Surgery II

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22. Oesophagus and Diaphragm

Management of bleeding esophageal varices
Devascularisation surgical procedures for esophageal varices
Oesophageal transection
Done through left thoracoabdominal route called ‘Milnes-Walker Operation’
During the transection, varices are disconnected, bleeders are ligated or under-run,
followed by oesophagogastric anastomosis
Gastric transection of Tanner
Division is made in the stomach through abdominal route
Sugiura and Futagawa operation
Extensive devascularization procedure
Aim → To interrupt the intramural and submucosal veins
Procedure →
Splenectomy
Devascularisation of the greater and lesser curvature of stomach
Oesophagogastric transection and suturing by using End-to-End anastomosis stapler.
Achalasia cardia - investigations and management // Achalasia cardia (x4) //
Achalasia cardia clinical features and treatment // Management of Achalasia cardia
(x2)
Clinical Features
Women around 30-40 years of age are commonly affected.
Dysphagia → develops slowly and is progressive. More to liquids than to solids
Recurrent respiratory tract infection
Features of anemia - glossitis, stomatitis, pallor
Retrosternal discomfort
Investigations
Barium swallow → Uniformly dilated esophagus above with smooth tapering
segment below - cucumber esophagus or bird beak appearance
X-ray chest →
Mediastinal mass produced by dilated esophagus can be seen
Aspiration pneumonitis can be diagnosed
X-ray abdomen → Fundic air bubble is absent due to stasis of fluid in the esophagus
Esophagoscopy →
It reveals a dilated sac containing stagnant food and fluid due to stasis which
splashes out with each heartbeat and with each respiratory movement
LES is closed with a rosette appearance
Esophageal manometry
Hypertensive LES
Aperistalsis of body of esophagus
Treatment
Aim is to cure the disease, most importantly the obstruction has to be relieved
Modified laparoscopic Heller’s cardiomyotomy is the treatment of choice
Complications
Carcinoma of the mid and lower esophagus (due to prolonged irritation)
Squamous cell carcinoma is most common type identified in patient with achalasia
List the premalignant lesions in the esophagus. Describe the clinical features
and management of Carcinoma esophagus.
Premalignant lesions
GERD with Barrett’s esophagus
Plummer Vinson syndrome
Achalasia cardia
Corrosive strictures
Clinical features of Ca esophagus
Men > 60 years
Dysphagia mainly for solids
Regurgitation
Loss of appetite, loss of weight, and cachexia
Backache indicates enlarged lymph nodes
Investigations
Low Hb
LFT is affected if secondaries to the liver occur
USG
Barium swallow - Rat tail or apple core appearance. Shouldering
Oesophagoscopy
Chest X-ray → Rule out aspiration pneumonia, mediastinal widening
Bronchoscopy to rule out involvement of bronchus
CT scan
Endoscopic USG → T&N staging
PET-CT using 18-FDG to known TNM staging
Treatment
Barrett’s esophagus: clinical features and treatment
Clinical features
History of GERD symptoms
Dysphagia Liquids > Solids
Heartburn
Early satiety, belching, bloating
Aspiration pneumonitis
Hoarseness of voice
Chest pain

Enumerate the pre malignant lesions and risk factors for carcinoma esophagus
Premalignant lesions
GERD with Barrett’s esophagus
Plummer Vinson syndrome
Achalasia cardia
Corrosive strictures
Risk factors
Carcinogens →
Tobacco, heavy smoking and alcohol abuse
Dietary carcinogenes liek nitrates in drinking water, baked bread, food (pickles, corn)
containing fungi - Geotrichum candidum
Viral → HPV
Hereditary
Bacterial → H. pylori infection. Has protective effect against adenocarcinoma of the
esophagus
Misc. → Obesity, Economic status
Palliative treatment for carcinoma esophagus
Intubation : The choice of intubation material is self-expanding metallic stent (SEMS).
The stent is deployed by endoscopy under fluoroscopic guidance. It is collapsed
during insertion and once confirmed position radiologically, it is expanded.
Laser therapy : Used to core the tumor and widen the lumen to relieve dysphagia.
Laser used is Nd:Yag laser of diode laser
Photodynamic therapy : Used for early esophageal cancers where the patients are
unwilling to go for surgery. A photosensitizer (porfimer sodium) is given. It will be
taken by dysplastic and malignant cells.
Radiotherapy, Brachytherapy : It is intraluminal radiation (RT) with short penetration
distance 1500 cGy radiation is given
Intratumor injection of absolute alcohol : Used as an adjunct to stenting to deal with
tumor overgrowth
Argon plasma photocoagulation
BICAP : Direct application of of electrical current. Limited to tumors which are
circumferential.
