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116
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mg/kg initial infusion then 5 mg/kg per hour. Fibrinogen
and prothrombin complex concentrate (PCC) transfusion
avoids packed cell and platelet transfusions significantly.
Cryoprecipitate and recombinant activated factor VIIa are
also beneficial.
Fluid and electrolyte management, sepsis control (antibi-
otics).
Further monitoring by hourly urine output, hemodynamic
stability, respiration, and estimation of lactic acid, base deficit,
fibrinogen, platelet, prothrombin INR, APTT, haematocrit,
arterial blood gas (ABG), liver and renal functions. Chest
ray may be required to check the lungs.
SRB's Manual of Surgery
Note:
• Blood transfusion is required if Hb% is <8 g%.
• One unit of blood should raise 1 g% of haemoglobin.
• On table management of bleeding during surgery: (HELP)—Haemostasis
(pressure, packing); Exposure (of the bleeding area by proper dissection or extension of incision or conversion into open in laparoscopy
if needed);
Precisely act to control bleeding (by bipolar or clips or suture or glue);
.
B
x Confirm shock, hypovolaemia and haemorrhage by clinical
assessment
x Immediate resuscitation by blood, oxygen, fluid
x Identify site of haemorrhage—ultrasound, endoscopy, CT scan,
diagnostic peritoneal lavage (DPL), blood tools
x Control of haemorrhage—surgery, endoscopic control, thera-
peutic embolisation
x Definitive treatment if any
x Sepsis control
x Prevention of coagulopathy by FFP, platelet concentrate, fresh
blood
x Critical care management
x End point resuscitation, fluid and electrolyte management, preven-
tion of organ failure
B
x Gelatin sponge (Gel foam), Oxidised cellulose (Surgicel)
x Collagen sponge (Helistat)
x Microfibrillar collagen powdeer (Avitene)
x Topical thrombin, Gelatin matrices (Floseal)
x Bone wax (derived from bees wax + almond oil)
x Topical EACA, topical cryoprecipitate
ocalize (the bleeding point specifically and accurately);
X
B C
Gel foam (gelatin sponge) is a good haemostatic
agent on oozing surface like gallbladder bed after cholecystectomy.
Oxidised regenerated cellulose is very good local
haemostatic agent; but it is much costlier than gelatin sopnge.
Acute blood loss following trauma, >15% of total body volume
in otherwise healthy individuals (liver, spleen, kidney, GIT
injuries, fractures, haemothorax, perineal injuries).
During major surgeries—abdominoperineal surgery, thoracic
surgery, hepatobiliary surgery.
Following burns; In septicaemia.
As a prophylactic measure prior to surgery.
Whole blood is given in acute blood loss.
Packed cells are given in chronic anaemia.
Blood fractions are given in ITP, haemophilias.
A
Donor should be fit without any serious diseases like HIV1
and HIV2 and hepatitis infections and malaria.
Weight of donor should be more than 45 kg.
Blood is collected in a sac containing 75 mL of CPD (Citrate
phosphate dextrose) solution and stored in special refrigerators at 4 degree celcius. CPD blood lasts for 3 weeks.
Adenosine can be added to increase the storage life of the
blood up to 5 weeks; it is called as CPDA solution. Currently
SAG-M (Saline, Adenine, Glucose-Mannitol) is used to
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store packed cells which increases the shelf life to 5 weeks
in 2–6 degree C.
In storage period, RBCs lose their ability to release oxygen in
7 days even though RBCs last for 3 weeks; so blood should
be transfused within 7 days ideally. WBCs are destroyed in 2
days. Platelets and clotting factors are destroyed very early
in 1–2 days.
B
x RBC’s last for 3 weeks
x WBC’s are destroyed rapidly
x Platelets also get reduced in 24 hours
x Clotting factors are labile and so their levels fall quickly
After grouping and cross-matching, 540 mL of blood is trans-
fused in 4 hours (40 drops per minute), using a filtered drip set.
One litre of blood contains 350 mg of iron. Normal excretion of
iron is 1 mg/day. Iron overload can occur after many transfusions.
Iron excretion can be increased by desferrioxamine infusion.
1. Packed cells
¾
It is obtained by centrifuging whole blood at
2000–2300 g for 15–20 minutes.
¾
It is used in chronic anaemias, in old age, in children.
¾
It minimises the cardiac overload due to trans fusion.
¾
It can be stored for 35 days at 1°–6°C.
