Surgical Site infection

1. Definition
- infection related to operative procedures occurring within one month of non-implant surgery or
within one year of implant surgery.

2. Duration
- Acute SSI (<30days): overt inflammatory process redness, pain, purulent drainage, fever and
spontaneous dehiscence
- Chronic SSI (>30days): delayed healing, formation of new sinus or fistula, persistent wound
drainage, infected prosthetic implant

3. Type of surgery
a. Clean surgery
- surgery without break in sterile technique and without breaching into any of the four system/
tracts: GI, GU, hepatobiliary & respiratory : mastectomy, thyroidectomy

b. Clean contaminated surgery

- surgery with entrance into any of the four system under controlled condition and no major break
in sterile technique encountered: appendicectomy

c. Contaminated surgery
- surgery with major break of sterile technique or gross spillage from any of the four tracts/ system.
-
d. Dirty surgery
- surgery done to existing extensive spillage of any of the four tracts, organisms causing post-op
infection present prior to surgery.

4. Clean surgery that requires prophylactic antibiotics

- Procedures with synthetic mesh or implant: hernioplasty, prosthetic joint (TKR)

- Thoracic and cardiac surgeries: pulmonary resection, valve replacement
- Neurosurgical procedures: craniotomy, shunt procedures.
- Modified radical mastectomy and axillary clearance
Acute Appendicitis
1. Clinical features
- right iliac fossa pain (typical is migratory RIF pain, initially from periumbilical/ epigastric
- vomitting/ nausea, reduced oral intake (usually pain started first)
- diarrhea/ constipationg
- Fever
- laboratory: raised white cells
ALVARADO scoring

2. Stages of appendicitis
Early: appendicial lumen obstruction leads to mucosal edema, bacterial diapedesis, clinically,
visceral pain at periumbilical area (poorly localised) due to distention and stretching of visceral
peritoneum.

Suppurative: increasing intraluminal pressure exceeded capillary perfusion, causes transmural

bacterial translocation, leading to serosal inflammation. Clinically, more well localised RIF pain is
felt due to inflamed serosa stimulate somatic nerve of parietal peritoneum

Gangrenous: Reduced capillary perfusion and venous drainage as a result of increasing intraluminal
pressure.

Perforated: Persistent appendiceal ischaemia causes perforation. Can be localised or generalised

peritonitis. Localised guarding and persistent tenderness. Generalised guarding if generalised
peritonitis.

Appendicular mass: Appendiceal phlegmon/ abscess, appendicular tumour

3. Management
a. Conservative management
• Indication:
- Non-complicated acute appendicitis: no appendicular abscess/ perforation/ mass with clinical
improvement.
- As a temporary treatment before interval or delayed appendicectomy: appendicular phlegmon or
perforated localised peritonitis with mild symptoms
• Antibiotics used :
- Cefuroxime/ Cefobid + Metronidazole

b. Operative management
- Laparoscopic appendicectomy
Procedures:
Infraumbilical small incision made under direct vision, 10mm port inserted. Peritoneal insufflation
with CO2 (airflow velocity 5-6L/min, pressure 10-12mmHg).
2 working ports of 5mm inserted at suprapubic and LIF.
Tracking down the caecum to look for appendix. Appendix ligated with with 2 laparotie, appendix
cut in between.
Follow through small bowel to look for Meckel’s diverticulum
- Open appendicectomy
Acute cholecystitis
-Inflammation of GB
1. Clinical fetaures/diagnostic criteria (TG18)
- Local inflammation: Murphy’s sign, RUQ pain
- systemic inflammation: fever, raised TWC/ CRP
- Imaging evidence of cholecystitis: thickening of GB wall (>5mm), GB distension/ enlargement,
GB sludge/ calculi, pericholecystic fluid, ultrasonographic Murphy’s sign, gas imaging

2. Severity Assessment (TG18)

Grade I/ Mild - cholecystitis in healthy patient with no organ dysfunction and mild inflammatory
changes, thus cholecystectomy is safe and low risk procedure

Grade II/ Moderate - elevated TWC (>18), palpable tender mass RUQ, duration from onset >72
hours, marked local inflammation

Grade III/ Severe - dysfunction of any of the organs (cardiovascular, neurological, respiratory, renal,
hepatic and haematological )

3. Management
Grade I -
Early lap. cholecystectomy is the first line. conservative management (antibiotics and supportive
care) if not fit for surgery.

Grade II -
Early lap (within 7 days) if successful antibiotics and general supportive care & fit for surgery

Delayed/ elective cholecystectomy if antibiotics and general supportive care able effective but pt
less fit for surgery.

Urgent GB drainage with PTBD if antibiotics and general supportive care not successful.

Grade III/ Severe -

Render best supportive care for organ dysfunction: ventilation, vasopressors etc
Immediate PTBD followed by delayed cholecystectomy

Stages of Cholecystitis
▪ Stage 1 (edematous)
▪ 2-4 days
▪ Gallbladder tissue intact with edema in subserosal layer
 ▪ Interstitial fluid with dilated capillaries and lymphatics
▪ Stage 2 (necrotizing)
▪ 3-5 days
▪ Edematous with areas of hemorrhage and necrosis due to elevated internal pressures
compromising blood flow
▪ Stage 3 (suppurative)
▪ 7-10 days
▪ Active inflammatory processes
▪ WBCs at necrotic and suppurative areas in wall
▪ Fibrous wall thickening
▪ Intramural abscesses
▪ Stage 4 (chronic)
▪ After repeated episodes of cholecystitis
▪ Mucosal atrophy
▪ Wall fibrosis
▪ PMN/lymphocyte/plasma cell infiltration
▪ Acute on chronic cholecystitis (chronic irritation by stones)

Subtype
1. Calculous
- 90% , caused by cystic duct obstruction by gallstone, then causing distension and inflammation of
GB.
2. Acalculous
- risk: bile stasis and reduced GB perfusion: sepsis, prolonged fasting, severe burn, infection
3. Emphysematous
- rare but life-threatening form of cholecystitis with air within gallbladder caused by gas-forming
bacteria: clostridium/ E.coli. U/S hyper echoic gas shadow within gallbladder wall and lumen.
Acute Cholangitis
1. Clinical features/diagnostic criteria (TG18)
- Systemic inflammation: fever, raised TWC/ CRP
- Cholestasis: jaundice, deranged LFT: raised ALP, r-GTP, AST & ALT
- Imaging: biliary dilatation & ethology on imaging (stricture, stone and stent)