Surgical palliation
Resection : Transhiatal esophagectomy
Bypass : Palliative bypass (gastric tube to cervical esophagus)
Feeding gastrostomy or jejunostomy : In very late cases
Metallic self expanding stents
Types of tracheoesophageal fistula
Type A : Isolated esophageal atresia - The esophageal ends do not communicate
with each other
Type B : Esophageal atresia with proximal tracheoesophageal fistula - When the
proximal part of esophagus has fistulous communication with trachea but distal part
is blind ending
Type C : Esophageal atresia with distal tracheoesophageal fistula - Here the proximal
part is blind ending but the distal part communicates with trachea (MOST COMMON
TYPE)
Type D : Esophageal atresia with double tracheoesophageal fistula - Both ends
communicate with trachea
Type E (H-type) : Isolated fistula - It is when the esophagus is patent but have a
fistulous communication with trachea
Type F : Esophageal stenosis (Not a fistula)

Surgical management of GERD (Gastro Esophageal Reflux Disease)

Indications for surgical management
No response to medical treatment
Patient’s suffering from complications of GERD like Barrett’s esophagus,
strictures/cancer
GERD associated with large hiatal hernia
Patient’s decision
Types of Surgery
Nissen’s total fundoplication →
Fundus of the stomach is mobilized by dividing the short gastric arteries
Fundus is brough behind the esophagus and wrapped in front of esophagus. It is a
loose wrap (Floppy Nissen)
Diaphragmatic defect is repaired by using non-absorbable sutures like nylon or silk
Laparoscopic fundoplication
Most popular today
Early discharge within two days
Early recovery
Most common early complication - Pneumothorax
Most common complication → Gas bloat syndrome
Partial fundoplication →
Done to minimize gas bloat syndrome
Types
Dorr’s - 180 degree anterior
Toupet - 180-270 degree anterior
Belsey Mark IV → Uses three layers of sutures
Hill’s repair → Median arcuate ligament repair
LINX device
Ring of interlinked titanium beads with magnetic cores
The magnetic beads are placed around the gastroesophageal junction
Transoral incisionless fundoplication - 270 degrees fundoplication
Diaphragmatic hernia clinical features and treatment
Maldevelopment of septum transversum results in diaphragmatic hernia
Can be acquired as well as congenital.
The acquired ones occur almost always due to road traffic accidents or stab injuries
to the abdomen.
Types
Bochdalek Morgagni
More common Less common
Left posterolateral defect Right anteromedial defect
Defective development of pleuroperitoneal canal Defective central tendon of diaphragm
Stomach, spleen and transverse colon can herniate Transverse colon usually herniates
Clinical features
Prenatally → Polyhydramnios on USG
Newborn → Bowel inside thoracic cavity → Hollowed out abdomen → Scaphoid
abdomen
Bowel sounds heard in thorax
NG tube can get coiled up
Bowel in thorax → Development of lungs impaired → Pulmonary hypoplasia →
Chronic hypoxia → Pulmonary vasoconstriction → Pulmonary hypertension
Management
Treat hypoxia
Bag and mask ventilation contraindicated
Intermittent positive pressure ventilation (IPPV) used
If IPPV fails → ECMO (Extracorporeal membrane oxygenation)
Inhaled nitrates to manage pulmonary hypertension
Definite management
Surgery
Circumferential incision over diaphragm → Contents reduced → Diaphragm repaired
with mesh → Chest tube placed in-situ
A 30 year old lady presents with progressive dysphagia of six months duration
which is more for liquids than solids. How do you investigate and treat this
patient?

23. Stomach and Duodenum

A 50 year male company executive come to the emergency department with
acute onset of severe pain abdomen with non-bilious vomiting. On evaluation
he is profoundly dehydrated in altered sensorium. Further enquiry reveals that
he was taking medications for chronic knee joint pain from a drug shop. What
is the likely clinical diagnosis? What could be the likely electrolyte imbalance in
this patient and explain its pathophysiology? How do you manage this
condition?
Gastric outlet obstruction secondary to chronic cicatrized juxtapyloric peptic ulcer
possibly due to long term NSAID use.
Electrolyte abnormality
Hypochloremia Hypokalemic Hyponatremic metabolic alkalosis with paradoxical
aciduria
Pathophysiology
Recurrent vomiting → Loss of H+ (metabolic alkalosis) and Cl- (hypochloremia) →
Kidney eliminates NaHCO3 to maintain acid-base balance (Renal compensation) →
Loss of Na+ (Hyponatremia) → RAAS activated → Conserves Na+ and excretes K+
(Hypokalemia) initially → Later H+ ions are secreted instead of K+ (Paradoxical
aciduria)
Management
Supportive care
Correction of dehydration and metabolic abnormality by fluids
Best fluid : N/2 NS + KCl + Dextrose
Alternative : Ringer lactate
Definitive surgery to relieve the obstruction
Blood supply of stomach
Left gastric artery is a direct branch of coeliac trunk. It ascends up to esophageal
hiatus and turns to the right along the lesser curvature of stomach. It branches and
anastomoses with branches of right gastric artery and supplies anterior and posterior
wall of the stomach.
Right gastric artery is a branch of hepatic artery which comes from coeliac trunk. It
also supplies lesser curvature and body of stomach, along with left gastric artery
Left gastroepiploic artery arises from splenic artery and supplies greater curvature of
stomach and anastomoses with right gastroepiploic artery.
Right gastroepiploic artery is a branch of gastroduodenal artery, which is a branch of
hepatic artery
Short gastric arteries are the branches of splenic artery. They supply the fundus of
the stomach. They are also called vasa braevia.
