Right Iliac Fossa Pain

and
Acute Appendicitis
ACUTE
APPENDICITIS
ANATOMY
Blind-ending tube
arising from caecum at
the meeting point of 3
taeniae coli, just distal
to the ileao-caecal
junction.

Mc-Burneys
point?
2/3 of the way
along a line from
umbilicus to ASIS.
Cardinal features of acute
appendicitis
Abdominal pain <72 hours
Vomiting 1-3x
Facial flush
Tenderness concentrated on RIF
Anterior tenderness on rectal examination
Fever ( 37.3 38.5 C)
No evidence of UTI on urine microscopy
DIAGNOSIS
CLINICAL DIAGNOSIS !
Useful investigations ( WBC, urinalysis, UPT, plasma
amylase)
Abdominal Ultrasound (detect abscess or mass)
CT scanning
Open Appendicectomy
Epigastric Pain
Approach to Epigastric Pain
Onset & Progression
Sudden/Gradual
Continuous/Intermittent
Character
Sharp
Dull
Tearing
Radiation
To the back
To right scapula
Alleviating factor
Lean forward
Food intake
Exacerbating factor
Food intake
Fatty meal
Timing
Differential Diagnoses of
Epigastric Pain
Stomach & Characteristics of Pain & Associated
Oesophagus Features
Peptic ulcer Intermittent epigastric pain which recurs
disease several times a year and lasts for days or
weeks at a time.
Gastritis Associated with heartburn, nausea,
vomiting, and hematemesis.
Gastroesopha Associated with heartburn, regurgitation,
geal reflux and dysphagia.
disease
Gastric cancer Mild, constant epigastric pain with early
satiety and constitutional symptoms.
Differential Diagnoses of
Epigastric Pain
Pancreas Characteristics of Pain & Associated
Features
Acute Acute-onset, persistent, severe upper
pancreatitis abdominal pain radiating to the back,
relieved by leaning forward
Chronic Epigastric pain radiating to the back
pancreatitis associated with pancreatic insufficiency.

Carcinoma of Dull pain radiating to the back, worse at

pancreas night with constitutional symptoms.
Differential Diagnoses of
Epigastric Pain
Biliary tract Characteristics of Pain & Associated
Features
Biliary colic Irregular recurrent bouts of severe pain
which last continuously for 1-12 hours,
may be associated with nausea &
vomiting, jaundice
Acute Prolonged (more than four to six hours),
cholecystitis steady, severe pain radiating to right
scapula, may be associated with fever,
nausea & vomiting, jaundice.
Ascending Charcots triad
cholangitis
Differential Diagnoses of
Epigastric Pain
Other causes:
Cardiac Myocardial infarction, pericarditis
Vascular Aortic Dissection, ruptured AAA
Abdomen Acute mesenteric infarct
Acute Pancreatitis
Common inflammatory disorder of the pancreas characterized by
abdominal pain.
Common pathophysiology of pancreatitis : Inappropriate
activation of the pro-enzymes causing auto-digestion of the
glands.
Acute Pancreatitis
Causes (I GET SMASHED):
Idiopathic
Gallstone
Ethanol
Trauma
Steroids
Mumps/Malignancy
Autoimmune
Scorpion/Snakes
Hyperlipidemia/Hypercalcemia
ERCP
Drugs (SAND Sulphonamides, Azathioprine, NSAIDs, Diuretics)
Acute Pancreatitis
Clinical features:
Cardinal symptoms:
Sudden onset epigastric pain radiating to the back, increasing severity,
relieved by leaning forward
Frequent vomiting with persistent nausea
Signs:
General: tachycardia, tachypnoea, fever, jaundice
Abdomen: distension due to ileus/ascites, Cullen/Grey-Turners signs,
tenderness and guarding at epigastrium, absent bowel sounds
Acute Pancreatitis
Mild attack Severe attack
Acute abdominal pain Severe acute abdominal
pain
Minimal or rapidly Generalised peritonitis
resolving abdominal sign
Minimal systemic illness Severe toxemia and
shock
Moderate tachycardia ARDS (may develop
during first few days)
Acute Pancreatitis
Investigations
Blood tests:
Serum amylase: >1000i.u./ml is diagnostic, often lower in alcoholic
pancreatitis, particularly during recurrent attacks
Serum lipase: more sensitive esp. if late-presenting cases (not commonly done)
LFT: elevated ALT (gallstone pancreatitis); bilirubin for obstructive jaundice
FBC: leukocytosis
Renal profile: increased urea; renal impairment; electrolyte imbalance
CRP: for monitoring of complications
Serum calcium: look for hypercalcaemia as a cause
Serum lipid: look for hyperlipidaemia as a cause
Urine diastase: can be used if serum amylase result is equivocal.
Acute Pancreatitis
Investigations
Imaging:
CXR (erect)
free gas under diaphragm (peforation)
Ultrasound
Posterior ascoutic shadowing gallstones
Pericholecystic fluid, wall thickening(>3mm) Cholecystitis
Dilated common bile duct (>0.8mm) Distal CBD stones
Endoscopic ultrasound (EBUS)
Most sensitive (98%) method to determine CBD stones.
CT scan (Contrast-enhanced)
Serum amylase not diagnostic
Look for complications in severe pancreatitis ( after 7-10days )
Acute Pancreatitis
Investigations
ERCP:
in patients with severe acute gallstone pancreatitis
Unresponsive to treatment within 48 hours
Diagnostic role once patient recovered from acute attack if a
cause has not yet evident.
Acute Pancreatitis
Modified Glasgow Scoring System (Imries Criteria)
Criterion Positive when
P aO2 < 8kPA / 60mmHg
A ge >55 years
N eutrophil count >15x109/L
C alcium (blood) <2mmol/L
R aised plasma urea >16mmol/L
E nzyme (plasma LDH) >600i.u./L
A lbumin (plasma) 32g/L
S ugar (plasma glucose) >10mmol/L

