hydroxylases. Prolyl
hydroxylase requires oxygen and iron as cofactors,
?-ketoglutarate as co-substrate, and ascorbic acid
(vitaminC) as an electron donor.
In the endoplasmic reticulum, The protocollagen
chain assumes an ?- helical configuration after its
glycosy-lated by the linking of galactose and
glucose at specific hydroxy-lysine residues.
Three ?-helical chains entwine to form a right-handed
superhelical structure Called procollagen .
Although initially joined by weak , ionic bonds, the
procollagen molecule becomes much stronger by
the covalent cross – linking of lysine residues.
Extracellularly, the procollagen strands by further
polymerization and cross- linking. The resulting
collagen monomer is further polymerized and
cross-linked by the formation of intra and
intermolecular covalent bonds.
Proteoglycan Synthesis :
lycosaminoglycans comprise a large portion of the “ground
substance” that makes up granulation tissue. Rarely found
free, they couple with proteins to form proteoglycans. The
polysaccharide chain is made up of repeating disacaride
units , composed of glucuronic or iduronic acid and
ahexosamine, which usually sulfated. The disaccharide
composition of proteoglycans varies from out 10 units in
the case of heparin sulfate to as much as 2000 units in the
case of hyaluronic acid.
The major glycosaminoglycans present in wounds are
dermatan and chonoitin sulfate. Fibroblasts synthesize
these compounds, increasing their concentration greatly
during the first 3 weeks of healing. The interaction between
collagen and proteoglycans is being actively studied. As
scar collagen is de-posited , the proteoglycans are
incorporated into the collagen scaffolding. However, with
scar maturation and collagen remodeling ,the content of
proteoglycans gradually diminishes.
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3- Maturation and 4- Remodeling :
The maturation and remodeling of the scar begins
during the fibroplastic phase, and is characterized
by a reorganization of previously synthesized
collagen. Collagen is broken down by matrix
metallo-proteinases (MMPs). The net wound
collagen content is the result of a balance between
collagenolysis and collagen synthesis. This will
shift toward collagen synthesis and eventually
establishment of extracellular matrix composed of a
relatively a cellular collagen-rich scar.
Wound strength and mechanical integrity in the fresh
wound are determined by both the quantity and
quality of the newly deposited collagen. The
deposition of matrix at the wound site follows a
characteristic pattern: fibronectin And collagen type
III constitute the early matrix scaffolding;
glycosaminoglycans and proteoglycans represent
the next significant matrix components; and collagen
type I is the final matrix. By several weeks post-injury
the amount of collagen in the wound reaches
aplateau, but the tensile strength continues to
increase for several more months. Fibril formation
and fibril cross-linking result in decreased collagen
solubility, increased strength, and increased
resistance to enzymatic degradation of the collagen
matrix. Scar remodeling continues for many(6–
12)months post-injury, gradually result in a mature,
avascular, and acellular scar. The mechanical
strength of the scar never achieves that of the
uninjured tissue.
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Epithelialization
Although tissue integrity and strength are being reestablished, the external barrier must also be restored.
This process, beginning within 1 day of the injury, is
characterized primarily by proliferation and migration
of epithelial cells adjacent to the wound. Marginal
basal cells at the edge of the wound lose their firm
attachment to the underlying dermis, enlarge, and
begin to migrate across the surface of the provisional
matrix. Fixed basal cells in a zone near the cut edge
undergo a series of rapid mitotic divisions, and these
cells appear to migrate by moving over one another in
a leapfrog fashion until the defect is covered. Once the
defect is bridged, the migrating epithelial cells lose the
flattened appearance, become more columnar in
shape, and increase their mitotic activity. Layering of
the epithelium is re-established, and the surface layer
eventually keratinizes.
Re-epithelialization is complete in less than 48 h in the
case of approximated Incised wounds, but may take
substantially longer in the case of larger wounds in
which there is a significant epidermal / dermal defect.
If only the epithelium and superficial dermis are
damaged, such as occurs in split-thickness skin graft
(STSG) donor sites or in superficial second – degree
burns ,then repair consists primarily of reepithelialization with minimal or no fibroplasia and
granulation tissue formation. The stimuli for reepithelialization remain incompletely defined;
however, it appears that the process is mediated by a
combination of a loss of contact inhibition; exposure
to constituents of the extracellular matrix, particularly
fibronectin; and cytokines produced by immune
mononuclear cells. In particular EGF, TGF-? ,basic
fibroblast growth factor (bFGF), PDGF,
Wound Contraction :
All wounds undergo some degree of contraction. For
wounds that donot have surgically approximated
edges, the area of the wound will be decreased by
this action (healing by secondary intention) .The
myofibroblast has been postulated as being the
major cell responsible for contraction, and it differs
from the normal fibroblast in that it possesses a
cytoskeletal structure. Typically this cell contains
smooth muscle actin in thick bundles called stress
fibers, giving myofibroblasts contractile capability.
The smooth muscle actin is un-detectable until day
6, and then is increasingly expressed for the next 15
days of wound healing. After 4 weeks this
expression fades and the cells are believed to
undergo apoptosis. the undifferentiated fibroblasts
may also contribute to wound contraction.
CLASSIFICATION OF WOUNDS ;
Wounds are classified as either acute or chronic.
Acute wounds heal in a predictable manner and
timeframe. The process occurs with few, ifany,
complications, and the end result is a wellhealed wound. Surgical wounds can heal in
several ways. An incised wound that is clean
and sutured closed is said to heal by primary
intention .Often, because of bacterial
contamination or tissue loss, a wound will be
left open to heal by granulation tissue
formation and contraction; this constitutes
healing by secondary intention. Delayed
primary closure, or healing by tertiary
intention, represents a combination of the first
two, consisting of the placement of sutures,
allowing the wound to stay open for a few
days, and the subsequent closure of the
sutures.
.