¾
One unit contains 300 mL with haematocrit about 70%.
One unit raises Hb% by 1.0 gram.
2. Plasma:
¾
This is obtained in the same way as packed cells by
centrifugation.
¾
It is indicated in burns, hypoalbuminaemia, severe protein
loss.
¾
It can be fractionalised into different fragments:
a. Human albumin 4.5% is obtained after repeated
fractionations and can be stored for several months
in liquid form at 4°C
b. Fresh frozen plasma (FFP)Fresh plasma obtained,
is rapidly frozen and stored at –40°C. It contains all
coagulant factors. 1 unit of FFP increases the clotting
factors levels by 3%. It can be stored for 2 years.
Rhesus D positive FFP can be transfused to Rhesus D
negative female.
Uses:
-
Severe liver disease with abnormal coa gulation
function.
-
Congenital clotting factor deficiency.
-
Deficiency following warfarin therapy, DIC, massive
transfusion.
-
To maintain prothrombin time at normal level. Dose
of FFP is 15 mL/kg.
c. CryoprecipitateWhen fresh frozen plasma is allowed to
thaw at 4°C, visible white supernatant layer develops and
is called as cryoprecipitate which is rich in Factor VIII and
fibrinogen. It is stored at minus 40°C and can be kept
for 2 years. Cryoprecipitate is used to raise fibrinogen
level at a dose to make plasma fibrinogen level 150 mg/
L. It is also used in inherited deficiency of factor VIII,
d
fibrinogen, factor XIII, von Willebrand’s disease.
d.
Fibrinogen is obtained by organic liquid fractionation
of plasma and is stored in dried form. It is very useful
in DIC and afibrinoge
naemia. It has risk of transmitting
hepatitis.
e
Factor VIII and IX concentrate: They are freeze dried
part from a large pooled plasma used in haemoplhilia
and von Willebrand’s disease.
Purified freeze dried human coagulation factor VIII
is available for use in haemophilia patients.
3.
Platelet-rich plasma: It is obtained by centrifu gation of freshly
donated blood at 150–200 g for 15–20 minutes. Platelet-rich
9
plasma contains 5.5 × 10
/L platelets in 50 mL plasma. It can
be random donor platelet or single donor platelet. Single donor
platelet is prepared by plateletapheresis containing 3 × 10
9
/L
platelets in 200 mL of plasma. One single donor platelet is
equal to 8 units of random donor platelet.
4.
Platelet concentrate:It is prepared by centrifu gation of
platelet rich plasma at 1200–1500 g for 15–20 minutes.
Used in thrombocytopaenia and drug (aspirin, clopidogrel)
induced haemorrhage. Platelet is transfused at a dose of
0.1 unit/kg, when platelet drops below 20,000/or episodes
of bleeding. Platelet stored at 4°C should be used within 48
hours; when stored at room temperature can be used up to
5 days. One platelet concentrate can increase up to 10,000
platelet/cumm in one hour.
Prothrombin complex concentrate (PCC) are derived from
5.
pooled plasma which contains factors II, IX and X; used in emergency reversal of warfarin therapy in uncontrolled haemorrhage.
A proportion of donations will have plasma removed and
will be replaced by crystalloid solution of SAG-M (Sodium
chloride; Adenine: Glucose anhydrate; Mannitol).
Features: It allows good viability of cells; very useful in
anaemias; but it is devoid of any proteins.
Precautions: For every four units of SAG-M blood, one whole
blood has to be given. Later for every two units of SAG-M
blood, one unit (400 mL) of 4.5% human albumin has to
be given. Coagulation status and platelet count should be
checked regularly.
117
CHAPTER 1H General Surgery: Haemorrhage and Blood Transfusion
Every obstacle introduces a person to himself.
118
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s
It is the most common complication due
to impurities like pyrogens in the blood or in infusion set.
Headaches, fever, chills and rigors, tachycardia, nausea
are the features. Transfusion is temporarily stopped or the
flow is slowed down with administration of antipyretic drug
to reduce fever. Often transfusion of that unit needs to be
discontinued.
Utricaria and allergy to specific proteins
in the donor’s plasma can occur. Usually it is mild and is treated
with steroid and antihistaminics. In severe utricaria that unit of
SRB's Manual of Surgery
blood is discarded; new washed RBC’s and platelets are used.