Mention causes of acute upper gastrointestinal bleed. A 65 yrs old male with a
past history of Myocardial Infarction was brought to casualty with massive
hematemesis. How will you investigate and manage the patient // Enumerate
causes of upper GI bleed
Causes of acute upper GI bleed
Esophageal causes
Reflux esophagitis
Esophageal varices
Ca Esophagus
Mallory weiss syndrome
Gastric causes
Gastric ulcer
Gastric varices
Acute erosive gastritis
Gastric cancer
Lymphoma
Gastric polyp
Duodenal polyp
Duodenal ulcer
Arteriovenous malformation
Duodenal carcinoma
Aortoduodenal fistula diverticulae
Other rare causes
Purpura
Haemophilia
Haemobilia
Pseudoaneurysms due to acute pancreatitis
Management of a patient with Upper GI bleed
Initial assessment

Investigations
Fibreoptic endoscopy → Should be done on an emergency basis within 6 to 36 hours
of admission
When endoscopy cannot yield diagnosis, selective coeliac angiography should be
done
Isotope studies → IV injection of 99m-Tch-pertechnetate can demonstrate
hypertrophic gastric like mucosa in Meckel’s diverticulum
CT angiogram is gold standard when haemobilia or haemosuccus pancreatitis is
suspected
Treatment
Initial resucitation →
Secure two large bore IV canula for volume replacement
Consider airway protection
Blood transfusion
Vitamin K
Octreotide (3-5 days)
Prophylactic IV antibiotics
Specific Treatment
Upper GI Endoscopy
Indications
Diagnostic
Peptic ulcers—acute and chronic
Gastritis
Carcinoma stomach
Oesophageal varices, ulcers, oesophagitis
Biopsy to rule out H. pylori infection
Brush cytology and biology, yield is better
Therapeutic
Injection of adrenaline into the bleeding vessel
Variceal injection
Snaring of polyps
Electrocoagulation of bleeders
Endoscopic cystogastrostomy
Foreign body removal
Percutaneous endoscopic gastrostomy (PEG)
Endoscopic mucosal resection for early carcinoma stomatch
Congenital hypertrophic pyloric stenosis // Congenital hypertrophic pyloric stenosis -
etiopathogenesis, clinical features and management (x2) // Write briefly on clinical
presentations and management of Hypertrophic Pyloric Stenosis of Infancy
Etiopathogenesis →
Hypertrophy involving the pyloric antral circular muslce fibres. Duodenum is normal
The lumen is so much narrowed to give rise to pyloric obstruction
Familial history
Prenatal incoordination of mucles, lack of nitric oxide relaxation of muscles may be
responsible
Clinical Features
First born male child is usually affected
First symptom is projectile vomiting which occurs 6-8 weeks after birth
Visible gastric peristalsis is seen on the abdomen wall
Loss of weight, dehydration
Olive like mass on palpation in the right hyperchondrium
Investigation
USG →
Thickening (>4mm) and lengthening (>16mm) of the pyloric sphincter
Long axis view of the pylorus → Cervix sign
Short axis view of the pylorus → Target sign
Treatment
Correction of dehydration and electrolyte disturbance by IV 0.45% NS
Ramstedt’s pyloromyotomy
Clinical features and metabolic effects of gastric outlet obstruction // Describe the
symptoms and signs of gastric outlet obstruction // Clinical features of Gastric outlet
obstruction
Chronic cicatrisation of a duodenal ulcer or juxtapyloric ulcer results in narrowing of
pyloric antrum which is described as pyloric stenosis.
Symptoms
Classical hunger pain of duodenal ulcer disappears. It may be replaced by the dull
aching colicky pain of gastric obstruction
Vomiting is profuse, projectile, persistent, fould smelling and non-bilious
Distension of upper abdomen with epigastric fullness
Signs
Visible gastric paralysis
Succussion splash → In pyloric stenosis, even on a fasting stomach there is residual
fluid left in the stomach which gives a splashing sound which can be heard
with/without stethoscope
Auscultopercussion test
Metabolic effects → Hypochloremic Hypokalemic Hyponatremic Metabolic Alkalosis
with Paradoxical aciduria
Describe clinical features, investigations and treatment of Carcinoma Stomach
Clinical features
Early satiety, flatulence, discomfort, pain in the upper abdomen
Anemia
Silent: Growth is silent but manifests as
Secondaries in the liver
Ascites
Left supraclavicular node (Virchow’s node)
Rectovesical deposits (Blumer’s shelf)
Umbilical nodule (Sister Mary Joseph Nodule)
Left axillary lymph nodes (Irish nodes)
Palpable ovarian mass (Krukenberg tumor)
Migratory thrombophlebitis (Trousseau Syndrome)
Leser Trelat Sign
Tripe palms
Obstruction at pylorus causing vomiting with/without blood. Visible gastric paralysis
can also be seen
Lump (mass) in the abdomen which is hard and irregular. Features
Moves with respiration
Upper border of the stomach mass can be made out
Pyloric mass is located in right hypochondrium; mass arising from the body is located
in epigastrium and left hypochondrium
Knee elbow position: Mass falls forward
Mass may have intrinsic mobility