Classification of wound
A wound can be caused by almost any injurious
agent and can involve almost any tissue or
structure. The most useful classification of
wounds from a practical point of view is that of
Rank and Wakefield into tidy and untidy wounds.
1- Tidy wounds
Tidy wounds are inflicted by sharp instruments and
contain no devitalised tissue ; such wounds can
be closed primarily with the expectation of quiet
primary healing. Examples are surgical incisions,
cuts from glass and knife wounds. Skin wounds
will usually be single and clean cut. Tendons,
arteries and nerves will commonly be injured in
tidy wounds, but repair of these structures is
usually possible . Fractures are uncommon in tidy
wounds.
2- Untidy wounds
Untidy wounds result from crushing, tearing, avulsion,
vascular injury or burns, and contain devitalised tissue .
Skin wounds will often be multiple and irregular.
Tendons, arteries and nerves may be exposed, and
might be injured in continuity, but will usually not be
divided. Fractures are common and may be multifragmentary. Such wounds must not be closed
primarily; if they are closed wound healing is unlikely to
occur without complications. At best there may be
wound dehiscence, infection and delayed healing, at
worst gas gangrene and death may result. The correct
management of untidy wounds is wound excision, by
this is meant excision of all devitalised tissue to create
a tidy wound. Once the untidy wound has been
converted to a tidy wound by the process of wound
excision it can be safely closed (or allowed to heal by
second intention).
Sutures
Suture materials are divided to :
1-absorbable & non-absorbable sutures:
1-1- absorbable sutures :
A- Plain catgut sutures : which are made
from the sub mucosa of the cat
intestine ,& usually absorbed in 1-2
weeks .
B- Chromic catgut: It is a plain catgut but
covered with chrome. It is absorbed in
3-4 weeks
C- Vicryl sutures :which are made of
polyglactinic acid & absorbed in 2-3
months.
D- Dexon sutures which absorbed in7-9
months.
1-2- non-absorbable sutures :
A- Silk :made of silky material that not
absorbed.
B- Nylon sutures
C- Stainless steel sutures
D- Cotton tape sutures
Sutures
2- According to the type of needle:
2-1- cutting needle .
2-2- round needle .
2-3- taper cut needle.
All these are curved needles & also there are
strait needles differ in its length & thickness
2-4- no needle sutures :which are used
for ligation .
The suture thread length about 75 cm & its
thickness measured by numbers (from thick
to thin) ,e.g. 2 , 1 , 0 , 2/0 , 3/0 , 4/0 up to 10/0
which is very thin suture used for eye
operations .
Sarcomas :
Sarcomas differ from carcinomas, not only in their derivation,
but in their earlier age incidence, as they are most common
during the first and second decades. Sarcomas often grow
rapidly and dissemination occurs early via the bloodstream
(e.g. ‘cannon-ball’ secondary deposits in the lung from an
osteogenic sarcoma).
The macroscopic appearance of a sarcoma varies
considerably. As the word implies, most tumours appear as
a fleshy mass, but their consistency depends on the
relative proportion of fibrous and vascular tissue.
Haemorrhage commonly occurs owing to the very thin
walls of the veins, which in some places are represented
merely by venous spaces.
Sarcomatous cells may reproduce tissue similar to that from
which the tumour originated, e.g. osteosarcoma or
chondrosarcoma. Sometimes a sarcoma develops in preexisting benign tumours, such as fibroma or a uterine
fibroid.
Fibrosarcoma :
Fibrosarcoma is composed of spindle cells of varying lengths (the
rounder they are the more malignant they are), and occurs in
muscle sheaths, scars and as a fibrous epulis. A fibrosarcoma of a
muscle sheath presents as an elastic or firm and slowly growing
swelling. Dilated veins over the tumour suggest malignancy, and if
not obvious they may be demonstrated by infrared photography. On
palpation the tumour often feels warm and pulsation may even be
detected. Fibrosarcomas not uncommonly arise in scar tissue,
sometimes many years after the scar developed. Sir James Paget
described this as a ‘recurrent fibroid’.
Treatment of sarcoma :
The spread of a fibrosarcoma is hastened by incomplete removal. The
moral is that wide excision with surrounding healthy tissues should
be practised in all cases. This may mean amputation in the case of a
limb. If untreated or if wide local excision is unsuccessful, a
fibrosarcoma eventually fungates through the skin. Metastases are
widely scattered and, unfortunately, radiotherapy has but little effect
on either the primary growth or the secondary deposits. Sarcomas
are often susceptible to anticancer drugs, but fibrosarcomas are
more resistant than other types. Sarcoma of bone is sensitive to
radiotherapy, which is used in some cases as an alternative to
amputation .
Lymphomas :
Lymphomas arise in lymph nodes, tonsils, Peyer’s
patches or lymph nodules in the intestines. Lymph
nodes of the neck or mediastinum are most commonly
affected . They have a bad prognosis.
Endothelioma; mesothelioma :
The endothelial linings of blood vessels, lymphatic spaces
and serous membranes occasionally give rise to
neoplasms. They can be malignant. They arise from the
pleura and rarely from the pericardium or peritoneum.
Asbestos inhalation may provoke their development.
‘Blue’ asbestos fibres especially have been shown to be
a cause. The original cells are flattened, but they
become spheroidal or cuboidal when neop]astic
changes occur. The ‘endothelioma’ (meningioma) of the
dura mater is thought to arise from the arachnoid
membrane, which is not an endothelial structure .
Benign to malignant transformation :
Certain benign neoplasms are prone to undergo malignant
changes, and it is important, for both treatment and
prognosis, to realise when this occurs. Some or all of
the following changes may be recognised:
• increase in size: comparatively rapid enlargement is
always suspicious, e.g. a neurofibroma which is
becoming sarcomatous;
• increased vascularity: dilated cutaneous veins,
ulceration and bleeding in the case of a superficial
growth (e.g. melanoma);
• fixity: due to invasion of surrounding structures;
• involvement of adjacent structures: e.g. facial palsy suggests malignant change in an otherwise longstanding
parotid pleomorphic adenoma;
• dissemination: discovery of secondary deposits.