2. Severity & management

Grade I Mild acute cholangitis Antibiotics & general supportive care.
Grade II Antibiotics & general supportive care.
2 of the followings Early biliary drainage: ERCP and stenting.
- abnormal WBC count
- High fever Perform pre-antibiotic bile or blood C&S.
- Age >75 Treating etiology with endoscopic,
- Hyperbilirubinemia (total bilirubin > 5mg/dl) percutaneous or operative intervention once
- Hypoalbuminemia acute illness resolved.
Grade III Antibiotics & general supportive care.
- acute cholangitis that is associated with onset Urgent biliary drainage: ERCP and stenting.
of dysfunction in at least one of the following
organ/system: Intensive organ support: inotrope, ventilators
- Cardiovascular dysfunction: hypotension etc.
- Neurological dysfunction: disturbed Perform pre-antibiotic bile or blood C&S.
consciousness
- Respiratory dysfunction Treating etiology with endoscopic,
- Renal dysfunction: oliguria, serum creatinine percutaneous or operative intervention once
>2mg/dL acute illness resolved.
- Hepatic dysfunction: INR>1.5
- Hematological dysfunction: Plt < 100 000/
mm3

Biliary colic Acute cholecystitis Acute cholangitis

- a symptom characterised by
right hypochondriac or
epigastric intermittent pain
- no sign of inflammation: no
fever
- liver enzymes and bilirubin
normal. Calculi seen but no
evidence of cholecystitis.
- inflammation of gall bladder,
with local and systemic
inflammatory signs
- no bile flow stasis or
obstruction
- Clinically, Murphy’s sign
positive. No jaundice.
Laboratory
Normal bilirubin, normal ALP
- inflammation of bile duct
causing narrowing or
obstruction to bile flow
- obstructive jaundice
- Right hypochondriac pain
- Fever
- significantly raised ALP,
ALT AST, GGT may raised.
- Direct bilirubin surged
Cholelithiasis
- gallbladder stone
- Maybe asymptomatic or
causing biliary colic or
cholecystitis
- no clinical jaundice
Choledocholithiasis Mirizzi syndrome
- common bile duct stone - common hepatic duct
- primary : formation within obstruction caused by
biliary tract with bile stasis compression by impacted stone
- Secondary : migration of in the cystic duct or
gallbladder stone to bile infundibulum of gallbladder.
duct
Clinically, fever, RHC pain and jaundice. Bile obstructions can
cause obstructive jaundice: jaundice+ pale stool+ dark coloured
urine.

Mirizzi syndrome has been classified based on the presence and extent of a cholecystobiliary
fistula:
Type I (11 percent of Mirizzi syndrome): External compression of the common hepatic duct due to a
stone impacted at the neck/infundibulum of the gallbladder or at the cystic duct
Type II (41 percent of Mirizzi syndrome): The fistula involves less than one-third of the
circumference of the common bile duct.
Type III (44 percent of Mirizzi syndrome): Involvement of between one-third and two-thirds of the
circumference of the common bile duct.
Type IV (4 percent of Mirizzi syndrome): Destruction of the entire wall of the common bile duct.
Acute Pancreatitis

1. Clinical features
- epigastric pain radiating to the back, may relieved by bending forward
- Nausea, vomitting, loose stool
- Loss of appetite
- Fever
- Identifiable risk factors: post-ERCP, alcohol intake
- Reduced bowel sound, abdominal distension

2 Diagnostic criteria
At least 2 of the followings:
- acute abdominal pain at upper abdomen
- Elevated serum amylase to 10x of the normal
- Abnormal imaging findings in the pancreas suggestive of pancreatitis
Oedematous pancreas, peripancreatic fluid collection, increase peripancreatic fat streakiness

3. Common cause of death

- Shock followed by severe dehydration
- Multiple organ dysfunction syndrome: Shock, ARDS ( PaO2 <60), AKI (Creat > 200), GI
bleeding

Severity scoring

1. Revised Atlanta classification

Determinant of Severity
Local: Presence of pancreatic necrosis
Sterile or persistent
Systemic: Presence of organ failure
Transisent or persistent
Severity
Mild: Absence of organ failure, absence of local and systemic cx
Moderate: Organ failure less than 48 hours and local or systemic complications without persistent organ
failure.
Severe: Organ failure> 48 hours
Clinical Phases
Early < 1 week: severity depends on presence of systemic organ failure
Late > 1 week: severity depends on presence of local complication or persistent systemic organ failure.
Classifications
- Interstitial oedematous pancreatitis
- Necrotizing pancreatitis (parenchymal, peripancreatic and combination)
Fluid collection
Interstitial oedematous pancreatitis:
- Acute peripancreatic fluid collections (< 4 weeks)
- Pseudocysts (>4 weeks)
Necrotizing pancreatitis
- Acute necrotic collections (< 4 weeks)
- Walled-off (pancreatic) necrosis (>4weeks)
2. Glasgow-Imrie scoring

P aO2 < 8kPa/ 60mmHg

A ge >55

Neutrophils : WBC> 15

C calcium <2mmol/L

R penal function/Urea > 16

E nzyme (AST/ALT >200iu/L or LDH> 600iu/L)

A albumin <32g/L

S sugar > 10mmol/L

Severe disease if presence of 3 or more within 48 hours, warrant ICU admission

3. Ranson Criteria

Criteria present on admission include the following:

• Age> 55 years


• WBC > 16,000/µL


• Glucose level > 200 mg/dL


• Serum LDH level > 350 IU/L


• AST level > 250 IU/L


Criteria developing during the first 48 hours include the following:

• Hematocrit fall of more than 10%


• BUN level increase > 8 mg/dL


• Serum calcium level < 8 mg/dL


• Pa O2 < 60 mm Hg


• Base deficit > 4 mEq/L


• Estimated fluid sequestration > 6 L

Score 0-2 Mild disease, admit to regular ward
Score 3 or above Higher mortality rate, require ICU admission.
4. APACHE II

>8 - Severe pancreatitis; APACHE II scoring can be done as daily ongoing assessment.