3 or more in first 48 hours indicate severe

pancreatitis.
Acute Pancreatitis
Ransons criteria
On Admission Within 48 hours of Admission
Age >55 years Fall in haematocrit >10%
White cell >16 x Blood urea >0.9
count 109/L mmol/L
Blood glucose >10 increase
mmol/L Ca2+ (uncorrected) <2.0
LDH >350 IU/L mmol/L
AST >250 IU/L Po2 <60 mmHg
Base deficit >4 mmol/L
3 or more features severe pancreatitis
0-2: minimal mortality Fluid sequestration >6 L
3-5: 10-20% mortality
>5 : >50%, associated with more systemic complications
Acute Pancreatitis
Management
Mild attacks
Initial mx: Fluid resuscitation, analgesia, no dietary restriction
Later mx: treat predisposing factors cholecystectomy/ERCP, discourage
alcohol abuse
Severe attacks
Oxygen supplementation
IV fluid resuscitation
Nil by mouth, gastric decompression with NG tube.
Simple anagelsic : Opoid (tramadol) preferrable, avoid NSAIDS & morphine
Frequent monitor for vital signs and complications
Treat underlying causes
Management
Gallstones pancreatitis
Monitor daily LFT.
Urgent therapeutic ERCP and sphincterotomy.
Approach in ERCP : Balloon catheter, Dormia basket stone extraction,
lithtotripsy (>1cm)
Early cholecystectomy before discharge (within 72 hours) to prevent
another attack.
Indication for ERCP
Severe pancreatitis, ductal stones, cholangitis and no response to
treatment within 48 hours.
Acute Pancreatitis
Complications
Early (1st week)
CVS: Haemodynamic instability shock due to fluid shifts
RS: ARDS & pleural effusion
Renal: Renal failure worsened by hypotension
Haemato: DIVC
GI: haemorrhage, ileus
Bacteraemia
Acute Pancreatitis
Complications
Late (after 1st week)
Pacreatic necrosis & infection
Acute peripancreatic fluid collection
Pancreatic pseudocyst
Collection of pancreatic enzymes, inflammatory fluids & necrotic debris,
encapsulated within lesser sac
Endoscopic drainage if >6cm & persists more than 6 weeks
Pancreatic abscess
Recurrent swinging fever
Hyperglycemia, hypocalcemia & hyperlipidemia
RENAL CALCULI
Introduction
-Stones disease is second only to prostatic disease in
the overall urological problem
It provokes symptoms due to obstruction or by
predisposing to urinart tract infections
Upper tract calculi are much more common than
bladder calculi
Stone composition : Calcium oxalate or calcium
phosphate 75%
Magnesium ammonium
phosphate (struvite)
15%
Pathophysiology
Chemical composition
- Stones are formed from a mixture of chemical
substances and minerals (calcium and oxalate)
- Occurs when their concentration exceeds their solubility
in urine such as in dehydration , meals, medical condition
----> crystal formation
- Lack of crystallisation inhibitors also play role
Mechanism
Calcium-containing stones
- Eg : Some patients excrete excessive calcium (idiopathic
hypercalciuria) without being hypercalcemic
- There may be increased intestinal absorption of Ca ---->
increased urinary excretion
Stones caused by excessive urinary excretion of a
stone constituent
- Eg : Hyperparathyroidism ( calcium), hyperoxaluria (oxalate),
gout (uric acid), cysteinuria (cysteine stones) , xanthinuria
(xanthine stones)
Other predisposing factors
- Eg: Chronic infection, urinary stasis, foreign bodies
 Clinical features
-Depends on the size, morphology and site of stone
- Incidental finding in Xray
Obstruction of urinary flow
- Pelvicalyceal obstruction : Obstruction of renal calyces---> local urinary obstruction
(hydrocalyx)-----> chronic or recurrent loin pain
- Obstruction of the pelviureteric junction (PUJ)/ ureter -----> hydronephrosis (dilatation
of renal pelvis)-----> progressive renal parenchymal damage ------> renal failure