Cysts :
The word cyst is derived from the Greek word meaning
‘bladder’. The pathological term ‘cyst’ means a swelling
consisting of a collection of fluid in a sac which is lined
by epithelium or endothelium.
True cysts :
True cysts are lined by epithelium or endothelium. If
infection supervenes, the true lining may be destroyed
and replaced by granulation tissue. The fluid is usually
serous or mucoid and varies from brown-staining by
altered blood to almost colourless. In epidermoid,
dermoid and branchial cysts the contents are like
porridge or toothpaste, as a result of the shedding of
desquamated cells. Cholesterol crystals are often found
in the fluid of branchial cysts.
False cysts (pseudocysts) :
Walled-off collections of fluid not lined by epithelium are not
regarded as true cysts. A pseudocyst of the pancreas is an
encysted collection of pancreatic enzymerich fluid lined by
granulation tissue or fibrous tissue. Pancreatic
pseudocysts are often in the retroperitoneum deep to but
bulging into the lesser sac; they may occur anywhere in
the abdominal cavity and even track into the mediastinum
and pleural cavities. In tuberculous peritonitis, fluid may be
walled off in cystic form by adherent coils of intestine.
Fluid may collect in the centre of a tumour (cystic
degeneration), due to haemorrhage or necrosis. This can
also happen in the brain as a result of ischaemia, and an
‘apoplectic cyst’ is formed. In acute pancreatitis fluid
collections loculated by viscera and fibrin are called ‘acute
fluid collections’; these often occur in the lesser sac but
are neither cysts nor pseudocysts as they are not lined by
either epithelium, granulation tissue or fibrous tissue.
A classification of cysts
Congenital
Sequestration dermoids
Tubuloembryonic (tubulodermoid)
Cyst of embryonic remnants
Acquired
Retention
Distention
Exudation
Cystic tumours
Implantation dermoids
Trauma
Degeneration
Parasitic
Hydatid, trichniasis,
cysticercosis
.
Congenital cysts
The sequestration dermoid is due to dermal cells being buried along the
lines of closure of embryonic clefts and sinuses by skin fusion. The
cyst therefore is lined by epidermis and contains paste-like
desquamated material. The usual sites are:
• the midline of the body — especially in the neck;
• above the outer canthus (external angular dermoid, ;
• in the anterior triangle of the neck (branchial cyst.
Tubuloembryonic (tubulodermoid) cysts occur in the track of an
ectodermal tube used in development, e.g. a thyroglossal cyst from
the thyroglossal duct or a postanal dermoid from the postanal gut. In
the brain, ependymal cysts arise from the sequestration of cells of
the enfolding neurectoderm.
Cysts of embryonic remnants. These arise from embryonic tubules and
ducts which normally disappear or are only present as remnants.
They should not be confused with teratomatous cysts, e.g. dermoid.
There are many examples in the urogenital system, e.g. in the male
from remnants of the paramesonephric duct (Müllerian) — the hydatid
of Morgagni, or from the mesonephric body and duct (Wolffian) .
Cysts of the urachus and the vitellointestinal duct are other examples
of cysts of embryonic remnants
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Acquired cysts
Retention cysts are due to the accumulated secretion of a gland behind an
obstruction of a duct. Examples are seen in the pancreas, the parotid, the
breast, the epididymis and Bartholin’s gland. A sebaceous cyst starts with
the obstruction of a sebaceous gland, but this is followed by the downgrowth and the accumulation of desquamated epidermal cells, thus
turning it into an epidermoid cyst. In the epididymis, if the retention cyst
contains sperms, it is known as a ‘spermatocele’.
Distension cysts occur in the thyroid from dilatation of the acini, or in the
ovary from a follicle. Lymphatic cysts and cystic hygromas are distension
cysts. Exudation cysts occur when fluid exudes into an anatomical space
already lined by endothelium, e.g. hydrocele, a bursa, or when a collection
of exudate becomes encrusted.
Cystic tumours. Examples are cystic teratomas (dermoid cyst of the ovary)
and cystadenomas (pseudomucinous and serous cystadenoma of the
ovary).
Ganglia. See Chapter 29.
Implantation dermoids arise from squamous epithelium which has been
driven beneath the skin by a penetrating wound. They are classically found
in the fingers of women who sew assiduously and metal workers (Fig.
12.13).
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Trauma
A haematoma may resolve into a cyst. This sometimes happens to haematomas of
muscle masses in the loin and anterolateral aspects of the thigh or the skin. They are
located between muscle, facial or subcutaneous planes and contain straw- or browncoloured fluid containing cholesterol crystals. They become lined by endothelium and
calcium salts may be laid down. Aspiration is only of temporary value, and a cure
depends upon complete excision of the lining. Within the cranium, a haematogenous
cyst can cause the same problems as any expanding, space-occupying lesion.
Degeneration cysts
These have already been discussed under false cysts.
Parasitic cysts
These are encrusted forms in the life cycle of various worms:
• Hydatid cyst of Taenia echinococcus. This is described later according to the organ
involved, e.g. liver, Chapter 52; lung, Chapter 47.
• Trichiniasis. Cysts of Trichina spiralis, affecting muscle.
• Cysticercosis. Cysts of Taenia solium. A disease of the pig, humans being rarely
affected. Eosinophilia is present. The cysts occur in any organ. They calcify and may
cause clinical effects according to their situation, especially in the brain. Only those
cysts which are actually causing symptoms should be excised.