Insidious in onset: Anemia anorexia and aesthesia of short duration
Dyspepsia
Investigations
CBC → Anemia (iron deficiency)
Routine examination for fitness before surgery → FBS, PPBS, ECG, RFT
Flexible upper GI endoscopy
To know extent of lesion
To confirm the diagnosis
To take multiple biopsy - 6 pieces
USG abdomen
To rule out secondaries in the liver
To look for enlarged celiac nodes
To look for ascites
To detect Krukenberg tumor of the ovary
Useful in detecting metastatic disease
CECT abdomen, pelvis and chest → To know about resectability
Endoscopic ultrasonography → Can be used to stage
Laparoscopy → To detect small liver and peritoneal metastasis
PET scan → To rule out metastatic disease
CEA → Indicator of extent of disease
Barium meal - intrinsic, persistent, irregular filling defect
Treatment
Consists of following
Surgical management - Primary tumor resection and lymph node resection
Chemotherapy
Radiotherapy
Primary Tumor Resection
Tumor at the pylorus or antrum → Distal gastrectomy + Gastro-jejunal anastomosis
Tumor in the body of stomach → Subtotal gastrectomy + Gastro-jejunal anastomosis
Tumor at the fundus or Siewert type III → Total gastrectomy + Esophago-jejunal
anastomosis
Lymph node resection
D1 clearance → Group 1 to 6 (perigastric) lymph nodes removed
D2 clearance → Group 1 to 11 (major arterial trunks) lymph nodes removed (Optimal
clearance)
D3 clearance → More than 11 groups of lymph nodes removed (Not done routinely)
Chemotherapy
Indications
Lymph node positive cases
Muscle invasion
Advanced cancer
Chemotherapeutic agents used → 5-FU and cisplatin
Radiotherapy → Given to gastric bed after gastric cancer surgery
Premalignant condition of carcinoma stomach
Atrophic gastritis
Pernicious anemia
Patients with hypogammaglobulinemia
H. pylori infection
Adenomatous polyps
Menetrier’s disease
Gastric ulcer (benign)
Previous gastrojejunal anastomosis or gastric resection
Enumerate the investigations done to evaluate a patient with carcinoma stomach
Investigations
CBC → Anemia (iron deficiency)
Routine examination for fitness before surgery → FBS, PPBS, ECG, RFT
Flexible upper GI endoscopy
To know extent of lesion
To confirm the diagnosis
To take multiple biopsy - 6 pieces
USG abdomen
To rule out secondaries in the liver
To look for enlarged celiac nodes
To look for ascites
To detect Krukenberg tumor of the ovary
Useful in detecting metastatic disease
CECT abdomen, pelvis and chest → To know about resectability
Endoscopic ultrasonography → Can be used to stage
Laparoscopy → To detect small liver and peritoneal metastasis
PET scan → To rule out metastatic disease
CEA → Indicator of extent of disease
Barium meal - intrinsic, persistent, irregular filling defect
Carcinoma stomach: investigations and treatment
Investigations
CBC → Anemia (iron deficiency)
Routine examination for fitness before surgery → FBS, PPBS, ECG, RFT
Flexible upper GI endoscopy
To know extent of lesion
To confirm the diagnosis
To take multiple biopsy - 6 pieces
USG abdomen
To rule out secondaries in the liver
To look for enlarged celiac nodes
To look for ascites
To detect Krukenberg tumor of the ovary
Useful in detecting metastatic disease
CECT abdomen, pelvis and chest → To know about resectability
Endoscopic ultrasonography → Can be used to stage
Laparoscopy → To detect small liver and peritoneal metastasis
PET scan → To rule out metastatic disease
CEA → Indicator of extent of disease
Barium meal - intrinsic, persistent, irregular filling defect
Treatment
Consists of following
Surgical management - Primary tumor resection and lymph node resection
Chemotherapy
Radiotherapy
Primary Tumor Resection
Tumor at the pylorus or antrum → Distal gastrectomy + Gastro-jejunal anastomosis
Tumor in the body of stomach → Subtotal gastrectomy + Gastro-jejunal anastomosis
Tumor at the fundus or Siewert type III → Total gastrectomy + Esophago-jejunal
anastomosis
Lymph node resection
D1 clearance → Group 1 to 6 (perigastric) lymph nodes removed
D2 clearance → Group 1 to 11 (major arterial trunks) lymph nodes removed (Optimal
clearance)
D3 clearance → More than 11 groups of lymph nodes removed (Not done routinely)
Chemotherapy
Indications
Lymph node positive cases
Muscle invasion
Advanced cancer
Chemotherapeutic agents used → 5-FU and cisplatin
Radiotherapy → Given to gastric bed after gastric cancer surgery
Complications of peptic ulcers
Acute complications
Perforation - Anterior duodenal ulcers perforate
Bleeding - Posterior duodenal ulcers bleed. Most commonly from the
gastroduodenal artery.
Chronic complications
Gastric outlet obstruction → Due to chronic cicatrization of duodenal ulcer or
juxtapyloric ulcer, there is narrowing of pyloric antrum which is described as pyloric
stenosis.
Teapot deformity or handbag stomach → Due to long standing lesser curvature
gastric ulcer there is shortening of the lesser curvature due to fibrosis.