5. CT severity index

CT pancreatic protocol should be done in

- all severe pancreatitis between 3-10 days of admission
- Mild disease which show no response towards analgesia and antibiotics after 72 hours;
0-3: mild acute pancreatitis
4-6: moderate acute pancreatitis
7-10: severe acute pancreatitis

Management
- Fluid resuscitation
- Nutrition - enteral vs parenteral
- MUST perform early U/S to look for CBD stone or dilated biliary tree
- ERCP if confirm presence of bile duct stone and severe pancreatitis to achieve early duct
clearance
- For gallstone pancreatitis:
- mild gallstone pancreatitis: interval cholecystectomy and bile duct clearance(CBD exploration)
can be done between 2-4 weeks
- Severe gallstone pancreatitis with less favourable response to initial treatment: urgent ERCP and
sphinterotomy is indicated within 48 hours

Complications
1. Systemic
- Shock
- ARDS/ hypoxia
- Renal failure
- DIC/ Portal or splenic vein thrombosis
- Metabolic derangement: acidosis, hypocalcemia, hyperglycaemia, hyperlipidaemia
- Ileus

2. Local - commonly occur after 1st week

- acute peipancreatic fluid collection
- Pseudocyst - CT localisation before definitive tx
percutaneous/ endoscopic transpapillary or transmural/ surgical drainage
- Sterile pancreatic necrosis
- Infected necrotising pancreatitis - broad spectrum antibiotics/ necrosectomy/ total
pancreatectomy
- Pleural effusion
- Pseudoaneurysm - bleeding into gastrointestinal tract or peritoneal cavity; commonly affected
splenic artery; mx with endovascular transarterial catheter embolisation/ ligation of vessels/
resection of pseudo aneurysm
- Recurrence or progression to Chronic pancreatitis

Chronic pancreatitis
- is a progressive inflammatory disease characterised by pancreatic fibrosis, irreversible destruction
of pancreatic parenchyma.
- clinical features: epigastric pain radiating to back, weight loss, anorexia, steatorrhea, bleeding
tendency secondary to malabsorption to fat-soluble vitamin, cachexia, diabetes mellitus
- Risk factor: chronic alcoholism, hypercalcemia/hyperthyroidism, pancreatic diversum, duct
obstruction(periampullary carcinoma)
- CECT pancreatic calcification
- Mx
- Cessation of tobacco and alcohol
Pain management (celiac nerve block)
Pancreatic enzyme replacement - Creon
Pancreatic sphinterotomy and stent placement for relief of obstruction
Low-fat high protein small meals
Vitamin supplementation/ Kabiven (aminoacid, electrolyte, dextrose, lipid)
Perforated Gastric Ulcer

Peptic ulcer disease is the disruption of gastric or duodenal mucosal integrity, caused by local
inflammation/ decreased mucosal resistance/ hyperacidity which leads to a well-defined
mucosal defect.

1. Risk factors: smoking, alcohol, aspirin use, H. Pylori infection

2. Clinical presentation
- sudden onset of severe, generalised abdominal pain, abdomen board-like rigidity, tachycardia,
pyrexia
- Eventually, circulatory failure ensues, cold clammy peripheries, sunken eyes, dry tongue, thready
pulse
3. Causes of mortality
Sepsis Hypovolumic shock
Perforated gastric ulcer, leakage of gastric Persistent vomiting or GI losses.
content which irritate peritoneal lining, causing Severe bleeding peptic ulcer.
peritonitis.
SSC Hour-1 Bundle of Care Elements: Fluid resuscitation
• Measure lactate level* Blood transfusion
• Obtain blood cultures before
administering antibiotics.
• Administer broad-spectrum antibiotics.
• Begin rapid administration of 30mL/kg
crystalloid for hypotension or lactate
level ≥ 4 mmol/L, minimum of 30ml/kg
in 3 hours.
• Apply vasopressors if hypotensive during
or after fluid resuscitation to maintain
MAP ≥ 65 mm Hg.
* Remeasure lactate if initial lactate is elevated
(> 2 mmol/L).

Management

- supportive:
a. fluid replacement and electrolyte correction
b. PPI
c. Insertion of nasogastric tube for gastric decompression
d. Strict and cautious monitoring of input/output: CBD and CVL inserted

- definitive:
a. oversewing the ulcer and Graham omental patch (omentoplasty).
b. Partial gastrectomy with Billroth I/Billroth II
c. A definitive ulcer procedure can be performed if contamination of the upper abdomen is
minimal and the patient is stable. This may include a highly selective vagotomy, a truncal vagotomy
and pyloroplasty, or vagotomy and antrectomy for a perforated duodenal ulcer.
UGIB
1. Difference between UGIB vs LGIB
- UGIB: bleeding proximal to ligament of Treiz
usu. presented with black tarry, sticks or loose stool and coffee ground vomitus -
degradation of blood by gastric acid
higher BUN/Cr ratio, >30
- LGIB: bleeding distal to ligament of Treiz
presented with fresh per rectal bleeding/ hematochezia

2. Variceal vs non-variceal bleeding

Non variceal bleeding

3. Risk factor:
- smoking/ alcohol consumption
- NSAID or aspirin use
- H. Pylori infection

3. Management
- Initial resuscitation: insertion of large bore cannula, GSH/GXM, transfuse if needed
- Indication for blood transfusion:
a. SBP BP< 110mmHg
b. Postural hypotension
c. Pulse rate >110/min
d. Hb <8g/dl
e. Angina or cardiovascular disease with Hb<10
- Start IV PPI loading dose and infusion for 72hours for effective haemostasis.
- Early OGDS to assess ongoing bleeding and haemostasis
- FORREST classification of bleeding ulcer
- Endoscopic intervention:
Pharmacological tx with adrenaline acts as vasoconstrictor and tamponade to stop bleeding, but
could not serve as sole treatment, must be combined with other mode of tx.

Rockall scoring
- for prognostication, esp pos-endoscopy
Blatchford scoring
- assessment stool for risk stratification and timing endoscopic intervention

AIMS 65 scoring

Albumin <3 g/dL (30 g/L)

INR >1.5
Alteration in mental status
sBP ≤90 mm Hg
Age ≥65 years

Variceal bleeding

- suspect vatical bleeding with presence of stigmata of chronic liver disease, deranged LFT,
ultrasound cirrhotic liver changes
- Management
a. Pharmacological
- 1. IV Terlipressin 2mg loading, 1mg TDS
- 2. Secondary prophylaxis with beta blocker: propranolol 20mg BD, Octreotide 50microgram
bolus, followed by 50microg/ hr infusion.
b. endoscopic therapy
- injection of histoacryl glue
c. Surgical intervention
- transjugular intrahepatic portosystemic shunt
d. Balloon tamponade as an immediate temporary resort of haemostasis - Sengstaken-Blakemores
tube
Mechanism of PPI
Loading dose of PPI 80mg stat, followed by IVI PPI at 8mg/hr for 72 hrs
Blocks the gastric H+K+ATPase, that reduce gastric acid secretion, subsequently lower gastric pH.
Low pH interferes clot stabilisation, thus PPI helps platelet aggregation/ haemostasis and bleeding
may stopped.