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Clinical features
The swelling usually has a smooth, spherical appearance. Fluctuation depends upon
the pressure of fluid within: a tense cyst feels like a solid tumour, although careful
palpation between two fingers may elicit a characteristic elasticity. In addition, a solid
tumour is most hard at the centre; a cyst is least hard at the centre. If fluctuation is
present, a cyst may be confused with a cold abscess or a lipoma. A cold abscess
usually has a peculiar rim of thickening surrounding the soft centre. A lipoma may
well test clinical acumen. Transillumination,while brilliantly clear in cysts containing
serous fluid, does not really distinguish between a lipoma and a dermoid or branchial
cyst. There is even an old axiom that ‘when in doubt, hedge on fat’. According to
circumstances, ultrasonography, computerised tomography (CT) or magnetic
resonance imaging (MRI), a test aspiration or excision reveals the true nature of the
swelling.
Cysts may be painful, especially when infection or haemorrhage causes a sudden
increase in intracystic tension. Sometimes they change in size for no apparent
reason. Occasionally, they diminish owing to rupture through a facial plane.
Effects are according to site and size. As with benign tumours, a cyst may compress
ducts and blood vessels, e.g. the main bile duct may be obstructed by a choledochal
cyst, a renal cyst or a hydatid cyst. The pelvic veins may be obstructed by an ovarian
cyst, the patient presenting for treatment of her varicose veins. The sheer size of an
ovarian cyst (Fig. 12.14) may so increase intra-abdominal tension as to bring the
patient to hospital with symptoms of a hiatus hernia.
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Complications
Infection
The cyst becomes tense and painful, and adherent to surrounding tissues. An abscess
may form and discharge on the surface and result in an ulcer or a sinus (viz. Cock’s
peculiar tumour, Chapter 13). Healing will not occur until the whole lining of the cyst
or the embryonic track is excised.
Haemorrhage
Sudden haemorrhage, as may occur in a thyroid cyst, causes a painful increase in
size. In this particular case, breathing may be difficult because of pressure on the
trachea.
Torsion
Torsion may occur in cysts which are attached to neighboring structures by a vascular
pedicle. Ovarian dermoids are sometimes brought to notice in this way as acute
abdominal emergencies. The cyst (or cysts — they may be bilateral) turns to a purple
or black colour as the venous and then the arterial supply is cut off.
Calcification
Calcification follows haemorrhage, or infection, and may be the result of reaction to a
parasite, e.g. hydatid cyst.
Cachexia ovarica
Enormous cysts are rarely seen nowadays (Fig. 12.14).
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Ulcers
An ulcer is a discontinuity of an epithelial surface. There is usually progressive
destruction of surface tissue, cell by cell, as distinct from death of macroscopic
portions, e.g. gangrene or necrosis. Ulcers are classified as nonspecific, specific (e.g.
tuberculous or syphilitic) or malignant.
Nonspecific ulcers are due to infection of wounds, or physical or chemical agents.
Local irritation, as in the case of a dental ulcer, or interference with the circulation,
e.g. varicose veins, are predisposing causes.
Trophic ulcers [trophe (Greek) = nutrition] are due to an impairment of the nutrition
of the tissues, which depends upon an adequate blood supply and a properly
functioning nerve supply. Ischaemia and anaesthesia therefore will cause these
ulcers. Thus, in the arm, chronic vasospasm and syringomyelia will cause ulceration
of the tips of the fingers (respectively painful and painless). In the leg, painful
ischaemic ulcers occur around the ankle or on the dorsum of the foot. Neuropathic
ulcers due to anaesthesia (diabetic neuritis, spina bifida, tabes dorsalis, leprosy or a
peripheral nerve injury) are often called perforating ulcers (Fig. 12.15). Starting in a
corn or bunion, they penetrate the foot, and the suppuration may involve the bones
and joints and spread along fascial planes upwards, even involving the calf.
The life history of an ulcer consists of three phases.
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Extension
During the stage of extension the floor is covered with exudate and
sloughs, while the base is indurated. The discharge is purulent and even
blood stained.
Transition
The transition stage prepares for healing. The floor becomes cleaner, the
sloughs separate, induration of the base diminishes and the discharge
becomes more serous. Small, reddish areas of granulation tissue appear
on the floor and these link up until the whole surface is covered.
Repair
The stage of repair consists of the transformation of granulation to fibrous
tissue, which gradually contracts to form a scar. The epithelium gradually
extends from the now shelving edge to cover the floor (at a rate of 1 mm
per day).
This healing edge consists of three zones — an outer of epithelium, which
appears white, a middle one, bluish in colour (where granulation tissue is
covered by a few layers of epithelium), and an inner reddish zone of
granulation tissue covered by a single layer of epithelial cells. The red
colour of granulation tissue is due to the high density of new capillaries
(neo-angiogenesis).
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Clinical examination of an ulcer
This should be conducted in a systematic manner. The following are, with brief
examples, the points which should be noted.
Site, e.g. 95 per cent of rodent ulcers occur on the upper part of the face. Carcinoma
typically affects the lower lip, while a primary chancre of syphilis is usually on the
upper lip.
• Size, particularly in relation to the length of history, e.g. a carcinoma extends more
rapidly than a rodent ulcer, but more slowly than an inflammatory ulcer.
• Shape, e.g. a rodent ulcer is usually circular. A gummatous ulcer is typically
circular, or serpiginous due to the fusion of multiple circles. An ulcer with a square
area or straight edge is suggestive of ‘dermatitis artefacta’ (Fig. 12.16).
• Edge (Fig. 12.17). A healing, nonspecific ulcer has a shelving edge. It is pearly,
rolled or rampant if a rodent ulcer, and raised and everted if an epithelioma, undermined and often bluish if tuberculous, vertically punched out if syphilitic.
• Floor. The floor is that which is seen by an observer, e.g. watery or apple-jelly
granulations in a tuberculous ulcer, a wash-leather slough in a gummatous ulcer.
• Base. The base is what can be palpated. It may be indurated as in a carcinoma or
attached to deep structures, e.g. a varicose ulcer to the tibia.