Hourglass contracture
Penetration into pancreas
Early gastric cancer
H. pylori
Cause of 90% duodenal ulcer and 75% gastric ulcers
Spiral gram negative bacilli
Resides in the gastric epithelium within or beneath the mucus layer, which protects it
from both acid and antibiotics
Locally produced toxin mediators
Urease which breaks down urea into ammonia and uric acid which creates an alkaline
microenvironment protecting the bacteria from acidic environment of stomach
Cytotoxins
Vacuolating cytotoxin (VacA) causes the release of cytochrome C from mitochondria
and induces apoptosis
Mucinase that degrades mucus and glycoproteins
Phospholipase that damages epithelial cells and mucus cells
Platelet activating factor, which is known to cause mucosal injury
Diagnosis
Non-invasive methods
Urea-breath test - Sensitivity and specificity greater than 90%
Serology
Detection of antigen in stool samples
Invasive methods
Endoscopic antral biopsy can be taken and the organism is cultured in agar
containing urea and pH-sensitive colorimetric agent
Due to activity of urease the pH of the medium changes and this changes the color
of colorimetric agent
Treatment
PPI triple therapy
PPI BD
Amoxicillin 1000 mg BD
Clarithromycin / Metronidazole 500 mg BD
Quadruple therapy
PPI BD
Metronidazole 250 mg TID
Tetracycline 500 mg QID
Bismuth 2tabs QID
Complications of H. pylori infection
Chronic duodenal ulcer
Chronic gastritis
GERD
Gastric carcinoma
Gastric MALToma
ITP
H. pylori eradication therapy (x2)
PPI triple therapy
PPI BD
Amoxicillin 1000 mg BD
Clarithromycin / Metronidazole 500 mg BD
Quadruple therapy
PPI BD
Metronidazole 250 mg TID
Tetracycline 500 mg QID
Bismuth 2tabs QID
Management of GIST (Gastro Intestinal Stromal Tumor) of stomach
Investigations
CECT : GIST is a radiological diagnosis. So biopsy in not mandatory.
PET-CT : Used for monitoring therapy in metastatic GIST
Immunohistochemistry
CD117/c-KIT → Most common. Seen in >90% GIST
CD34 → 60-70% patients are positive
DOG1 → Most specific marker for GIST
CD117 negative → Wild type GIST
Management
Surgery is the primary management
Margin taken is 2 cm
Gastric GIST : Wedge resection is done. Gastrectomy is not necessary
Intestinal GIST : Resection and anastomosis is done.
Routine lymph node clearance is not done
Adhesions are seen with surrounding structures. Structures/organs with adhesions
are removed to prevent local recurrence.
If malignant GIST/metastatic GIST
GISTs are classified according to their malignancy risk by Fletcher’s classification
which takes into account :
Size of tumor
Number of mitotic figures
Imatinib (tyrosine kinase inhibitor) is used.
If resistance to imatinib : Sunitinib, sorafenib are used
GIST
What are the features of duodenal ulcer perforation? How duodenal ulcer
perforation is managed?
Features
Stage of chemical peritonitis
Symptoms and History
Severe agonizing pain in the right hypochondrium
Episode of coffee-ground vomitus, maybe followed by melena later
General examination
Pulse rate increases, patient is anxious and pale
Per abdomen examination
Guarding and rigidity of abdominal wall
Rebound tenderness (Blumberg’s sign)
Liver dullness obliterated because of collection of free air under the right dome of
diaphragm
Bowel sounds absent
Stage of reaction/illusion/dilution
General examination
Pulse is feeble, more than 120 beats per minute
Hypotension persists
Evidence of dehydration due to loss of fluid into peritoneal cavity
Per abdomen examination
Abdominal distension due to fluid and paralytic ileus
Guarding and rigidity are worsened
Shifting dullness is present
Bowel sounds absent
Stage of bacterial peritonitis
Patient becomes severely ill, dehydrated, toxic with drawn in cheeks
Tongue is dry and coated but with bright eyes (Hippocratic facies)
Features of hypovolemia and septic shock such as feeble thready pulse, cold
peripheries, shallow respiration, high grade fever and persistent hypotension present
Gross abdominal distension, guarding, rigidity, abdominal tenderness suggest
generalized peritonitis
Investigations
CBC and electrolytes
Plain X-ray chest or abdomen in erect position shows free air under the right dome
of diaphragm. If patient is not able to stand a left lateral decubitus view is taken
CT scan with contrast - pneumoperitoneium, fluid in the abdomen, site of perforation
Treatment (ABCDEF)
Aspiration of stomach contents with Ryle’s tube to reduce further contamination and
decrease biliary and pancreatic juice
Blood grouping and cross matching may be necessary for surgery
Charts: Temperature, pulse, BP, respiration, urinary output
Drugs:
Inj. ampicillin 500 mg IV, STAT and 6th hourly (Gram positive)
Inj. gentamicin 60-80 mg IV, 8th hourly (Gram negative)
Inj. metronidazole 500 mg IV, 8th hourly (Anaerobes)
Cephalosporins can also be used depending on the severity of shock
Explorative laparotomy is done through a midline incision. The perforation is
identified and closed with interrupted non-absorbable silk sutures, which is
strengthened by placement of omentum. Peritoneal toilet/wash is given to avoid
residual abscess, Abdomen is closed with a drain which is removed after 3-5 days. If
its a large gastric ulcer, it is better to do gastrectomy if the condition of patient
permits
Vagotomy and GJ is not done at this stage as the condition of patient is very poor
and there is peritoneal sepsis
Postoperatively the patient is put on anti-ulcer drugs
An endoscopy is done after 2 months. If the ulcer persists, it may be worthwhile
giving a course of H. pylori eradication treatment. Inspite of this treatment, if
symptoms and ulcer persists it is likely to be a chronic ulcer and an elective operation