: It is the most dangerous
complication. It is due to ABO incompatibility. Usually it is
nonfatal but occasionally can be fatal. It is commonly due
to technical error at different levels. It amounts for criminal
negligence in court of law. Intravascular destruction causes
haemoglobinemia, haemoglobinuria, acute renal failure
and DIC. Dyspnoea, chest pain, sweating, fever with chills,
tachycardia, hypotension, and cardiac arrest occurs in
fatal type. Jaundice is a common feature in nonfatal type.
Free haemoglobin level in blood will be above 5 mg/d
Condition is treated as an emergency in critical care unit/
ICU. Transfusion is stopped immediately; blood sample of
recipient and transfusing blood is sent immediately for two
laboratories for rechecking. Smoky urine of the patient is
typical. Injection hydrocortisone/dexamethasone IV is given
immediately. Fluid therapy, alkalization of blood is done
using sodium lactate and sodium bicarbonate. Mannitol 20
gram in 100 mL is infused in 5 minutes; furosemide 120
mg is injected intravenously. Haemodialysis is needed if
there is renal failure. Often ventilator support, defibrillator
if cardiac arrest occurs is needed. Correction of acidosis,
electrolytes is needed.
: It is due to donor
plasma antibody against HLA and leucocyte specific antigens of
recipient. Occasionally it is due to recipient’s antibody against
donor’s leucocytes. Features are—breathlessness, saturation drop, fever, hypotension which is observed 4 hours after
transfusion. Chest X-ray shows bilateral diffuse infiltrate. They
need ventilator support for short period with eventual rapid and
complete recovery.
This
very serious, very rare complication occurs due to recognition and reaction against host tissues by infused donor
lymphocytes. It is common in immunosuppressed, lymphoma,
leucaemic patients. Any type of blood products including
leukocyte reduced blood can cause the condition. Features
are—pancytopaenia, toxic epidermal necrosis, liver dysfunction with more than 90% mortality. It is difficult to treat.
It occurs if especially large
quantities of whole blood are transfused in chronic severe
anaemia, pregnancy, elderly patients, in patients who have
cardiac problems.
E
B
x Congestive cardiac failure
x Transfusion reactions HBV, HCV
– Incompatibility: Major and minor reactions with fever, rigors,
pain, hypotension
– Pyrexial reactions due to pyrogenic ingredients in the blood
– Allergic reactions
– Sensitisation to leucocytes and platelets
– Immunological sensitisation
x Infections: Serum hepatitis, HIV, Bacterial infection, Malaria,
Barr virus/Cytomegalovirus infection, Syphilis, Yersinia,
EpsteinBabesia microti infection, Trypanosoma cruzi infection.
x Air embolism, Thrombophlebitis
x Coagulation failure due to—Dilution of clotting factors, Dissemi-
nated intravascular coagulation, Dilutional thrombocytopenia
occurs in patients with massive blood transfusion
x Circulatory overload causing heart failure
x Haemochromatosis in patients with CRF receiving repeated blood
transfusions
x Citrate intoxication causes bradycardia and hypo cal caemia. For
every four units of blood 10 m
gluconate should be infused intravenously
x Iron overload
L.
x It is defined as replacement or transfusion of blood equivalent
to patient’s blood volume in <24 hours corresponding to that
particular age (In adult it is 5–6 litres, in infants it is 85 mL/kg
body weight.) Or single trans
continuously or transfusion >4 units in one hour or replacement
of 50% of blood volume in 3 hours or rate of loss >150 mL/hour.
x Massive transfusion is used in severe trauma asso ciated with liver,
vessel, cardiac, pulmonary, pelvic injuries. Often it is required
during surgical bleeding (primary haemorrhage on table) of
major surgeries
x Adverse effects of massive transfusion
a. Severe electrolyte imbalance (hypocalcaemia, hyperkalaemia,
acidosis)
b. Coagulopathy—altered platelet and coagu lation factors—
dilutional thrombocytopaenia
c. Citrate toxicity, hyperammonaemia
d. Hypothermia
e. Poor oxygen delivery—due to reduced 2,3 DPG
f. Infections, iron overload
g. Incompatibility and transfusion reactions
h. Acute respiratory distress syndrome (ARDS), disseminated
intravascular coagulation (DIC), congestive cardiac failure (CCF)
Note:
• Autologous blood transfusion: An healthy individual with no infection
and haematocrit of >30% can predonate blood few weeks prior to any
elective surgeries, which in turn, can be used at the time of surgery.
Autologous blood is used in orthopaedic, gynaecologic and urologic
surgeries. Patient donates one unit of blood weekly; last one if at all
being 72 hours before the date of surgery.