Indication for Eradication therapy

Pantoprazole 40mg BD, Amoxycillin 1g BD, Clarithromycin 500mg BD for 1/52
Indicated in H.pylori colonisation/ positive CLO test
Intestinal Obstruction
1. Clinical features
4 cardinals symptoms: abdominal pain, abdominal distension, reduced bowel output/
constipation, vomitting

2. Etiology
Extraluminal: Volvulus, herniation, adhesion
Mural: Cancer, inflammatory stricture ( Crohn’s ds), intussusception
Intraluminal: gallstone impaction, impacted fecolith, foreign body

3. Classification
Mechanical: presence of obstruction
Extraluminal: Volvulus, herniation, adhesion
Mural: Cancer, inflammatory stricture ( Crohn’s ds), intussusception
Intraluminal: gallstone impaction, impacted fecolith, foreign body

Functional: absence of obstruction, no abdominal pain.

Paralytic ileus
Electrolyte imbalance (hypoK)
Mesenteric vascular occlusion
Spinal injury

4. Differentiating obstruction at different level

Gastric Outlet Proximal small bowel Distal small bowel Large bowel
Obstruction
- Projectile vomitting is - Vomiting is the early - Prominent abdominal - Constipation is the
the earliest and symptoms. Vomiting pain and distension. cardinal sign,
prominent features. is profuse, gastric - Vomiting of gastric abdominal distension
Vomitus is non-bilious content and bilious content, then bile and is marked at flanks.
- early satiety later. become feculent at - Vomiting is late
- No abdominal - Dehydration last. feature
distension. - No marked distension
and constipation.
- presence of gastric • dilated loops of small bowel proximal to the - AXR shows dilated
dilatation, no bowel obstruction (see 3-6-9 rule) large bowel (presence
dilatation seen. • predominantly central dilated loops of haustral folds,
• three instances of dilatation > 2.5 - 3 cm ref which spaced
required irregularly and do not
• valvulae conniventes are visible cross whole diameter
• gas-fluid levels if the study is erect, of bowel.
especially suspicious if 8 - Small bowel fluids
◦ >2.5 cm in width level if IC valve
◦ in same loop of bowel but at incompetent.
different heights (> 2 cm difference
in height)
5. Differentiating closed loop vs volvulus vs intussusception
Close loop obstruction Volvulus Intussusception

- a form of complete bowel - torsion of a segment of - Segment of intestine invaginate

obstruction where a segment of
intestine, usu small bowel is
obstructed at 2 points (loss of
proximal and distal outlets)
- classical form seen as malignant
stricture of colon with competent
ileocaecal valve.
- causes: volvulus, hernia,
Complications arise more rapidly:
ischaemia, necrosis & perforation
distended, fluid-filled, sometimes
C-shaped or U-shaped bowel
segment with prominent
mesenteric vessels converging on
a point of torsion (CT whirl sign)
or incarceration
alimentary tract, usually sigmoid
colon
whirl pattern, caused by the
dilated sigmoid colon around its
mesocolon and vessels, and a
bird-beak appearance of the
afferent and efferent colonic
segments
into adjoining intestinal lumen
- Intussuseptum - part that
invaginate
intussuscipiens - receiving
invagination
- usually seen in paediatric
- Classical presentation:
vomiting, intermittent colicky,
passage of blood per rectum
Target sign

6. Pathophysiology
- presence of mechanical obstruction causes proximal dilatation and while distal to the blockage
will be decompressed as the content passed out
- Swallowed air and gas from bacterial fermentation add up to bowel distention.
- bowel wall becomes edematous, normal absorptive function is lost, and fluid is sequestered into
the bowel lumen. There may also be transudative loss of fluid from the intestinal lumen into the
peritoneal cavity.
- Intestinal necrosis or gangrene caused by twisting of bowel around mesentery or intramural
vessels compromise that causes reduced perfusion.

7. Management
a.Initial supportive non-operative management
- gastric decompression for nausea and vomiting pt, Ryle’s tube insertion for free flow and
aspiration regularly
- Electrolytes replacement according to deficit and losses
- Endoscopic decompression of sigmoid volvulus - high risk of recurrence, risk of perforation

b. Surgical intervention
- generally definitive management varies according to underlying cause
- Immediate surgical exploration is indicated for either suspected bowel compromise (ie,
perforation, necrosis, or ischemia) or for treating a surgically correctable cause of small bowel
obstruction (SBO), except adhesions.
- Resection with primary anastomosis or decompress with diverting stoma created.
- Palliative care for advanced malignancy - diverting colostomy or endoscopic stenting
Shock
Shock is a state of circulatory insufficiency that creates an imbalance between tissue oxygen supply
and oxygen demand that causes global tissue hypo perfusion which is associated with reduced
venous oxygen content and metabolic acidosis.
1. Type of shock
- Hypovolumic shock - in adequate circulating volume : massive haemorrhage, burn
- Cardiogeneic - inadequate cardiac pump function : AMI, arrythmia, severe valve dysfunction
- Distributive - peripheral vasodilatation and maldistribution of blood flow: septic, anaphylactic
and spinal shock
- Obstructive - extracardiac obstruction of cardiac output : tension pneumothorax, pulmonary
embolism

2. Stages of hypovolumic/haemorrhagic shock

- compensated stage: tachycardia but normotensive, maintained by baroreceptor reflex, RAA
system, chemoreceptors and vasopressin
- Decompensated stage: failed compensatory mechanism
- refractory/ irreversible: circulatory failure continues deteriorate despite fluid or blood
resuscitation.
 CLASS I CLASS II CLASS III CLASS IV