Passage of stones into ureter

- Intermittently pass gravel and sand, dysuria,hematuria (exit via urethra)
- Bladder outlet obstruction , urinary retention ( stone pass into bladder)
- Loin pain
- Severe, unilateral colicky pain
- Pain radiates from loin to groin/ tip of penis
 Predisposition to infection
- By causing urinary stasis, preventing proper flushing of
tract, bacteria multiplication -------> acute pyelonephritis,
perinephric abscess
Local irritation and tissue damage
- Simple inflammation -----> bleeding -----> hematuria
- Chronic inflammation -----> fibrosis------> stricture ( at PUJ and
ureter)
- Also may cause squamous metaplasia-----> squamous carcinoma
Predisposing factors
- Idiopathic (common)
- Stasis of urine eg : congenital abnormality,
hydronephrosis, chronic obstruction d/t BPH, neurogenic
bladder
- Chronic urinary infection eg : Proteus ---> alkaline
urine---> magnesium, ammonia, phosphate stone
- Excess urinary excretion of stone forming substances
- Foreign bodies
- Dietary (dairy or high Ca content)
- Multifactorial eg: prolonged immobility, multiple
fracture, paralysis(skeletal decalcification)
Investigation
Aim :
- to confirm the presentation of stone
- to locate stone
- to look for any effects of stone on renal function and UT
- to identify any structural d/o
- to identify any metabolic predisposing factors
1. Urine test- dipstick, UFEME, urine culture and sensitivity
- Haematuria, pyuria, microorganisms (UTI)
2. Kidney, ureter, bladder plain abdominal Xray
- 90% stones are radiopaque because they contain calcim.
- Urate stones are radiolucent
-Kidney size, bladder stones

3. Intravenous urogram
- To visualize the stone, show dilated urinary system (hydroureter/hydronephrosis)

4. US of kidney or bladder
- Features of stones, echogeneic rim, posterior acoustic shadowing
5. MAG-3 renogram
- If pyelonephritis occurs d/t stone obst, use this to measure renal function
- Normal kidney function : 50% on each side
- If one of kidney <15% , it is not worth to salvage the kidney

6. CT scan of abdomen and pelvis

Management
CONSERVATIVE ( stones smaller than 5mm, as 60%'ll be
passed out. Only treat if do not pass out after 4-6
weeks/symptomatic)
- Treatment of any urinary tract infection
- Hypercalcaemia----> treat disease if possible
- High fluid intake
- Low salt intake
- Restriction of red meat, dairy products
 Surgical intervention
- Indication of removal of stone:
1. Obstruction of urinary flow
2. Infection
3. Persistent, recurrent or severe pain
4. Stone likely to cause future obstruction or infection
5. Small metabolic stones likely grow rapidly in size
6. In patients where colic could be disastrous eg :
airline/military pilot
7. Patients with a solitary kidney
 Types of treatment available :
1. Percutaneous nephrolithotomy
(PCNL)
- Done for renal stones that are too
large for ESWL to disintegrate
- Contraindicated in uncorrected
bleeding diathesis, unfit for GA