• Recycled blood: In major surgeries if there is significant blood loss, then
patient’s bled blood is carefully sucked out through a sterile system and
is filtered and reused again to the patient. This will reduce the number
of transfusions.
L of 10% calcium chloride or
fusion of blood more than 2,500 mL
• Erythropoietin—injection 1000–3500 units preoperatively also used to
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increase the RBC count. It is used in CRF patients who are on haemodialysis. It is given twice weekly but it is costly.
cs
1. Perfluorocarbon (Fluosoleda; perfluoro decalin; Fluosol DA):
Abiotic RBC substitute as synthetic oxygen carrier with half life is
7 days with high affinity for O
. It is inert, colourless, odourless,
2
dense, poorly soluble, biocompatible liquid. It is emulsified with
albumin or lipids before infusion. Its emulsion alone injection
can cause pulmonary embolism. It can bind and release oxygen.
But as it reduces the PPO
quickly, it is a disadvantage. Patient
2
ideally to be kept in hyperbaric place. It is oily in nature hence
has to be emulsified. It releases 1.3 m
L of oxygen/100 mL. It
should be kept frozen. It can cause anaphylaxis.
2.
Stroma-free haemoglobin: Biomimetic haemoglobin based
substitute which has more affinity for oxygen as it does not
contain 2, 3 DPG but has short half life. It is nephrotoxic.
3. Chelates which reverse bound O
: It is intraoperative—
2
salvage of blood: On table blood is collected, washed, filtered
and transfused; used in major trauma.
s
1. Human albumin Hererisk of transmitting hepatitis is
absent. Plasma fractionation is done using organic liquids
and heat to extract albumin which is stored at 4°C for many
months. It can be used in patients with cirrhosis, burns,
nephrotic syndrome, ovarian hyperstimulation syndrome
(occurring after ovarian stimulation with gonadotrophin injections during in vitro fertilization (IVF) therapy). One gram of
albumin binds with 14 mL of water so it increases the blood
volume also. Albumin is infused daily as needed until good
response is observed. Albumin is expensive.
2. Dextrans are useful to improve plasma volume. They are
polysaccharides of varying molecular weights.
This is derived from Leuconostoc mesenteroides bacteria
after adding yeast. One gram of dextran binds with 20 m
water to raise the plasma volume.
a. Low molecular weight dextran (40,000 mol wt) (Dextran
40, Rheomacrodex). Dextran 40 is very effective in
restoring blood volume immediately. But small molecules
are readily excreted in kidney and so effect is transitory.
It may be useful in prevention of sludging in kidney and
hence renal shut down.
b. High molecular weight dextran (Dextran 110 and Dextran
70). It is less effective but long acting and so useful to
have prolonged effect.
¾
Blood samples for blood group and cross-matching
should be taken before giving dextrans as it interferes
with rouleaux formation of red cells.
L of
¾
Dextrans also interfere with platelet function and so may
precipitate abnormal bleeding.
¾
Total volume of dextrans should not exceed 1,000 mL.
¾
It causes hyperchloraemic acidosis and central pontine
myelinolysis.
3.
Gelatin, in a degraded form of mol wt 30,000S, is used
as a plasma expander. Up to 1000 m
L of 3.4–4% solution
containing anions and cations is given intravenously—
Haemaccel. But it is less effective than dextran and after 4
hours of its infusion, only 30% remains intravascular.
Hydroxyethyl starch: It contains starch, sodium hydroxide,
4.
ethylene oxide. It is a good plasma volume expander but lasts
only for 6 hours.
Tourner means to turn (Greek). A tourniquet is used to cut off
the blood supply to a limb temporarily so that a bloodless field
is created while performing the surgery. Limb should be exsanguinated before applying/inflating the cuff of the tourniquet. It is
done using a bandage or pressurized Rhys-Davis exsanguinator.
A tourniquet is applied in mid-thigh above the knee joint in lower
limb and in mid-biceps level above the elbow in upper limb. It
should not be closer to joints. It is not applied over the forearm
or leg. It is applied over layers of gauze or cotton, not over a bare
skin. Pressure used in upper limb is 250 mmHg; lower limb is
300 mmHg (In children, it is 150 and 250 mmHg for upper and
lower limbs respectively).
Esmarch rubber tourniquet.
Automatic gauged pressure tourniquet.
119
CHAPTER 1H General Surgery: Haemorrhage and Blood Transfusion
The very act of believing creates strength of its own.