Blood loss (ml) Up to 750 750-1500 1500-2000 >2000

Bld loss (%bld vol) Up to 15% 15-30% 30-40% >40%

PR <100 100-120 120-140 >140

BP Normal Normal Decreased Decreased

Pulse press (mmHg) Normal/ Decreased Decreased Decreased

Increased

RR 14-20 20-30 30-40 >35

U/output (ml/Hr) >30 20-30 5-15 Negligible

Mental status Slightly anxious Mildly anxious Anxious, Confused, lethargic

confused

Fluid replacement Crystalloid Crystalloid Crystalloid & Crystalloid & blood

blood

3. Clinical features
Hypotension
Tachycardia
Oliguria
Abnormal mental status
Tachypnea
Cool, clammy, cyanotic skin
Metabolic acidosis (high anion gap)
Hyperlactatemia (initial lactate >2mmol/L)

Haemorrhagic Resuscitation with fluid or blood transfusion

Deinitive treatment to stop bleeding
Cardiogenic - cardioversion for arrhythmia
- ACS protocol
Septic shock Sepsis bundle care
Anaphylactic M epinephrine (1 mg/mL preparation): Give epinephrine 0.3 to 0.5 mg
intramuscularly, preferably in the mid-outer thigh. Can repeat every 5 to 15
minutes (or more frequently), as needed. If epinephrine is injected promptly
IM, most patients respond to one, two, or at most, three doses. If symptoms
are not responding to epinephrine injections, prepare IV epinephrine for
infusion.
Place patient in recumbent position, if tolerated, and elevate lower
extremities.
Oxygen: Give 8 to 10 L/minute via facemask or up to 100% oxygen, as
needed.
Normal saline rapid bolus: Treat hypotension with rapid infusion of 1 to 2
liters IV. Repeat, as needed. Massive fluid shifts with severe loss of
intravascular volume can occur.
Albuterol (salbutamol): For bronchospasm resistant to IM epinephrine,
give 2.5 to 5 mg in 3 mL saline via nebulizer, or 2 to 3 puffs by metered dose
inhaler. Repeat, as needed.
Alternative: IV anti-histamine/ glucocorticoid

Obstructive 1. Tension pneumothorax

emergent tube thoracostomy (24 or 28 Fr, 36 Fr for trauma; fifth intercostal
space, midaxillary line) or needle decompression using a 14 to 16 gauge
intravenous catheter (second or third intercostal space, midclavicular line)
followed by immediate tube thoracostomy; tube thoracostomy is indicated
should decompression fail

Massive Transfusion Protocol

1. Massive transfusion
- Massive transfusion is defined as transfusion of a volume equal to the patient’s total blood
volume in less than 24 hours (national transfusion guideline MOH)

- requirement for >10 units of PRBCs within the first 24 hours of injury.
- transfusion of >4 RBC units in 1 h with anticipation of continued need for blood product support
- replacement of >50% of the TBV by blood products within 3 hours

- aim to abrupt lethal triad: hypothermia, acidosis and coagulopathy

2. Regime
FFP, platelets, and RBCs at 1:1:1 unit ratios

3. Indication to initiate
- actual or anticipated 4 units RBC in less than 4 hours + haemodynamically unstable with or
without anticipated ongoing bleeding
- Severe thoracic, abdominal, pelvic or multiple long bone trauma.
- Major obstetric, surgical or gastrointestinal bleeding.
 4. Indication to terminate
- bleeding controlled
- Blood parameters achieved:
- INR <1.5 normal/ Plt > 50/ fibrinogen >1/ Ca >1.1/ Lactate < 4/ pH > 7.2/Base excess< -6
- Temp > 35

5. Complication of massive transfusion

• volume overload
• over-transfusion
• hypothermia
• dilutional coagulopathy of clotting factors and platelets (regular and early monitoring of
coagulation, involvement of haematology for replacement therapy )
• excessive citrate causing metabolic alkalosis and hypocalcaemia (monitor pH and ionised
calcium, replace calcium as necessary)
• hyperkalaemia (use of younger blood, monitor regularly, may require specific therapy)

6. Adverse reaction of blood transfusion

Acute (w/I 24 h) Delayed (after 24h)

o Acute haemolytic reactions (ABO or Rh o Infections (viral, parasites etc)

incompability) o Iron overload
o Anaphylaxis *** o Transfusion associated graft-versus-host disease
o Bacterial contamination o Post-transfusion purpura
o Febrile non haemolytic transfusion reaction (from o Delayed haemolytic and serologic transfusion
HLA Ab) reactions
o Allergic reactions (itch, utricaria, mild fever)*** o Hypotensive reactions
o Transfusion- Associated Circulatory Overload o Immunomodulation
o Transfusion-related acute lung injury (TRALI) o Alloimmunization
o Hypothermia
o Electrolyte toxicity
o Air embolism
Pre-operative assessment
1. American Society of Anaesthesiology
defines the overall health status of the patient and is used by anesthesiologists, surgeons, and other
clinicians involved in perioperative care

ASA 1 Healthy normal Healthy, non-smoking, no or minimal alcohol use

individual
ASA 2 A patient with mild Mild diseases only without substantive functional limitations.
systemic disease Examples include: current smoker, social alcohol drinker,
pregnancy, obesity (30 < BMI < 40), well-controlled DM/HTN,
mild lung disease
ASA 3 A patient with severe Substantive functional limitations; One or more moderate to
systemic disease severe diseases. Examples include: poorly controlled DM or
HTN, COPD, morbid obesity (BMI ≥40), active hepatitis,
alcohol dependence or abuse, implanted pacemaker, moderate
reduction of ejection fraction, ESRD undergoing regularly
scheduled dialysis, premature infant PCA < 60 weeks, history
(>3 months) of MI, CVA, TIA, or CAD/stents.
ASA 4 A patient with severe recent ( < 3 months) MI, CVA, TIA, or CAD/stents, ongoing
systemic disease that cardiac ischemia or severe valve dysfunction, severe reduction
is a constant threat to of ejection fraction, sepsis, DIC, ARD or ESRD not undergoing
life regularly scheduled dialysis
ASA 5 A moribund patient ruptured abdominal/thoracic aneurysm, massive trauma,
who is not expected to intracranial bleed with mass effect, ischemic bowel in the face
survive without the of significant cardiac pathology or multiple organ/system
operation dysfunction
ASA 6 A declared brain-dead
patient whose organs
are being removed for
donor purposes

2. Eastern Cooperative Oncology Group (ECOG) performance status

- assess the ability of patient to tolerate therapies in serious illness, specifically for chemotherapy
- Assess disease impacts patient’s ADL