• Discharge. A purulent discharge indicates active infection. A blue—green coloration
suggests infection with Pseudomonas pyocyaneus. A watery discharge is typical of
tuberculosis. It is bloodstained in the extension phase of a nonspecific ulcer.
Bacteriological examination may reveal colonisation by coagulase-positive
staphylococci. Spirochetes are found in a primary chancre (Chapter 8).
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Lymph nodes are not enlarged in the case of a rodent ulcer, unless
due to secondary infection. In the case of carcinoma, they may be
enlarged, hard and even fixed. The inguinal nodes draining a
syphilitic chancre of the penis are firm and ‘shotty’, but contrarily
the submandibular nodes draining a chancre of the lip are greatly
enlarged.
• Pain. Nonspecific ulcers in the extension and transition stages
are painful (except for the anaesthetic trophic type). Tuberculous
ulcers vary, that of the tongue being very painful. Syphilitic ulcers
are usually painless, but an anal chancre (of a homosexual) may
be painful (cf. anal fissure, Chapter 61).
• General examination. Evidence of debility, cardiac failure, all
types of anaemia, including sickle-cell anaemia, or diabetes must
be sought.
• Pathological examinations, e.g. biopsy, will confirm carcinoma.
The serological and Mantoux tests may be of value for syphilis and
tuberculosis, respectively.
• Marjolin’s ulcer. See Chapter 13
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local (topical) treatment of nonspecific ulcers
Any underlying cause is treated, e.g. varicose veins (Chapter 16),
diabetes, arterial disease. Many lotions and nonadhesive
applications are used to aid the separation of sloughs, hasten
granulation and stimulate epithelialisation. The basic requirements
of an ideal dressing are that should:
•maintain a high humidity between the wound and the dressing;
•remove excess exudate and toxic compounds;
•permit gaseous exchange of oxygen, carbon dioxide and water
vapour;
•provide thermal insulation to the wound surface and be
impermeable to microorganisms;
•be free from particles and toxic wound contaminants
•allow easy removal with no trauma at dressing change;
•be safe to use and be acceptable to the patient;
•be cost-effective.
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Antiseptics and topical antibiotics
Antiseptics can do more harm than good when used
inappropriately. They can interfere with the normal healing
process, are toxic to fibroblasts and may permit more virulent
organisms to dominate. The routine use of antiseptic and
hypochlorite solutions should be avoided. If a wound needs
cleaning, this can be achieved safely and more economically with
normal saline warmed to body temperature prior to use. If a
topical antiseptic is necessary, aqueous chlorhexidine 1 in 5000
solution is effective against a wide range of Gram-positive and negative organisms and some fungi, but not spores. Povidone
iodine has a broad spectrum of activity but its antibacterial effect
is reduced by contact with pus or exudate. It should not be used
on patients who are sensitive to iodine. Topical antibiotics are not
recommended routinely as resistance and sensitisation following
application may arise. Flamazine is a hydrophilic cream containing
silver sulphadiazine 1% which is a broad-spectrum antibacterial
agent and very effective against Pseudomonas, useful for the
prevention of Gram-negative sepsis in patients with severe burns.
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Wound dressings
Hydrocolloid dressings such as Granuflex or Comfeel consist of a thin polyurethane
foam sheet bonded on to a semipermeable polyurethane film, which is impermeable
to exudate and microorganisms. When the dressing comes into contact with wound
exudate it interacts to form a gel which expands into the wound. The moist
conditions produced under the dressing promote angiogenesis and wound healing
without causing maceration. They can be used in the treatment of leg ulcers,
pressure sores, minor burns and many types of granulating wound. A hydrocolloid
dressing can be applied to small wounds containing dry slough or necrosis: the
dressing prevents the loss of water vapour from the surface of the skin, and this
effectively rehydrates the dead tissue which is then removed by autolysis.
Hydrogel (Intrasite gel) is a pale yellow/colourless transparent aqueous gel. When it
comes into contact with a wound, the dressing absorbs excess exudate and produces
a moist environment at the surface of the wound without causing tissue maceration.
It may be applied to many different wounds including leg ulcers, pressure sores,
surgical wounds and granulating tissue. It is particularly useful in the treatment of
dry, sloughy or necrotic wounds, promoting rapid débridement by facilitating
rehydration and autolysis of dead tissue. It reduces the feeling of pain and can be
used as a carrier of other medicines, e.g. metronidazole, for the control of odour
caused by infection with sensitive organisms. (It is useful in fungating tumours where
the aim is not to heal the wound but to manage the distressing symptoms caused by
it.) Intrasite should be secured with a secondary dressing such as an absorbent pad
or Tegaderm depending on the wound.
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Alginates (Kaltostat) consist of an absorbent fibrous fleece composed of the mixed
sodium and calcium salts of alginic acid. In the presence of exudate or other body
fluids containing sodium ions, the fibres absorb liquid and swell, calcium ions present
in the fibre are partially replaced by sodium, causing the dressing to take on a gellike appearance which promotes healing. The fibres are held in place with a
secondary dressing such as an absorbent pad or Tegaderm depending on the amount
of
exudate. Alginate dressings can be used for the management of bleeding wounds
including cuts and lacerations and also for a wide range of exuding lesions including
leg ulcers, pressure sores and most other granulating wounds. Most suitable for
heavy to moderately exudating wounds. In the presence of low exudate the Kaltostat
must be moistened with saline before application to avoid adherence. The alginates
are biodegradable so it is not necessary to remove every fibre if it will damage the
healing tissue.