such as vagotomy and GJ is done. Simple suturing cures majority of acute ulcers
Fluids are given preoperatively to treat dehydration and postoperatively for 3–4 days
till the paralytic ileus settles down (soft abdomen and bowel sounds present)
Stages and signs of duodenal ulcer perforation
Stage of chemical peritonitis
Symptoms and History
Severe agonizing pain in the right hypochondrium
Episode of coffee-ground vomitus, maybe followed by melena later
General examination
Pulse rate increases, patient is anxious and pale
Per abdomen examination
Guarding and rigidity of abdominal wall
Rebound tenderness (Blumberg’s sign)
Liver dullness obliterated because of collection of free air under the right dome of
diaphragm
Bowel sounds absent
Stage of reaction/illusion/dilution
General examination
Pulse is feeble, more than 120 beats per minute
Hypotension persists
Evidence of dehydration due to loss of fluid into peritoneal cavity
Per abdomen examination
Abdominal distension due to fluid and paralytic ileus
Guarding and rigidity are worsened
Shifting dullness is present
Bowel sounds absent
Stage of bacterial peritonitis
Patient becomes severely ill, dehydrated, toxic with drawn in cheeks
Tongue is dry and coated but with bright eyes (Hippocratic facies)
Features of hypovolemia and septic shock such as feeble thready pulse, cold
peripheries, shallow respiration, high grade fever and persistent hypotension present
Gross abdominal distension, guarding, rigidity, abdominal tenderness suggest
generalized peritonitis
Management of Perforated duodenal ulcer
Investigations
CBC and electrolytes
Plain X-ray chest or abdomen in erect position shows free air under the right dome
of diaphragm. If patient is not able to stand a left lateral decubitus view is taken
CT scan with contrast - pneumoperitoneium, fluid in the abdomen, site of perforation
Treatment (ABCDEF)
Aspiration of stomach contents with Ryle’s tube to reduce further contamination and
decrease biliary and pancreatic juice
Blood grouping and cross matching may be necessary for surgery
Charts: Temperature, pulse, BP, respiration, urinary output
Drugs:
Inj. ampicillin 500 mg IV, STAT and 6th hourly (Gram positive)
Inj. gentamicin 60-80 mg IV, 8th hourly (Gram negative)
Inj. metronidazole 500 mg IV, 8th hourly (Anaerobes)
Cephalosporins can also be used depending on the severity of shock
Explorative laparotomy is done through a midline incision. The perforation is
identified and closed with interrupted non-absorbable silk sutures, which is
strengthened by placement of omentum. Peritoneal toilet/wash is given to avoid
residual abscess, Abdomen is closed with a drain which is removed after 3-5 days. If
its a large gastric ulcer, it is better to do gastrectomy if the condition of patient
permits
Vagotomy and GJ is not done at this stage as the condition of patient is very poor
and there is peritoneal sepsis
Postoperatively the patient is put on anti-ulcer drugs
An endoscopy is done after 2 months. If the ulcer persists, it may be worthwhile
giving a course of H. pylori eradication treatment. Inspite of this treatment, if
symptoms and ulcer persists it is likely to be a chronic ulcer and an elective operation
such as vagotomy and GJ is done. Simple suturing cures majority of acute ulcers
Fluids are given preoperatively to treat dehydration and postoperatively for 3–4 days
till the paralytic ileus settles down (soft abdomen and bowel sounds present)
A man previously on long term NSAID’S presents with features of peritonitis.
What could be the two most likely causes for his peritonitis? How will you
investigate and treat the causes?
The most likely cause for his peritonitis is peptic ulcer perforation.
Investigations
CBC and electrolytes
Plain X-ray chest or abdomen in erect position shows free air under the right dome
of diaphragm. If patient is not able to stand a left lateral decubitus view is taken
CT scan with contrast - pneumoperitoneium, fluid in the abdomen, site of perforation
Treatment (ABCDEF)
Aspiration of stomach contents with Ryle’s tube to reduce further contamination and
decrease biliary and pancreatic juice
Blood grouping and cross matching may be necessary for surgery
Charts: Temperature, pulse, BP, respiration, urinary output
Drugs:
Inj. ampicillin 500 mg IV, STAT and 6th hourly (Gram positive)
Inj. gentamicin 60-80 mg IV, 8th hourly (Gram negative)
Inj. metronidazole 500 mg IV, 8th hourly (Anaerobes)
Cephalosporins can also be used depending on the severity of shock
Explorative laparotomy is done through a midline incision. The perforation is
identified and closed with interrupted non-absorbable silk sutures, which is
strengthened by placement of omentum. Peritoneal toilet/wash is given to avoid
residual abscess, Abdomen is closed with a drain which is removed after 3-5 days. If
its a large gastric ulcer, it is better to do gastrectomy if the condition of patient
permits
Vagotomy and GJ is not done at this stage as the condition of patient is very poor
and there is peritoneal sepsis
Postoperatively the patient is put on anti-ulcer drugs
An endoscopy is done after 2 months. If the ulcer persists, it may be worthwhile
giving a course of H. pylori eradication treatment. Inspite of this treatment, if
symptoms and ulcer persists it is likely to be a chronic ulcer and an elective operation
such as vagotomy and GJ is done. Simple suturing cures majority of acute ulcers
Fluids are given preoperatively to treat dehydration and postoperatively for 3–4 days
till the paralytic ileus settles down (soft abdomen and bowel sounds present)
Duodenal ulcer: Causes and treatment
Causes
Neurological causes → Stimulation of vagus increases secretion of acids. This is
brought about by anxiety, worry, hurry and curry.