Criteria Score Description

Fully active, able to carry on all predisease activities
Asymptomatic 0
without restriction.
Symptomatic but Restricted in physically strenuous activity but ambulatory
completely 1 and able to carry out work of a light or sedentary nature.
ambulatory For example, light housework, office work.
Symptomatic, Ambulatory and capable of all self care but unable to carry
<50% in bed 2 out any work activities. Up and about more than 50% of
during the day waking hours.
 Symptomatic, Capable of only limited self-care, confined to bed or chair
>50% in bed, but 3
50% or more of waking hours.
not bedbound
Completely disabled. Cannot carry on any self-care. Totally
Bedbound 4
confined to bed or chair.
Death 5

3. New York Heart Association (NYHA) score

- assess severity of heart failure, its impact on carrying out daily living

4. Pre-op anaesthesia assessment

History
Assess heart failure symptoms (NYHA) , functional capacity
Past medical history
Tobacco use
Previous hx of difficult intubation

Examinations
Vital signs & BMI
Cardiopulmonary examinations: heart rythm, murmurs
Features of difficult intubation: LEMON, Mallampati scoring
Dentures

Investigation
Blood: FBC, RP and electrolytes, Coagulation profile
Cardiac marker
ECG: ischaemic changes
Chest X Ray: lung pathology (TB/ COPD), cardiomegaly/ heart failure
Echocardiogram: ejection fraction, regional wall motion abnormalities, valvular abnormalities
Blood grouping for screen and hold

Cardiovascular disease
- recent angioplasty may warrant for postpone of surgery, recent MI elective surgery postponed
6-12 months
- Use of antiplatelet should be withheld 1 day prior, warfarin require bridging with LMWH 5 days
prior
- ACEi or ARB stopped 24 hours before surgery

Renal disease
- CAPD or HD prior to surgery, post dialysis, blood monitoring
Chronic respiratory disease
- stop smoking, compliant to inhaler

Diabetes mellitus
- first on the list, monitor refill closely, maintained 5-10
- Omit morning dose of hypoglycaemic agent
Pain management
1. Type of pain
- Nociceptive
- Neuropathic
- Psychogenic

2. Acute vs chronic pain

Acute Chronic

- intense pain for short duration - long duration, continuous and recurring

- result from noxious stimuli that activates

nociceptors neuron
- associated with surgery, traumatic injury, tissue - associated with chronic disease: cancer, spine
damage/ ischaemia and inflammatory processes. disease, diabetic neuropathy
- duration days to weeks - duration longer than 3 years

- accompanied by anxiety and restlessness - result in depression, financial and social burden

3. Assessment of Pain score

- MOH Numeratic Rating Scale
- Wong’s Baker Face
- FLACC pain scale : <4yo

3. Type of analgesia

Mechanism of action Example

Acetaminophen - central action and peripheral Paracetamol
blockage of COX
NSAID - Inhibit prostaglandin Ibuprofen, diclofenac sodium
synthesis as an inflammatory
Selective COX-2 inhibitor Celecoxib
process.
Opiates -bind to pre-synaptic opiates Morphine, Codeine
receptor and inhibit Pethidine, Fentanyl
neurotransmitter release Tramal
Gabapentin - for neuropathic pain
management
- depression of dorsal horn
sensitivity through a multitude
of mechanisms
Antidepressant - increasing noradrenaline in SSRI: fluoxetine
the spinal cord by reuptake TCA: amitriptyline, duloxetine
inhibition directly inhibits
neuropathic pain through α2-
adrenergic receptors
Post-op Monitoring
- monitored in recovery room (postoperative anaesthesia care unit)
- Vital signs ( BP, HR, SPO2, Temp, pain score, every 5 mins for 15 mins, then once in every 15
mins)
- Common post-op complications
1. Hypotension : drop of BP 20-30% of baseline, dizziness and nausea, disorientated, decreased
urine output. Mx: continue close observation, fluid bolus, vasopressor agents or eliminate
underlying cause
2. Hypertension : usually due to pain, irritation from CBD, ETT, hypoxaemia, acidosis. Mx:
analgesia, antihypertensive and correcting underlying problem: correcting metabolic
derangement.
3. Tachycardia/ bradycardia: bradycardia maybe an effect from muscarinic blocking agent
4. Post-operative nausea and vomiting (PONV) :
identify underlying cause, avoid medications that may
cause nausea, give antiemetic.

5. Hypothermia and shivering

Distributive heat loss, evaporation from skin prep,
impaired function of normal thermo- regulation from
anesthetics and the higher rate of heat loss from
patients with burns, traumatic injuries, or cachexia.
Mx: warm blanket, reassurance.

6. Altered mental status/ emergence delirium : possible

caused by hypoxaemia, metabolic derangement,
hypotension/hypoperfusion to cerebrum, effect of
scopolamine or atropine

7. Peripheral nerve injury: malposition of patients

hand, causing stretching of peripheral nerve. Usually
conservative management

8. Urinary retention : anaesthesia affecting the central

or peripheral micturition reflex, medication, pelvic
surgery

Post-operative examination
1. Bromage score : to assess degree/intensity of motor block in spinal anaesthesia that determine
recovery from anaesthetic effect, should be assessed 4 hourly
Individuals who required extra post-op attention
1. Extreme ages: paediatric and elderly
2. Comorbidities: ischaemic heart disease, previous stroke, chronic lung disease,
immunocompromised, poor nutritional status
3. previous complicated surgery: intraoperative/post-operative complication
4. Major surgery: cardiothoracic surgery, intracranial surgery
Fluid and electrolyte
- Daily requirement
- fluid 30-40ml/kg
- Sodium 1-2 mmol/kg
- Potassium 0.7-1.5mmol/lg
- Magnesium & Calcium 0.1mmol/kg
- Phosphorus 0.4 mmol/kf
- Glucose 2-4g/kg
- Protein 1-1.25 g/kg

Definition of level Signs and symptoms

Lethargy, altered consciousness, coma, convulsion, peripheral

Hypernatremia
oedema, ascites, pleural effusion, myoclonus, tremor, rigidity,
(>145mmol/L)
Na hypereflexia
Weakness, n/v, altered consciousness, altered vision, cramps,
Hyponatremia
myoclonus (<120mmol/L cerebral oedema, <100mmol/
(<135mmol/L)
Lcardiac symptoms

Muscular weakness and paralysis, Arrhythmias and ECG

Hyperkalemia
changes (6-7 tall T-waves, prolonged PR interval;10-12 may
K (>5.5mmol/L)
caused widen QRS, VF, systole)
Hypokalemia Arrhythmias (eg. AF, PVC) and ECG changes (eg. sagging ST,
(<3.5mmol/L) T-wave depression, U-wave elevation

Abdominal groans (constipation, nausea, vomiting), psychic

Hypercalcemia
moans (lethargy, depression), bones and stones (kidney),
(>2.6mmol/L)
Ca (>3.75mmol/L may leads to coma and cardiac arrest)
Increased cardiac and neuromuscular excitability, eg. Tetanic
Hypocalcemia
syndrome, prolonged PR interval and ventricular arrhythmias,
(<2mmol/L)
impaired mental status,

Shortness of breath, bibasal crepitations, pedal edema. Bibasal

Fluid overload
hazziness/ pleural effusion
Water
Poor hydration, tachycardia, hypotension. VBG metabolic
Dehydation/ Shock
acidosis with increased lactate.