Lyofoam is a low-adherent conformable polyurethane foam sheet. The side of the
dressing that is to be placed in contact with the skin has been heat treated to render
it hydrophilic, whilst the outer surface remains hydrophobic. The dressing is freely
permeable to gases and water vapour but resists the penetration of aqueous
solutions and exudate. The dressing absorbs blood and any other tissue fluids but the
aqueous component is lost by evaporation through the back of the dressing. Strikethrough occurs laterally and not at the top of the dressing. The dressing maintains a
moist warm environment at the surface of the wound, which is conducive to
granulation and epithelialisation. Foam sheet dressings may be used on a variety of
exudating wounds including leg ulcers, pressure sores, sutured wounds, burns and
donor sites.
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Tegaderm consists of a thin polyurethane membrane coated with a layer of an acrylic adhesive. The
dressing allows for a moist environment at the surface of the wound by reducing water vapour loss
from the exposed tissue. It is permeable to both water vapour and oxygen and impermeable to
microorganisms, providing an effective barrier to external contamination. Scab formation is
prevented and epidermal regeneration takes place at an enhanced rate, compared with that which
occurs in wounds treated with traditional dry dressings. Tegaderm may be used in the treatment of
minor burns, pressure areas, donor sites, postoperative wounds and a variety of minor injuries. It
is also effectively used as a protective cover to prevent skin breakdown due to friction or
continuous exposure to moisture.
Alleyvncavity wound dressing is a highly comfortable absorbent dressing consisting of a soft,
polymeric outer membrane with a three-dimensional honeycomb-like structure containing a mass of
hydrophilic polyurethane chips. The outer membrane is perforated to allow exudate to be drawn
into the interior of the dressing where it is absorbed and retained by the ‘chips’. This type of
dressing is used for heavily exudating, full-thickness sloughy wounds, usually combined with
Intrasite gel; it can be used alone with clean, deep, ex~ daring wounds.
Most of the above dressings are also available with added properties which improve their basic
function, such as Kaltocarb. This is Kaltostat with a layer of activated charcoal cloth attached. This
is effective as a primary dressing in the management of infected malodorous wounds.
As the wound heals if granulation tissue continues to grow past the epidermal layer, the dressing
used to stimulate granulation should be discontinued and a Lyofoam dressing should be applied. If
after 1 week there is no improvement Tetra-cortil ointment containing hydrocortisone and
oxytetracycline applied sparingly to the wound may be effective. This should be covered with a
Lyofoam dressing and should be used for no longer than 5 days. Silver nitrate may be used with
heavy overgranulating tissue but it is not recommended, usually because of its toxicity and the risk
of sensitivity and staining.
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Oriental sore (syn. Delhi boil, Baghdad sore, etc.)
This disease is due to infection by a protozoal parasite,
Leishmania tro pica, and is a common condition in Eastern
countries which is occasionally imported to Western zones. An
indurated papule appears on an exposed surface, usually the face.
If untreated, this breaks down to form an indolent ulcer, which
eventually leaves an ugly, pigmented scar. The condition readily
responds to intravenous injections of antimony tartrate, but very
small lesions can be treated by carbon dioxide snow, and also
curettage.
Bazin’s disease (syn. erythema induratum) is due to localised
areas of fat necrosis and particularly affects adolescent girls.
Symmetrical purplish nodules appear, especially on the calves,
and gradually break down to form indolent ulcers, which leave in
their wake pigmented scars. Tuberculosis may be a cause in many
instances, the ulcers responding to antituberculous drugs (Fig.
12.17) (Chapter 8).
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Sinuses and fistulas
A sinus (Latin a hollow; a bay or gulf) is a blind track (usually lined with granulation tissue) leading from an epithelial
surface into the surrounding tissues. Pathological sinuses must be distinguished from normal anatomical sinuses (e.g.
the frontal and nasal sinuses). A fistula (Latin = a pipe or tube) is an abnormal communication between the lumen or
surface of one organ and the lumen or surface of another, or between vessels. Most fistulas connect epitheliallined
surfaces (Fig. 12.18). Sinuses and fistulas may be congenitalor acquired. Forms which have a congenital origin include
preauricular sinuses (Chapter 37), branchial fistulas (Chapter 43), tracheo-oesophageal fistulas (Chapter 50) and
arteriovenous fistulas (Chapter 15). The acquired forms often follow inadequate drainage of an abscess. Thus, a
perianal abscess may burst on the surface and lead to a sinus (erroneously termed a blind external ‘fistula’). In other
cases, the abscess opens both into the anal canal and on to the surface of the perineal stem resulting in a true fistulain-ano (Chapter 61). Acquired arteriovenous fistulas are caused by trauma or operation (for renal dialysis).
Persistence of a sinus or fistula
The reason for this will be found among the following:
• a foreign body or necrotic tissue is present, e.g. a suture, hairs, a sequestrum, a faecolith or even a worm (see
below);
• inefficient or nondependent drainage: long, narrow, tortuous track predisposes to inefficient drainage;
• unrelieved obstruction of the lumen of a viscus or tube distal to the fistula;
• high pressure, such as occurs in fistula-in-ano due to the normal contractions of the sphincter which force faecal
material through the fistula;
• the walls have become lined with epithelium or endothelium (arteriovenous fistula);
• dense fibrosis prevents contraction and healing;
• type of infection, e.g. tuberculosis or actinomycosis;
• the presence of malignant disease
• ischaemia;
• drugs, e.g. steroids, cytotoxics;
• malnutrition;
• interference, e.g. artefacta;
• irradiation, e.g. rectovaginal fistula after treatment for a carcinoma of the cervix;
• Crohn’s disease;
•high-output fistula, e.g. duodenocutaneous fistula.
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Treatment
.
The remedy depends upon e removal or specific treatment of the cause
(see appropriate pages).
Guinea worm (syn. dragon worm, Dracunculusmedinensis) (Fig. 12.19)
This is a cause of a persisting sinus on the lower leg. The larval form
enters through the wall of the stomach or duodenum in drinking water
contaminated by a tiny cyclops crustacean which has consumed the
larvae. Settling in the abdominal connective tissue, the male and female
mate, the pregnancy lasting about a year, and the female wanders in the
subcutaneous tissues to select for egg laying a part of the anatomy likely
to be submerged in water (containing the cyclops), usually the lower leg.