120
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¾
Uses:
¾
To attain bloodless field in limb surgeries—upper and
lower limbs, orthopaedic surgeries, soft tissue tumours,
amputations.
¾
It is used (rubber tourniquet) to access veins for IV injections and IV sampling.
¾
Tourniquet is used in diagnostic tests for varicose veins,
purpura (ITP), carpal tunnel syndrome, tetany.
¾
It is used as a first aid in bleeding conditions of limbs,
snake bite (it is controversial).
¾
Tourniquets are often used for small procedures in fingers
and toes.
SRB's Manual of Surgery
Types:
¾
Simple red rubber catheter is used
for drawing blood, to have access to veins.
¾
Martin’s tourniquet made up of India rubber.
¾
Used in limbs, will give the arterial
pressure and also acts as a tourniquet (Sphygmomanometer cuff is simpler and easily available type).
¾
Esmarch rubber
¾
Conn pneumatic tourniquet is manually operated tourniquet where air is pumped up to the required pressure.
¾
Specialised sophisticated tourniquets are available
which gauge pressure and time accurately—automatic
tourniquet.
¾
Tourniquet time for upper limb is one hour and for lower
limb is two hours.
Contraindications:
¾
In all peripheral vascular diseases and atherosclerosis.
¾
Infection; Deep venous thrombosis.
¾
Crush injuries; Sickle cell disease.
Complications:
¾
Crushing effect on muscles in thigh occurs leading to
crush syndrome.
¾
Tourniquet palsy in upper limb (radial nerve involve-
ment)—neuropraxia.
¾
Improper application of tourniquet leads to more
bleeding.
¾
Forgetting the removal of tourniquet or taking more time
to release may compromise the blood supply of the limb
leading to severe ischaemia and gangrene. It occurs
especially when tourniquet is used in finger or toe.
¾
Infection, Skin blistering and necrosis.
Acute pancreatitis can cause DIC by releasing proteolytic
enzymes which activate prothrombin and factor X.
¾
Septic abortion, abruption, retained dead foetus, amniotic
fluid embolism are obstetric causes of DIC.
¾
Carcinoma of pancreas, prostate, acute promyelocytic
leucaemia often cause DIC.
¾
Haemolysis, snake bite, liver dysfunction are other
causes.
Types of DIC:
¾
Acute DIC presents with bleeding in gums, GIT, venepunc-
ture site, haematuria, petechiae, oozing from surgical or
traumatic wounds. Massive bleeding also can occur.
¾
Chronic DIC is a low grade type with thrombotic features.
Investigations:
¾
In DIC—bleeding time, platelet counts are reduced.
Thrombin time (TT), prothrombin time (PT) and activated
partial thromboplastin time (APTT) are prolonged. Fibrinogen degradation product (FDP), D-dimer test are raised.
¾
Complete haematocrit, investigations relevant to cause,
renal function tests, LFT, electrolyte estimation, blood/
discharge/pus/urine culture.
Treatment of DIC:
¾
Treatment of specific cause as per protocol. Correction
of haemodynamic instability by fluid therapy, transfusion
of packed cells or whole blood. Dopamine/dobutamine
therapy.
¾
Factor replacement—specific therapy for DIC—FFP, cryo-
precipitate, platelet concentrate transfusions are essential. FFP is given at a dose of 15 mL/kg. Cryoprecipitate
is used to raise fibrinogen level at a dose to make plasma
fibrinogen level 150 mg/dL. Platelet is transfused at a
dose of 0.1 unit/kg, when platelet drops below 20,000/
or with episodes of bleeding.
¾
Heparin use is often controversial. It is used mainly in
chronic DIC, DIC with purpura, DIC of obstetric cause,
cancer induced DIC, DIC due to acute antiphospholipid
antibody syndrome.
¾
EACA, tranexamic acid can be used but with questionable benefits.
Disseminated intravascular coagulation (DIC) is a manifestation
due to widespread intravascular coagulation resulting in microthrombi formation, consumption of platelets and clotting factors
and production of breakdown products eventually leading into
severe bleeding and tissue ischaemia.
Causes:
¾
Major trauma causes DIC due to release of tissue thromboplastin. Burns, major surgery can also cause DIC.
¾
Sepsis is the most common cause of DIC. Common
sepsis causing DIC are gram-negative, meningococcal,
malarial, histoplasmosis, aspergillosis, etc.