Correction with
- T. Slow K, 1 tab/ 600mg can raise 8mmol
usually taken 2-3 tab/ day
- Mist KCL 13.4mmol
- Injection KCL 13.4mmol (must be diluted with normal saline)
- Injection KHPO43 10mmol
-
Trauma
- traumatic chest injury: injury to rib, pulmonary, airway and cardiac
- Flail chest: segmental fracture of 2 or more consecutive rib
Paradoxical movement, where segment of chest wall that has loss continuity moves inward as the
rest of chest expand during inspiration
- Bulky dressing as splintage

Pneumothorax Haemothorax Tension pneumothorax

Closed or open Massive hemothorax is can be rapidly fatal as
Open: communication defined by the need for intra-thoracic pressure
between pleural space to thoracotomy — the rises cause decreased
external environment via indications are: venous return and kinking
chest wall defect which is - Blood loss > 1,500 mL of great vessels resulting
larger than 2/3 tracheal or 1/3rd of blood volume in obstructive shock
diameter. @sucking chest - Blood loss >200 mL/h
wound (3 mL/kg/h) for 2-4 hours
Examination Pleuritic chest pain. S & S of haemorrhagic Features similar to
Hyperresonance on shock, hypotensive, pneumothorax, except that
auscultation and tachycardia mediastinum displacement
percussion. Reduce breath sound. causing tracheal deviation
Dull on percussion away from affected side.
Ipsilateral hyper
expansion and decrease
chest expansion.
Distended neck vein,
hypotension,tachycardia
Findings X ray shows loss of lung Pleural effusion, blunting Mediastinum displaced to
markings and of costophrenic and the contralateral side.
hyperlucency at affected cardiophrenic angle. Loss Ipsilateral hyper inflated.
side. Ipsilateral of cardiac silhouette *tension pneumothorax
hyperinflated. does not need Xray for
Occasionally diagnosis
subcutaneous emphysema
and pneumomediastinum.
Resuscitation ATLS protocol
Resuscitation according to ABC
Airway: Determine airway obstruction (blood pooling etc), airway maneuver,
adjunct airway or definitive airway (ETT),
Breathing: high flow O2 to maintain saturation,
Circulatory: Insert 2 large bore cannula. maintenance of BP with inotropes, fluids
or blood products if blood loss is significant.
Stabilise cervical spine.
Open pneumothorax: 3 way occlusive dressing
Definitive Chest tube insertion Chest tube insertion. Needle decompression
Simple closed Transfuse with blood with thoracotomy at 5
pneumothorax maybe ongoing intercostal space mid-
managed conservatively axillary line. 14G needle
(paed: 2nd ICS
midclavicular line)
Followed by chest tube
inserted at safety triangle.
Rehabilitativ - supportive care to optimise pain control
e - Deep breathing exercise and incentive spirometry
- Active coughing
- Mucus mobilisation: vigorous chest physiotherapy, saline nebulisation,
mucolytics T. Bisolvan
- Supplemental oxygen

Life-threatening chest trauma (primary survey)

1. Open pneumothorax
2. Tension pneumothorax
3. Massive haemothorax
4. Cardiac tamponade
5. Flail chest
6. Airway obstruction or disruption

Potentially life-threatening chest injuries (secondary survey)

1. Aortic injury
2. Simple pneumothorax, non-massive haemothorax
3. Oseophageal perforation
4. Diaphragmatic injury
5. Tracheobronchial injury
6. Pulmonary or cardiac contusion
FAST scan
- area to check:
1. Morrison pouch/ hepatorenal pouch
2. Splenorenal pouch
3. Subxiphoid pericardial window
4. Pouch of Douglas
5. Bilateral hemithoraces
6. Upper anterior chest - position the probe in the longitudinal orientation along the midclavicular
line at the third to fourth intercostal space (the most anterior area of thoracic cavity where air
accumulate as pneumothorax)

- assess peritoneal free fluid, pericardial blood

- Sliding sign present - no pneumothorax

- Management
a. Cardiac tamponade - pericardiocentesis

- Using aseptic technique, Insert at least 3” needle at the angle of the Xiphoid Cartilage at the 7th
rib
- Advance needle at 45 degree towards the clavicle while aspirating syringe till blood return is
seen - Continue to aspirate till syringe is full then discard blood and attempt again till signs of no
more blood 

- Closely monitor patient due to small about of blood aspirated can cause a rapid change in blood
pressure

b. Peritoneal free fluid

- diagnostic laparotomy to ascertain source of bleeding and therapeutic haemostasis

Head Injury
- Glasgow Coma Scale: assessment tool for level of consciousness and awakefulness
Score 13-15 Mild injury
9-12 Moderate injury
3-8 Severe injury
Eye opening 4- spontaneously
3- speech
2- pain
1- No response
Verbal response 5- Orientated to time, place and person
4- Confused
3- Inappropriate words
2- Incomprehensible sound
1- No response
Motor response 6- Obeys command
5- Localising pain
4- Withdrawal from pain
3- Abnormal flexion (decorticate)
2- Abnormal extension (decerebrate)
1- No motor response

- indication of intubation
1. GCS score less than or equal 8 (reduced conscious ness for airway protection)
2. Severe metabolic acidosis or shock
3. Upper airway edema: laryngoedema
4. Respiratory failure, with RR>35 or PaO2 <60mmHg
5. Severe musculoskeletal disorder with impaired respiratory effort
- type of intracranial bleed
- aneurysmal bleed-
Risk factors: hypertension, family history of aneurysm, comorbidities (polycystic kidney disease,
Ehler-Danlors)
preceding thunderclap headache, unconscious/altered mental status