It is a minimally-invasive
procedure to remove stones from
the kidney by a small puncture
wound (up to about 1 cm) through
the skin. It is most suitable to
remove stones of more than 2 cm
in size and which are present near
the pelvic region.
.2.Extracorporeal shock
wave lithoripsy (ESWL)
- Calcium oxalate, uric acid, struvite
stones fragment easily, but calcium
phosphate and cystine do not
- For stone < 10mm
- For renal stone and upper ureter
stone- not good for lower system d/t
difficult to access
- Contraindicated in pregnancy,
untreated UTI, untreated bleeding
diathesis, distal obstruction
3. Ureteroscopy with
lithoripsy - for stone along
ureter
4. Cystolitholapaxy
( procedure to break up bladder
stones into smaller pieces and
remove them )- for blader
stone
5. Open surgery
(pyelolithotomy,
ureterolithotomy) - rare,
Location Size Treatment
Renal < 5mm Conservative mx unless symptomatic/persistent
5-10mm ESWL
10- Either ESWL or PCNL
20mm
> 20mm PCNL

Location Size Treatment

Upper ureter < 5mm Conservative mx unless symptomatic/persistent
5- ESWL
10mm
>10mm URS with lithoripsy
Location Size Treatment
Middle ureter/distal ureter < 5mm Conservative mx unless symptomatic/persistent
> 5mm URS with lithotripsy
Location Size Treatment
Bladder < Cystolitholapxy
30mm
> 30 Open cystolithotomy (also if there are multiple
 Intestinal Obstruction
Most common emergency surgical disorder of the intestines
It occurs when intestinal contents fail to move distally
80% occur in small bowel ; 20% occur in large bowel
2 most common causes of intestinal obstruction are adhesions and hernia.
 Outline
1.Classification
2.Causes
3.Clinical features
4.Specific investigations
5.Treatment
 Aetiology
Classification
Site
Dynamic
Speed of
onset
Intestinal
Obstructio Blood
n supply
Paralytic ileus
Adynami &
Pseudoobstruct
c ion
 Aetiology
Intraluminal Intramural Extramural
Faecal impaction Stricture, e.g. TB Strangulated
Foreign bodies Malignancy hernia
Bezoars Diverticulitis Adhesions /
Gallstone ileus Crohns disease Bands
Parasites: Intussusception Volvulus
ascaris worms Congenital
atresia
 Site
High Low

Small bowel Large bowel

obstruction obstruction
 Speed of onset

Acute Chronic Acute on

obstruction obstructio chronic
n obstruction
Signs and Affects large Develops in
symptoms bowel colon cancer
appear very Colic comes Acute
early first, distension obstruction is
Affects small later due to
bowel, accumulation of
obstructed fecal matter in
hernia, bands proximal bowel
 Blood supply /
Nature
Simple Closed loop
obstruction obstruction
Blood supply Both proximal
is not and distal ends
impaired are blocked
Occurs in
Strangulat carcinoma of
ed right colon with
constrictive
obstruction
Blood supply
lesions or
is seriously
volvulus
impaired
 Common causes according to
age groups
Neonatal Infants Young adults Elderly
and Middle
age
Congenital Intussusceptio Strangulated Strangulated
atresia n hernia hernia
Congenital Hirschsprungs Adhesions Carcinoma of
stenosis disease Bands colon
Imperforate Strangulated Crohns disease Colonic
anus hernia diverticulitis
Volvulus Obstruction Impacted
neonatorum due to faeces
Hirschsprung Meckels
s disease diverticulum
Meconium
ileus
 Clinical features
1. Intestinal obstruction is diagnosed by the 4
cardinal symptoms:
Colicky abdominal pain
Distension
Absolute constipation
Vomiting
2. Examination should always include a search
for:
Surgical scars
Hernia
3. Determine is it simple or strangulation?
Change in character of pain from colicky to
continuous
Tachycardia
Pyrexia
Peritonism
Bowel sounds absent or reduced
Specific investigations
1. Erect and supine
Abdominal X-rays
Localize the site of
obstruction
Findings: Loop or
loops of distended
bowel with fluid
levels on erect film
 Small bowel obstruction
Findings:
Ladder pattern of
dilated loops
Centrally located
Striations that pass
completely across
the width of the
distended loop
produced by the
circular mucosal folds
 Large bowel obstruction

Findings:
Loops Located
peripherally
Striations that do not
completely extend
across the width of
the distended loop
(haustration of the
taenia coli)
Bowel is considered dilated if:

Small intestine: > 3cm in diameter

Proximal colon: >9cm in diameter

Sigmoid colon: > 5cm in diameter

2. CT Abdomen, with
oral water-soluble
contrast
(gastograffin)
Detecting obstructive
lesions and colonic
tumours
Localize the site of
obstruction
May detect unusual
hernia (obturator
hernia)
3. Ultrasound abdomen
Dilated loops of
intestine
Presence of fluid in
abdomen
Gall stone ileus
Gas in portal vein or
intrahepatic gas
Intussusception and
assessment of
vascularity with duplex
scan
 Treatment
1.Chronic large bowel obstruction, slowly
progressive and incomplete can be investigated at
some leisure and treated electively.
2.Acute obstruction, of sudden onset, complete and
with risk of strangulation is invariably in urgent
problem requiring emergency surgical intervention.
3. Management:
Preoperative preparation
Operative treatment
Conservative treatment
Preoperative preparation in
acute obstruction
1. Gastric aspiration
Nasogastric suction
Decompress bowel and lessen risk of aspiration

2. Intravenous fluid replacement

Replace of fluid sequestration into gut, vomiting.
Hartmanns and normal saline, potassium if low.
Resuscitation with plasma expanders in shock patients.

3. Antibiotic therapy
Given in intestinal strangulation is likely or found during
operation.
 Operative treatment
1. The affected bowel is inspected to determine its
viability
At the site of obstruction (e.g. band or margins of hernia orifice
pressing on bowel)
Whole segment of bowel involved in a closed loop obstruction.
2.Non-viability is determined by 4 signs:
Loss of peristalsis
Loss of normal sheen
Colour (greenish and black bowel is non-viable, purple bowel may
recover)
Loss of arterial pulsation in the supplying mesentery
3. Small bowel in intestinal obstruction can be resected and
primary anastomosis performed (safe because of excellent
blood supply)

Jejunal artery Ileal artery

4. Large bowel obstruction is treated by resection of the

obstructing lesion, with primary ileocolic anastomosis in
case of lesions proximal to splenic flexure.
5. Left sided lesions are managed by excision of the affected
6. If distal end will not reach the surface it is closed as in
Hartmanns procedure.
7. The difference in
managing small
bowel obstruction
and large bowel
obstruction is due to:
Intraluminal flora
Poorer blood supply
of the large bowel
A colonic primary
anastomosis is very
liable to leak in
presence of obstruction
7. If colo-colonic anastomosis is done, proximal bowel is
first lavaged via a catheter passed through the appendix
stump, flushing effluent along the colon and out via a
large-bore tube in proximal end of colon.
8. A defunctioning loop ileostomy may be performed to
minimize complications of an anastomotic leak if it
occurs.
 Conservative treatment (drip and suck)
Intravenous fluid
Nasogastric aspiration

Indications:
When distinction from postoperative paralytic ileus is uncertain
When a period of careful observation is indicated
When the obstruction is one of the repeated episodes due to
massive intra-abdominal adhesions
An increase in distension, pain and pulse rate are indication to
abandon conservative treatment and to re-explore the abdomen
When chronic obstruction of large bowel occurs
May attempt removing obstructing faeces by enema, prepare bowel
and carry out elective operation
 Peritonitis
Inflammation of peritoneal cavity/

inflammation of the serosal membrane that lines the abdominal cavity and the organs contained

CLINICAL DIAGNOSIS

Peritonitis Abdominal Sepsis, Medscape

Peritonism= specific sign
Any of the following clinical findings:
1) rebound tenderness;
2) percussion tenderness;
3) indirect tenderness;
4) guarding

Peritonitis Abdominal Sepsis, Medscape

1. Most often caused by introduction of infection through organ perforation

2. From other irritants, such as foreign bodies, bile from a perforated gall bladder or a lacerated liver, or gastric
acid from a perforated ulcer