Haemostasis is the spontaneous arrest of bleeding. When an
injury occurs platelet adhesion occurs to injured vessel/capillary
wall which activate the release of ADP (Adenosine diphosphate)
which makes more platelet to aggregate (platelet aggregation).
These activated platelets release thromboxane A2 which further
increases the adhesion and aggregation of platelets. Circulating
fibrinogen binds to an activated platelet receptors glycoprotein
IIb and IIIa and fibrinogen gets converted into fibrin.
Clotting factors are proteins synthesised by the liver which
with a series of cascade reaction activates clotting factors and
achieves blood coagulation by a complex mechanism. Factor
II, VII, IX and X are vitamin K dependent for their synthesis
T
Plasma thromboplastin component (PTC; Christmas
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in liver (carboxylation of glutamic acid). In the process of
coagulation each factor gets activated to an enzyme by partial
proteolysis, which in turn, activates other needed coagulation
factors. Eventually fibrinogen gets converted into soluble fibrin
and later into insoluble fibrin.
Two types coagulation system are there:
Intrinsic pathway
Extrinsic pathway
In vitro coagulation occurs by intrinsic coagulation system.
Cascade gets activated by vessel wall injury, shear stress of
vessel or other factors. It activates the cascade to get final result.
cs
Factor
No.
Common name
I Fibrinogen
II Prothrombin
III Thromboplastin
IV Ionic calcium
V Hereditary labile factor, activator (AC) globulin,
proaccelerin
VI Accelerin, supposed to be active form of factor V
VII Proconvertin; serum prothrombin-conversion
accelerator (SPCA)
VIII Antihemophilic factor (AHF)
IX
factor)
X Stuart-Prower factor
XI Plasma thromboplastin antecedent (PTA)
Hageman factor
XII
Fibrin stabilizing factor, fibrinase
XIII
Prekallikrein
XIV
Kallikrein
XV
Platelet factor
XVI
121
CHAPTER 1H General Surgery: Haemorrhage and Blood Transfusion
They are the two most common inherited bleeding disorders
due to deficiency of factor VIII.
Factor VIII has two components; smaller one—factor VIII
C is needed for activation of factor X in intrinsic coagulation pathway; its deficiency leads to classic haemophilia. It
is inherited as an X-linked recessive trait, thus it occurs in
males and homozygous females. The larger component of
factor VIII called von Willebrand’s factor, facilitates the adhesion of platelets to subendothelial collagen, hence crucial for
haemostasis, its absence leads to von Willebrand’s disease.
is called haemophilia A is caused by
deficiency of factor VIII C with X linked recessive trait. It occurs
in males or homozygous females. Recurrent haemarthroses is
a common presentation. Petechiae and echymoses are absent.
Bleeding time is normal but coagulation time is prolonged.
Treatment is replacement of factor VIII haemophilic factor. If
not known patient may go for a life-threatening bleeding even
after dental extraction.
is deficiency of larger component
(99%) of the factor VIII-vWF. It is an autosomal dominant
disease with normal bleeding time and normal platelet count.
Common presentations are spontaneous bleeding from mucous
membrane, excessive bleeding from wounds and severe
menorrhagia. Haemarthroses is not common in von Willebrand’s disease. Treatment is replacement of specific factors.
also called as Christmas disease is due to
factor IX deficiency is inherited as X linked autosomal recessive trait.
Our greatest glory is not in never falling, but in rising every time we fall.
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C hapter Outline
·
Burns
·
Management of Burns
·
Eschar
·
Contracture in Burn
Wound
BURNS
TYPES OF BURNS
B
x Thermal injury
– Scald—spillage of hot liquids
– Flame burns
– Flash burns due to exposure of natural gas, alcohol, combus-
tible liquids
– Contact burns—contact with hot metals/objects/materials
x Electrical injury
x Chemical burns—acid/alkali
x Cold injury—frost bite
x Ionising radiation
x Sun burns
Depending on the Percentage of Burns (Burn Severity
Classication)
Mild (Minor):
Partial thickness burns <15% in adult or <10% in children.
Full thickness burns less than 2%.
Can be treated on outpatient basis.
Moderate:
Second degree of 15–25% burns (10–20% in children).
Third degree between 2–10% burns.
·
Electrical Burns
·
Inhalation Injury
·
Chemical Burns
Burns which are not involving eyes, ears, face, hand, feet,
perineum.
Major (severe):
Second degree burns more than 25% in adults, in children
more than 20%.