NSAIDs → More responsible for gastric ulcer rather than duodenal ulcer
Genetic causes → Family history of duodenal ulcer may be present which suggests a
genetic cause. Patients with blood group ‘O’ are more prone, for the development of
chronic duodenal ulcer because of increased parietal cell population.
Food habits → Spicy food, diet poor in vitamins, smoking and alcohol, alone or in
combination precipitate the development of chronic duodenal ulcer.
Bacteriological causes → H. pylori is implicated in 60-80% of duodenal ulcers
Endocrinal causes
Zollinger-Ellison syndrome is a non-beta cell tumor of pancreas with
hypergastrinemia
Hyperparathyroidism → Increased calcium levels → Stimulates parietal cells →
Hyperacidity
Investigations
Esophagogastroduodenoscopy (EGD) →
Ulcer appears as a crater with/without slough or bleeding.
In gastric ulcers, take routine biopsy to rule out malignancy
In duodenal ulcers biopsy is done in recurrent cases to rule out H. pylori.
Tests for H. pylori
Non-invasive tests
Urea breath test
Serology
Detection of antigens in stool
Invasive
EGD and biopsy
Treatment
Medical
H2 blockers → Chances of relapse are more
Ranitidine (150 mg BD x 6 weeks)
Famotidine (20 mg BD)
Roxatidine (75 mg BD)
PPIs
Omeprazole (20 mg OD)
Esomeprazole (40 mg/day)
Lansoprazole (30 mg/day)
Pantoprazole (40 mg/day)
Regular antacids - calcium or magnesium based
Given in high doses (120 ml/day) they will neutralize the acid (not practical)
Instead small dose of antacids added to H2 blocker for psychological benefit of
patient
Diet → Spicy food, coffee, alcohol, and smoking to be discouraged. Discontinue
aspirin or NSAIDs and other gastric irritants
Eradication therapy
Bismuth Tiple Therapy
Bismuth 2 tablets QID
Metronidazole 250 mg TID
Tetracycline 500 mg QID
PPI triple therapy
PPI BD
Amoxicillin 1 g BD
Clarithromycin or Metronidazole 500 mg BD
Quadruple therapy
PPI BD
Bismuth 2 tablets QID
Metronidazole 250 mg TID
Tetracycline 500 mg QID
Surgical
Indications
Intractable pain in spite of treatment with PPIs
Frequent replapses
Complications - Gastric outlet obstruction, hemorrhage
Procedures
Highly selective vagotomy →
The branches of the nerves of Latarjet supplying parietal cell mass are divided.
Hence, it is called parietal cell vagotomy.
The terminal fibres of the nerve of Latarjet which supply pylorus are preserved (5–7
cm of ‘Crow foot’). Hence no drainage procedure is required because pyloric function
is preserved
Total truncal abdominal vagotomy with gastrojejunostomy or with pyloroplasty
Most popular and most commonly done
Anterior and posterior trunks of the vagus are divided just below the diaphragm.
Drainage procedure : Any of the following two
Gastrojejunostomy : Posterior, vertical, retrocolic, isoperistaltic, no sloop, no tension,
GJ of Mayo (PVRING) preferred
Pyloroplasty - Heinke-Mikulicz pyloroplasty or Finney pyloroplasty
Vagotomy and antrectomy
Post gastrectomy dumping syndrome

Differences between gastric and duodenal ulcers

Gastric ulcer Duodenal ulcer
Pain Increases with meals - weight Decreases with meals - weight gain
loss
H. pylori ~70% ~90%
infection
Mechanism Decreased mucosal protection Decreased mucosal protection or increased gastric acid
secretion
Other causes NSAIDs Zollinger-Ellison Syndrome
Risk of More Generally benign
carcinoma
Other Biopsy margins to rule out Hypertrophy of Brunner glands
malignancy
Complications of gastro-jejunosotmy.
Anastomotic leaks
Bilious vomiting
Bowel obstruction (Internal hernias) :
Peterson’s hernia → Seen in antecolic approach when another piece of bowel
herniates behind the roux limb
Stemmer’s hernia → Seen in retrocolic approach when one or more loop of bowel
herniates through the transverse mesocolon window.
Peptic ulcer at anastomotic site
Stenosis of gastrojejunostomy
Iron and Vitamin B12 deficiency
Complications due to vagotomy
Gallstone formation
Impaired gastric emptying
Dumping syndrome

Gastrinoma // Clinical features and management of Zollinger-Ellison syndrome //

Zollinger Ellison syndrome
Clinical features
Clinical triad - gastric acid hypersecretion, severe PUD and non-islet cell tumors of
pancreas
Abdominal pain
Diarrhea
Weight loss and steatorrhea also secondary to decreased duodenal and jejunal pH
and inactivation of lipase
Esophagitis from gastro-esophageal reflux
Investigation
Endoscopy →
Peptic ulcer disease
Gastric rugal folds, reflecting the trophic effect of hypergastrinemia on the gastric
fundus
Serum gastrin levels
Elevated fasting levels (>200 pg/mL) mostly present
Values > 1000 pg/mL are diagnostic
Secretin/Pentagastrin test
Secretin (2 mg/kg) is administered intravenously and serum gastrin samples are
measured before and after secretin administration at 5-minute interval for 30
minutes.