- hypertensive bleed
Account the most frequent cause of intracerebral/intraparenchymal bleeding
• basal ganglia hemorrhage (especially the putamen) - ipsilateral deviation of the eyes due to
descending capsular pathways from the frontal eye field
• thalamic hemorrhage - downward deviation of eyes and lack of pupillary response to light
• pontine hemorrhage - LOC, comatose due to affected reticular activating system
• cerebellar hemorrhage
Burn Injury
-. Parkland formula:
4ml x body weight x BSA%, whereby first half given in first 8 hours, another half given over next
16 hours

- degrees of burn
First degree Superficial Involves Erythema, 3-6 days
- epithelium intact thickness epidermis blanchable
significant pain
but lack of
blisters/ dry
Second degree Superficial partial Superficial Blister formation/ 7-21 days
- loss of thickness dermis (papillary) wet, pain,
epidermis and blanches.
portion of dermis
Deep Partial Deep dermis White appearance
thickness (reticular) - most or fixed red
skin appendages staining ( no
destroyed blanching)pain
sensation on deep
pressure.
Third degree Full thickness Epidermis, dermis Waxy white to
and entire leathery dry and
subcutaneous fat, elastic. Non-
eschar formation blanchable, no
pain sensation.
Fourth Degree Penetrate deep Requires surgical
tissue to fat, intervention
fascia, muscle
and bone

- inhalation injury
Suspect if present of the followings
a. Symptoms:
Hoarse or weak voice 

Increasing stridor 

Brassy cough 

Restlessness 

Respiratory difficulty 

b. Signs
Soot around mouth / nose 


Singed facial / nasal hair 


Carbonaceous sputum 

Swollen upper airway 

Hypoxia 

Pulomanary oedema 

ARDS
c. Fire in enclosed space
d. Extensive head and neck burn injury
e. Supraglottic edema on fibreoptic examination
F. High concentration of carboxyhemoglobin

Intubation in indicated if
- Airway injury with pending airway obstruction (increasing SOB, stridor, hoarse voice)
- Decrease conscious level, unprotected airway
- Severe respiratory failure
- Moderate to severe facial or oropharyngeal burn
- Uncooperative/combative patient leading to distress and further risk of injury
- Burn TBSA >40%

Indication for transferring to burn unit

• Extremes of age (<5 or >60 years)
• Site of injury
◦ Face, hands or perineum
◦ Feet (dermal or full thickness loss)
◦ Any flexure, particularly the neck or axilla
◦ Circumferential dermal or full thickness burn of limb, torso or neck
• Inhalational injury – any substantial injury, including carbon dioxide poisoning
• Mechanism of injury
◦ Chemical injury >5% of the total body surface area (BSA)
◦ Exposure to ionising radiation
◦ High pressure steam injury
◦ High tension electrical injury
◦ Hydrofluoric acid burn >1% of total body surface area
◦ Suspicion of non-accidental injury
◦ Electrical burns (including lightning injury)
• Partial-thickness burns of >10% total BSA
• Large size (dermal or full thickness loss)
◦ <16 year - >5% of total BSA
◦ >16 year - >10% of total BSA
• Coexisting conditions
◦ Any serious medical condition
◦ Any associated injuries
• Patients requiring social, emotional or rehabilitation intervention
• Refer all significant burn injuries to surgery for proper wound debridement
• Patients with worsening wounds within the past 72 hours, with wounds starting to produce
scarring, & presence of any degree of contracture
• Burns with or without trauma at high risk for morbidity & mortality

1. Second- and third-degree burns greater than 10% TBSA in patients under 10 or over 50
years of age
2. Second- and third-degree burns greater than 20% TBSA in other age groups
 3. Second- and third-degree burns that involve the face, hands, feet, genitalia, perineum, and
major joints
4. Third-degree burns greater than 5% TBSA in any age group
5. Electrical burns, including lightning injury
6. Chemical burns
7. Inhalation injury
8. Burn injury in patients with pre-existing medical disorders that could complicate
management, prolong recovery, or affect mortality (e.g., significant chemical exposure)
9. Any patients with burns and concomitant trauma (e.g., fractures, blast injury) where burn
injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the
greater immediate risk, the patient may be treated initially in a trauma center until stable
before being transferred to a burn center. Physician judgment will be necessary in such
situations and should be in concert with the regional medical control plan and triage
protocols appropriate for the incident
10. Hospitals without qualified personnel or equipment for the care of children should transfer
children with burns to a Verified Burn Center with these capabilities
11. Burn injury in children who will require special social/emotional and/or long-term
rehabilitative support, including cases involving suspected child abuse or substance abuse

Burn in adult vs Pediatric

- paediatric patients have larger BSA, more susceptible to hypovolumic shock
- Burn area estimation for paediatric using Lund-Browder, more precise.
- Fluid therapy should be started if TBSA >10%
2000 ml /m2 BSA  +  5000 ml /m2 BSAB (Body 
Surface Area Burned).

Total requirement for first 24 hours  =  4 ml/kg/%TBSA 
+  1500 ml/m2 BSA
- Ringer lactate solution with 5% dextrose should be used for maintenance fluids.
- Aim for urine output 1ml/kg/hr
- Think of NAI, require admission
- More susceptible to hypoglycaemia, hypothermia



Management
A. Initial resuscitation
- A - airway, watch out for obstruction, intubation in signs of airway obstruction
- B- Oxygen therapy CO poisoning, chest physio for smoke inhalation injury
- C- circulation resuscitation with Parkland formula using Ringer lactate to achieve desire u/o.
Take blood for ix and GSH
B. Wound care & analgesia
- Tetanus prophylaxis - ATT
- Toilet with aqueous chlorrhexidine
- Deroofing with topical antibiotics
▪ Silver sulfadiazine for deep burns
 ▪ Bacitracin and nonsticky dressings for more superficial burns
- Surgical intervention:
Immediate – escharotomy, tracheostomy
Early – tangential excision and skin graft < 72 hrs 

Intermediate – Tangential excision & Spilt Skin Graft > 72 hrs 

Late – post burn reconstruction 

**Escharotomy - circumferential eschar, esp thoracic or abdominal eschar
*** Tangential excision until punctate bleeding seen
**** spilt-skin graft is the removing of epidermis and portion of dermis from donor site