All third degree burns of 10% or more.
Burns involving eyes, ears, feet, hands, perineum.
All inhalation and electrical burns.
Burns with fractures or major mechanical trauma.
I. Depending on thickness of skin involved
a. First degree: Here the epidermis looks red and painful, no
blisters, heals rapidly in 5–7 days by epithelia lisation without
scarring. It shows capillary filling.
b. Second degree: The affected area is mottled, red, painful,
with blisters, heals by epithelialisation in 14–21 days.
¾
Superficial second degree burn heals, causing pigmenta-
tion.
¾
Deep second degree burn heals by causing scarring, and
pigmentation. Sensation is present but no blanching.
c. Third degree: The affected area is charred, parch ment like,
painless and insensitive, with thrombosis of superficial
vessels. It requires grafting. Charred, denatured, insensi-
tive, contracted full thickness burn is called as
These wound must heal by re-epithelialisation from wound
edge.
d. Fourth degree: Involves the underlying tissues—muscles,
bones.
II. Depending on thickness of skin involved
a.
Partial thickness burns: It is either first or second degree
burn which is red and painful, often with blisters.
b. Full thickness burns: It is third degree burns which is
charred, insensitive, deep involving all layers of the skin.
T
Head and neck 9% 18% 20%
Front of chest and abdominal wall 9 × 2 = 18% 18% 10 × 2 = 20%
Back of chest and abdominal wall 9 × 2 = 18% 18% 10 × 2 = 20%
Lower limb 18 × 2 = 36% 13.5 × 2 = 27% 10 × 2 = 20%
Upper limb 9 × 2 = 18% 18% 10 × 2 = 20%
Perineum 01% 01%
Note: It is head and lower limb percentage which differ in adults and children.
Adults Children Infants
Degrees of burns.
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123
CHAPTER 1I General Surgery: Burns
First and second degree burn.
A B
Percentage of burns in (A) Adults; (B) Children
(Wallace’s rule of 9).
B
x Wallace’s rule of nine is used for early assessment—refer Figures
1.219A and B.
x Using the Lund and Browder chart is better method for assessing
the burns wound. Here each part of the body is individually
assessed for involvement of burns.
x Patient’s entire hand area is 1%. Clean piece of paper is cut to the
size of hand and through that percentage of burns is assessed.
44°C temperature takes 6 hours to cause deep burns. 65°C takes
45–60 seconds to cause deep full thickness burn.
Burn is a dynamic wound and so assessment should be repeated
at regular intervals.
Second degree burns with blisters.
Extensive third degree burns with eschar.
Extensive burns more than 50%.
Action, to be effective, must be directed to clearly conceived ends.
124
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Altered pulmonary resistance causing pulmonary oedema
↓
Infection
↓
Systemic inflammatory response syndrome (SIRS)
↓
Multiorgan dysfunction syndrome (MODS).
There is increased capillary permeability, decreased plasma
oncotic pressure causing loss of protein and fluid from intravascular space. Vasoconstriction occurs due to raised capillary
hydrostatic pressure leading into cellular aggregation. Blockage
SRB's Manual of Surgery
Third degree burns with charred skin, with thrombosed
veins and eschar.
of lymphatics causes poor clearance of fluid and proteins from
interstitial spaces. Cell membrane function is impaired causing
intracellular fluid accumulation. Activation and release of various
complement factors, histamine, and prostaglandins results in
myocardial dysfunction, oedema of tissues, reduced immunoglobulin synthesis. Catecholamine levels are raised drastically in
patient with burn. There will be lipolysis, proteolysis, increased
release of glutamine and alanine from skeletal muscles. Urea
production is increased due to more proteolysis.
Face burns in an adult—severe third degree.
History of burn.
Pain, burning, anxious status, tachycardia, tachypnoea, fluid
loss.
In severe degrees features of shock.
Tolerable temperature to human skin is 40°C for brief period.
Heat causes coagulation necrosis of skin and subcutaneous tissue
↓
Release of vasoactive peptides
↓
Altered capillary permeability
↓
Loss of fluid →
↓
Decreased cardiac → Decreased myocardial
output function
↓
Decreased renal blood → Oliguria
flow (Renal failure)
Burn zones (Jackson's).
vein the body is due to altered pressure gradient
because of the injury to basement membrane.
is due to:
Hypovolaemia.
Release of cardiac depressants.
Hormonal causes like catecholamines, vasopressin, angio-
tensins.
are due to:
Release of ADH from posterior pituitary to cause maximum
water reabsorption.