3. Women :
localized peritonitis from an infected fallopian tube ,
or a ruptured ovarian cyst

Peritonitis Abdominal Sepsis, Medscape

Clinical features

Peritonitis Abdominal Sepsis, Medscape

 Causes of peritonitis by type

Localized (occur near any Generalized

primary intra-abdominal Chemical peritonitis:
inflammatory process) irritation of peritoneum by
Transmural noxious materials exp: bile,
inflammation of the stomach/bowel content
bowel (appendicitis, (due to perforation)
diverticulitis) Bacterial peritonitis :
Transmural spreading intraperitoneal
inflammation of other infection (rupture of intra-
viscera abdominal abscess or fecal
(cholecystitis,salpingiti contamination due to
s) bowel perforation, trauma
Peritonitis Abdominal Sepsis, Medscape
or surgical spillage)
Essential Surgery, 5th Edition
 The etiology of disease depends on the type, as well as location, of
peritonitis, as follows:

1. Primary peritonitis:
Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid
( heart failure and Budd-Chiari syndrome)

- The highest risk of SBP, is in patients with cirrhosis who are in a

decompensated state.Especially decreased hepatic synthetic function with
associated low total protein level, low complement levels, or prolonged
prothrombin time (PT) .

Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold
higher risk of developing SBP because of decreased ascitic fluid opsonic
activity.

- More than 90% of cases of SBP are caused by a monomicrobial infection.

The most common pathogens:
gram-negative organisms
(eg,E coli[40%],K
pneumoniae[7%],Pseudomonasspecies,Proteusspecies, other gram-
negative species [20%]) ,

gram-positive organisms
(eg,Streptococcus pneumoniae[15%], otherStreptococcusspecies [15%],
andStaphylococcusspecies
Peritonitis Abdominal Sepsis, Medscape
Anaerobic microorganisms are found in less than 5% of cases
2. Secondary peritonitis
- perforated appendicitis;
- perforated gastric or duodenal ulcer;
- perforated (sigmoid) colon caused by diverticulitis,
- volvulus, or cancer;
- Infecred necrotizing pancreatitis

The pathogens involved in SP differ in the proximal and distal GI

tract.
- Gram-positive organisms predominate in the upper GI tract,
with a shift toward gram-negative organisms in the upper GI tract in
patients on long- term gastric acid suppressive therapy.

- Contamination from a distal small bowel or colon source

initially may result in the release of several hundred bacterial
species (and fungialmost always polymicrobial,

3. Tertiary peritonitis
4. Chemical peritonitis
5. Peritoneal abscess

Peritonitis Abdominal Sepsis, Medscape

http://emedicine.medscape.com/article/180234-
overview#a5
Investigations
1. Blood tests

Full blood count

Leukocytosis (WBC >11000 cells/L)
Liver function test
Amylase and lipase levels
pancreatitis is suspected
Blood culture (33% positive in SBP)
Serum-to-ascites albumin gradient (SAAG)
> 1.1 is noted in SBP

Peritonitis Abdominal Sepsis, Medscape

http://emedicine.medscape.com/article/180234
2. Urinalysis ,
Patients with lower abdominal and pelvic infections often
demonstrate WBCs in the urine and microhematuria.
3. Imaging
Abdominal x-ray
Present of free air (common on anterior gastric and duodenal
perforation) under the diaphragm (perforated viscus)
Signs of perforation
Abdominal ultrasound and CT scan
Look for pathology in the right upper quadrant (eg, perihepatic
abscess, pancreatitis), right lower quadrant, and pelvis (eg,
appendicitis, tubo-ovarian abscess, Douglas pouch abscess)

Peritonitis Abdominal Sepsis, Medscape

http://emedicine.medscape.com/article/180234
Management
Local
o Treated according to diagnosis
o Example: appendicitis - appendicectomy
diverticulitis antibiotics

Generalized
o Is patient haemodynamically stable? Assess ABCDE
o As diagnosis made, high doses of antibiotics (IV)
o Urgent laparotomy (discover the cause, clear the
contaminating material- peritoneal toilet)
o Correction of fluid and electrolyte imbalance

Peritonitis Abdominal Sepsis, Medscape

Essential Surgery, 5th Edition
 SKIN
LESIONS BENIGN
&
MALIGNANT

By Nur Diyana Mohadi

http://obel.ee.uwa.edu.au/research/applications/skin-
 LOCATION EXAMPLES
Epidermis BENIGN: Skin tags (papillomas), warts,
seborrheoic keratosis, keratoacanthoma
PREMALIGNANT: Solar keratosis, Bowen's
disease, Erythroplasia of Queyrat
MALIGNANT: Squamous & basal cell carcinoma
Melanotic lesions Benign pigmented naevi, Malignant melanoma
Dermis Pyogenic granuloma, Histiocytoma, Keloid,
Secondary carcinomas, Karposi's sarcoma
Skin appendages Sebaceous cyst, Dermoid cyst, Pilonidal sinus,
benign appendages tumor
Subcutaneous/hypoder Lipoma & liposarcoma, Neurofibroma &
mis and deeper tissue sarcoma, Neurofibromatosis, Schwannoma,
Ganglion
Vascular origin Campbell de Morgan spots, spider naevi,
angioma, glomus tumours of digits
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 EPIDERMIS
(benign)