Cellulitis, abscesses, ulcers and sinuses follow, through which the embryos
are discharged, hopefully to be eaten by the cyclops. Baid travelled the
interior of India and in 500 cases discerned a syndrome of the infestation,
presenting with conjunctivitis (allergic) in 11 per cent, fibrous contracture
of joints in 19 per cent, periostitis with osteomyelitis in 21 per cent and
acute arthritis in 65per cent.
Wound Healing :
In human regeneration is limited to epithelium and the liver; most
tissues heal by repair resulting in scarring. Wound healing is the
summation of a number of processes which follow injury including
coagulation, inflammation, matrix synthesis and deposition,
angiogenesis, fibroplasia, epithelialisation, contraction,
remodelling and scar maturation . Where wound edges are apposed
healing proceeds rapidly to closure; this is known as healing by
first intention or primary healing . Where the wound edges are
apart, such as when there has been tissue loss, the same biological
processes occur, but rapid closure is not possible. Angiogenesis
and fibroblast proliferation result in the formation of granulation
tissue. This contracts to reduce wound area and allows
epithelialisation across its surface to achieve wound closure. This
is known as healing by second intention . This process is slower,
the contraction involved may cause contracture and functional
restriction ,and the resultant healed surface is a thin layer of
epithelium on scar tissue that may not prove durable in the long
term. In general, healing by second intention will give a worse
aesthetic outcome. It is because of the poor functional and
aesthetic results of healing by second intention that surgical
endeavour is usually directed towards achieving primary wound
healing.
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Wound excision
The most important step in the management of any untidy
wound is wound excision. This process is sometimes
called ‘wound toilet’ or ‘debridement’. The former implies
washing and the latter laying open or fasciotomy, all of
which may be important in wound management but do
not describe excision of devitalised tissue which is the
most important process. For this reason the term ‘wound
excision’ is preferred. In order to excise a wound
adequate anaesthesia — local, regional or general must
be provided. Where possible a bloodless field also aids
identification of structures. For superficial wounds the
use of local anaesthetic with 1 in 200 000 adrenaline
gives good haemostasis of skin edges. In the limbs a
pneumatic tourniquet is used. It is helpful to use a skin
marking pen to plan the skin excision and any wound
extensions. Excision should proceed in a systematic
fashion dealing with each tissue layer in turn, usually
starting superficial and moving deep.
Longitudinal structures such as blood vessels, nerves and
tendons are identified and exposed, but left in continuity.
With experience the surgeon learns to recognise dead
tissues. Devitalised dermis is pink rather than white;
devitalised fat is pink rather than yellow; devitalised
muscle is a dark colour, has lost its usual sheen and
turgor, and does not twitch when picked up with forceps.
Bone fragments with no soft-tissue attachment or non-vital
soft tissue attachments are also discarded. This approach
to radical wound excision is sometimes called a
‘pseudotumour’ approach, because the entire wound is
excised with an appropriate margin back to healthy tissue .
At the end of wound excision the wound should resemble
an anatomical dissection. Normal bleeding should be
observed from each layer. Occasionally in very extensive
wounds this radical approach must be modified. Where
radical wound excision would threaten the viability or
function of the limb it is reasonable to excise what is
definitely nonviable, carry out fasciotomy as appropriate
and dress the wound, with a view to returning 48 hours
later for a second look, and thereafter further serial wound
excisions until a tidy wound is achieved.
Wound closure :
Wound closure can be achieved by number of
differing techniques. Most tidy wounds that do not
involve loss of tissue can be closed directly.
Where there is tissue loss a technique to import
appropriate tissue is needed. Reconstructive
plastic surgical techniques can range from simple
skin grafts to complex composite free tissue
transfers . This list used to be described as a
‘reconstructive ladder’; unfortunately this implies
that the correct approach is to use the simplest
technique and only when it fails move to a more
complex technique. This approach is not
appropriate in modern surgical practice. The
available techniques should be regarded as a
‘toolbox’ from which to select the technique that
provides most rapid healing, earliest return to
function and superior aesthetic outcome.
Scars
The most superficial wounds such as superficial burns and abrasions will heal
by epithelialisation alone without scar formation. In these circumstances
adnexal structures are preserved and the epithelium regenerates from these
structures. This may leave alterations in keratinisation, texture or
pigmentation of the healed area, but not scarring as such.
A scar is the inevitable consequence of wound repair. The final phase of wound
repair is the process of remodelling and scar maturation . The fibroblasts,
capillaries, glycosaminoglycans, and immature collagen of granulation tissue
and the newly healed wound are replaced by relatively acellular, avascular
scar tissue composed of mature collagen with scattered fibroblasts. This
biological process is manifested by a change in appearance of the scar from
a red, raised, firm, contracting, perhaps itchy nodule to a pale, flat, softer,
static, symptomless plaque of mature scar. The rate at which any given scar
passes through this process can vary widely depending on the age of the
individual, the site of the wound, the time the wound took to heal, the
direction of the scar and the tension across it . In general, scars in younger
patients with wounds on the trunk that heal slowly, perhaps with infection or
dehiscence, and scars that have a lot of tension across them will take much
longer to mature than scars in older people, in thin-skinned areas, that heal
rapidly by first intention and that have minimal tension across them . It is
important to be aware of this variation in the natural history of scar
maturation in order to counsel patients regarding the likely progress and
outcome of their scar, advise those having elective surgery what the
consequences in terms of scarring will be, and to recognise the various
types of adverse scarring which can occur. One of the most frequent types of
adverse scar, a hypertrophic scar, is one that remains red, raised, itchy and
tender for longer than might generally be expected.