Release of aldosterone from adrenals to cause maximum
sodium reabsorption.
Toxins released from the wound along with sepsis causes
acute tubular necrosis.
Myoglobin released from muscles (in case of electric injury
or often from eschar) is most injurious to kidneys.
are due to:
Altered ventilation-perfusion ratio.
Pulmonary oedema due to burn injury, fluid overload, inhala-
tion injury.
ARDS; Aspiration; Septicaemia.
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B
BURNS
x Occurs in burns around face and neck, or trapped in burning room
x Presents with hoarseness or stridor
x Inhaled burning gases can cause upper airway burns and laryn-
geal oedema
x Smoke inhalation can cause chemical alveolitis, pulmonary
oedema, ARDS and respiratory failure
x Steam inhalation can cause damage to respiratory epithelium and
subglottic oedema
x Carbon monoxide inhalation more than 10% is dangerous as it
forms carboxyhaemoglobin (CO has got 240 times more affinity
to haemoglobin than oxygen) which blocks oxygen transport
completely causing respiratory arrest, hypoxia and metabolic
acidosis
x Chest wall burn causes mechanical block of ventilation—needs
escharotomy in chest wall and the procedure is painless
x Airway burn may require early elective intubation or tracheostomy
or emergency cricothyroidotomy as a life-saving method
are due to:
Acute gastric dilatation which occurs in 2–4 days.
Paralytic ileus, Curling’s ulcer (due to decreased mucosal
defence; not due to increased HCl).
Cholestasis and hepatic damage; Acute acalculous cholecy-
stitis, acute pancreatitis can occur.
Bowel mucosal ischaemia causes poor motility, reduced
food digestion and absorption with increased translocation of
bacteria causing peritoneal oedema, septicaemia and abdominal
compartment syndrome.
Hypermetabolic rate (BMR).
Negative nitrogen balance; Electrolyte imbalance.
Deficiencies of vitamins and essential elements.
Metabolic acidosis due to hypoxia and lactic acid.
BP
Focus may be at the burn site, catheter site, cannula/CVP line
site, or respiratory infection.
Low immunity, loss of proteins and immunoglobulins, loss of
barrier causes sepsis. Opportunistic infection is also common.
Associated conditions like diabetes, HIV infection, old age,
respiratory diseases worsen the sepsis in burn injury.
It may be local infection commonly by Staphylococcus aureus
in early period, Pseudomonas, Candida, Aspergillus, herpes
simplex virus in partial thickness nasolabial burns. It may be
suppurative thrombophlebitis also.
Systemic infection like pneumonia, bacteraemia, septicaemia
can occur.
Burns itself creates immunosuppression (cell-mediated
immunity).
Sepsis is identified by fever, lethargy, leucocytosis, throm-
bocytopenia.
B
x Streptococci (Beta haemolytic—most common)
x Pseudomonas
x Staphylococci
x Other gram-negative organisms
x Candida albicans
Burns over chest wall with eschar.
Note the extent of involvement.
Shock due to hypovolaemia—15% of burns causes shock.
Renal failure.
Pulmonary oedema, respiratory infection, adult respiratory
distress syndrome (ARDS), respiratory failure.
Infection by Staphylococcus aureus, beta hae mo lytic Strep-
tococcus, Pseudomonas, Klebsiella leads to bacteraemia,
septicaemia. Fungal and viral infections of dangerous types
can also occur.
GIT: Hypovolaemia, ischaemia of mucosa, erosive gastritis—
Fluid and electrolyte imbalance.
Postburn immunosuppression predisposes to severe oppor-
tunistic infection.
Eschar formation and its problems like defective circulation,
ischaemia when it is circumferential.
Electrical injuries often cause fractures, major internal organ
injury, convulsions.
Development of contracture is a late problem. It leads to
ectropion, microstomia, disability of different joints, defective hand functions, growth retardation causing shortening.
Inhalation burn causes pulmonary oedema, respiratory
arrest, ARDS.
Chemical injury causes severe GIT disturbances like erosions,
perforation, stricture oesopha gus (alkali), pyloric stenosis
(), mediastinal injury.
Other problems commonly seen are DVT, pulmonary embo-
lism, urinary infection, bed-sores, severe malnutrition with
catabolic status, respiratory infection.
125
CHAPTER 1I General Surgery: Burns
Success lies not in achieving what you aim at, but in aiming at what you ought to achieve.
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