1 2

3 4
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 EPIDERMIS
(malignant)
2
3

1
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 DERMIS

1 2

3
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 SKIN APPENDAGES

2 1
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 SUBCUTANEOUS/HYPODERMIS & DEEPER TISSUE

1 3
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 SUBCUTANEOUS/HYPODERMIS &
DEEPER TISSUE

4
5
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 VASCULAR ORIGIN

1 2
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 VASCULAR ORIGIN

5
3

4
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
 2
1

3
H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery, Churchill Livingstone, 2007, 4th ed, pg 662-698.
Surgical Sepsis
Sepsis
New definition :
Life-threatening organ dysfunction caused by a
dysregulated host response to infection.

Previously defined as : infection + Systemic

Inflammatory Response Syndrome (SIRS)
SIRS (Systemic Inflammatory Response Syndrome)
Two or more of:
Temperature >38C or <36C
Heart rate >90/min
Respiratory rate >20/min or Paco2 <32 mm Hg (4.3 kPa)
White blood cell count >12000/mm3 or <4000/mm3 or >10%
immature bands
 Pathogenesis
Local infection immune response (inflammation) occurs when the
immune system is weak or the infection is virulent infection spread
through bloodstream to other parts of body widespread inflammation
SEPSIS

qSOFA (quick SOFA) bedside criteria

qSOFA (Quick SOFA) Criteria :
( 2 )
Respiratory rate 22/min
Altered mental status
Systolic blood pressure 100
Septic shock : mm Hg
Sepsis with persisting hypotension requiring vasopressors to maintain
MAP 65 mm Hg and having a serum lactate level >2 mmol/L (18
mg/dL) despite adequate volume resuscitation.
How does sepsis occur after surgery?
Wound
Watch for signs of infection on incision wound (tender, warm,
erythematous, pus discharge, fever, fatigue)

Pneumonia
Important to get up and about as quickly as is possible after
operation.
Deep breathing and coughing exercises are also helpful in keeping
lungs clear.
Higher risk in patient using ventilator.

UTI
Bladder catheterization

Endogenous
Deep-sited infection
Eg: Anastomotic leak after colorectal anastomosis
 Management
Preventing sepsis is important
Appropriate use of prophylactic antibiotics
Adequate & early fluids resuscitation

All within 1 hour

Give high flow oxygen
Take blood culture & consider source control
Give IV antibiotics according to local protocol
Start IV fluid resuscitation with Hartmann's
Check lactate
Monitor hourly urine output (consider catheterisation
 Prevention
General prevention
Rapid resuscitation & early definitive treatment of major
injuries
Good surgical technique
Appropriate use of prophylactic & therapeutic antibiotics
Early diagnosis & treatment of infective surgical complication

Prevention for at-risk patients & early treatment

Rapid resuscitation & prevention of shock
Optimising of oxygen delivery
Nutritional support via an enteral route
References
1. H. G. Burkitt, C. R. G. Quick, J.B. Reed, Disorders of Skin, Essential Surgery,
Churchill Livingstone, 2007, 4th ed, pg 662-698.
2. N.S. Williams, C. J. K. Bulstrode & P. R. O'Connel, Skin and subcutaneous tissue,
Bailey & Love Short Practice of Surgery, CRC Press, 2013, 6th ed, pg 577-604.
3. M. Ramachandran, M. A. Gladman, Superficial Lesions, Clinical Cases and
OSCEs in Surgery, Churchill Livingstone, 2011, 2nd ed, pg 3-63.
4. http://emedicine.medscape.com/article/1083405-overview
5. http://www.webmd.com/digestive-disorders/abdominal-x-ray-of-a-bowel-obstruction
6. http://www.aafp.org/afp/2011/0115/p159.html
7. https://ptolemy.library.utoronto.ca/content/critical-care-and-trauma-part-8-surgical-sepsis
8. Images: Google image