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Adverse scar
There are many types of adverse scar (Table 3.3), many of which can be
avoided or prevented by correct incision planning and adequate wound
management. Some types, however, cannot be prevented and are
unpredictable in their occurrence. The appearance of some scars can be
improved by surgical or other means, but scars can never be removed
totally. The types of adverse scar will be discussed and suggestions for
avoidance or management made.
Wrong direction
Incisions that pass along ideal lines are more likely to leave acceptable
scars. There are many types of ‘lines of election’ for incisions, most of
which pass along skin wrinkles or along relaxed skin tension lines (that is
a line along which maximal skin tension passes when the part is in a
relaxed position). These lines have minimal tension across the wound
edges. A scar which crosses these lines will have a greater tendency to
stretch or become hypertrophic, and even if not hypertrophic will usually
appear more conspicuous than one which follows a relaxed skin tension
line. Other ideal positions for scars are at junctions between anatomical
areas such as the nose and the cheek, the cheek and the ear or the
junction between a hairy and hairless area
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Poor alignment of features
Where a scar crosses the junction between distinct anatomical features, such as the
vermillion of the lip, it is essential that these features are accurately realigned. Such
misalignments result in conspicuous adverse scars.
Stretched scar
Scars from excisional wounds on the trunk and limbs often stretch. It has been
shown that the width of a scar depends on the tension across the wound at the time
of wound closure. In general, steps to avoid excessive tension across the wound will
be rewarded with narrower scars. Where tension cannot be avoided there is evidence
that prolonged wound support with buried nonabsorbable or long-term absorbable
sutures can minimise scar stretching.
Contracted scar
The process of wound contraction continues in the remodeling phase of scar
maturation such that a scar will always be shorter than the incision from which it
results. Where a linear scar crosses a flexor surface this shortening may result in a
scar contracture which may prevent full extension of that part. This will occur on the
flexor surface of a finger if a straight-line incision is used. Curved or zigzag incisions
will avoid this problem. Where scarring is extensive such as burn scars then scar
contractures may be inevitable. Linear scar contractures can be corrected by
realignment of the scar; there are various techniques to do this including Z-plasty
and multiple Y—Vplasty. More extensive contractures will require release and
introduction of additional skin by means of grafts or flaps.
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Pigment alteration
The new epidermis of a scar will often not have the same degree
of pigmentation as surrounding unscarred areas. Most scars are
hypopigmented, but hyperpigmentation can also occur. The only
ways to deal with this problem are cosmetic camouflage or
tattooing. Contour deformity
Where wound edges are not anatomically aligned in the vertical
plane or where a bevelled cut is not repaired accurately there is a
risk of contour irregularity in the healed scar. This can usually be
avoided by accurate wound repair, if necessary excising bevelled
edges to restore even vertical edges for repair. A variation of this
problem occurs when a curved laceration heals, in that the scar
shortens and that portion of skin within the concavity of the
curved scar tends to become raised. This problem is known as
trapdooring or mushrooming. It will often improve with time, but
scar revision is sometimes indicated to correct it.
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Tattooing
In traumatic wounds it is possible for particles of grit, dirt or soot
to become implanted in the wound as it heals. Thisresults in
tattooed scars where the particles of foreign material show
through as blue or black discoloration of the scar. Adequate
primary wound management can avoid this. Abrasions with
ingrained dirt should be scrubbed with a stiff brush; more deeply
tattooed wounds should be excised. Late correction of tattooed
scars can be very difficult.
Stitch marks
If skin sutures are left in place for more than 7 days then scars
from the stitch marks will usually result. This problem can be
avoided by using subcuticular sutures wherever possible,
removing skin sutures before 7 days and, where prolonged wound
support is needed, supplementing skin sutures with subcuticular
sutures allowing early removal of the skin sutures. Adverse scars
due to prominent stitch marks can rarely be improved by scar
revision.
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Hypertrophic scars
In some circumstances scars remain in the remodelling phase for longer than is
usual. These hypertrophic scars are more cellular and more vascular than mature
scars, there is increased collagen production and collagen breakdown, but the
balance is such that excess collagen is produced. Clinically these scars are red,
raised, itchy and tender (Fig. 3.14). Such scars will eventually mature to become
pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic
scars from keloid scars. Hypertrophic scars typically occur in wounds where healing
was delayed, perhaps where complications such as infection or dehiscence occurred.
They are more common in children and where skin tension is high such as the tip of
the shoulder or any scar that runs across relaxed skin tension lines.
The risk of developing a hypertrophic scar can be minimised by ensuring quiet
primary healing. Where hypertrophy does occur patience is usually rewarded by
improvement with time. Massage of the scar with moisturising cream or the
application of pressure to the remodelling scar can accelerate the natural process of
maturation. Patients with hypertrophic bum scars are supplied with custom made
Lycra pressure garments that promote acceleration of scar maturation. Revision of
hypertrophic scars is appropriate where they cross skin tension lines or where a
specific wound healing complication occurred. In the absence of these factors scar
revision should be avoided as it will usually be met with recurrence.
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Keloid scars
In some situations there is an extreme overgrowth of scar tissue
that grows beyond the limits of the original wound and shows no
tendency to resolve. Keloid scars are biologically identical to
hypertrophic scars that fn turn are an extension of normal scar
behaviour. Whilst it is usually possible to make the distinction
between these scar types, they are best regarded as a spectrum
of scar behaviour (Table 3.4). Keloid scars are more frequent in
Afro-Caribbean and oriental racial groups (Fig. 3.15).They often
occur in wounds that healed perfectlywithout complications. They
are more common in certain sites such as the central chest, the
back and shoulders and the ear-lobes. Many keloid scars are
untreatable and surgical treatment as a single modality will
usually be met with recurrence. Some keloid scars will improve
with the application of pressure. Intralesional injections of steroids
such as triamcinolone can be helpful. The best cure rates are
achieved with a combination of surgery and postoperative
interstitial radiotherapy.