An increase in serum gastrin of greater than 200 pg/ml above basal levels is specific
for gastrinoma.
Treatment
Localization of the gastrinoma is performed before operative intervention is made
Noninvasive methods include
CT
MRI
Endoscopic ultrasound
111111In-octreotide scintigraphy
Invasive modalities include
Selective visceral angiography
Percutaneous transhepatic portal venous sampling for gastrin
Selective arterial secretin stimulation test
If the tumor is resectable
< 5 mm → Enucleation
> 5 mm → Full thickness removal
If the tumor in unresectable
Chemotherapy using 5-FU, streptozocin
High dose of PPIs
Octreotide

24. Liver
Describe etiology, clinical features and management of Hepatocellular
carcinoma.
Etiology
Hepatitis B virus
Hepatitis C virus
Hepatitis D
Cirrhosis
Aflatoxin consumption
OCPs
Heavy alcohol consumption, smoking, hemochromatosis
Type I glycogen storage disorder and familial polyposis coli alpha-1 antitrypsin
deficiency, Budd-Chiari syndrome
Clinical features
Age group: Highest incidence is found after 50 years
Sex: Male alcoholics
Hepatomegaly is the most common feature
Liver is hard on palpation
Weight loss
Weakness
Paraneoplastic syndromes - Hypoglycemia, hypercholesterolemia
Investigations
Complete blood picture → Hb is usually low
LFTs → High bilirubin, low albumin and high globulin levels
Chest X-ray → CT chest pulmonary metastasis
Abdominal USG
Diffuse distortion of hepatic parenchyma and a well-circumscribed hyperechogenic
mass suggests HCC
Mosaic pattern of tumor with thin halo and lateral shadows, nodule in nodular patter
with separating fibrous septa and posterior echo nehancement
Tumor thrombi in portal vein, hepatic vein or IVC
Triple Phase CT is the investigation of choice. It helps differentiate HCC from
metastasis
Non contrast phase → Both appear hypodense
Arterial phase
HCC appears hyperdense
Metastasis appears hypodense
Washout (Venous) phase
Rapid washout in HCC
Metastasis appear hypodense
Tumor markers
Alpha-fetoprotein
PIVKA 2 (Protein induced Vitamin K antagonism)
Glycipan
HepPar - 1
Neurotensin-B raised in fibrolamellar variant
MRI
Liver biopsy - Done for unresectable cases or metastatic disease before starting
chemotherapy.
Treatment
Resection → It is the best possible treatment for hepatocellular carcinoma. Up to 3
segments of the liver can be resected. Rest of the liver will be enough to maintain life
provided remaining liver is healthy/noncirrhotic
Functional liver remnant (FLR) should be >20% of standardised total liver volume
after resection.
The remnant liver should have vascular inflow, venous outflow, biliary drainage.
Two contiguous liver segments must be left behind
Transcatheter arterial chemoembolization
By introducing gel foam into the branches of hepatic artery some amount of tumor
necrosis occurs.
This arterial embolization combined with chemotherapeutic agents such as
doxorubicin, results are better because the tumor has prolonged exposure to the
drug. This is called transarterial chemoembolisation (TACE).
This method is followed only as a palliative procedure
Trans-arterial radioembolization
Another option for unresectable HCC
Also called internal radiation
Most commonly used radioactive material is Yttrium-90 (90Y).
It emits β-radiation.
It is delivered through feeding vessels of the tumour.
Thus, any tumor, any size, any nodules can be irradiated.
Survival is prolonged with this treatment.
Can be used in cirrhotic patients of poor liver function
It is indicated in advanced disease, portal vein thrombosis
Percutaneous ethanol ablation
Tumor necrosis occurs as a result of cellular dehydration denaturation of proteins
and occlusion of small tumor vessels.
It is cheaper and is a palliative treatment. Tumor less than 3 cm and nodules not
more than 3 are candidates. It reduces the tumor size and decreases pain
Radiofrequency ablation (RFA)
It is now being tried for inoperable tumours or patients who are not ideal candidates
for surgery, as per Milan’s criteria -
Single tumor < 5 cm
1-3 tumors < 3 cm with no distant metastasis/vascular invasion
Electrical energy (500 kHz) is delivered through a 18 G needle inserted under US or
CT guidance through the skin into the tumor. In the following few months, the tumor
is destroyed and the cells are killed
Injection octreotide
Sorafenib
Drug of choice in advanced liver disease with good liver function
Multi-tyrosine kinase inhibitor
Promotes apoptosis and inhibits angiogenesis
Side effects: Fatigue, skin rashes, hand-foot syndrome, hypertension
Describe the segmental anatomy of liver with the help of a neat labeled
diagram. Explain the pathology, clinical features and management of
hepatocellular carcinoma
Segmental anatomy of liver
The liver is divided into two lobes by the main portal fissure, which is also called
Cantlie’s line. This line extends from gall bladder fossa to the left side of IVC.
The right portal fissure contains the right hepatic vein. The fissure divides the right
lobe into
Anteromedial sector
Segment V anteriorly
Segment VIII posteriorly
Posterolateral sector
Segment VI anteriorly
Segment VII posteriorly
The left portal fissure contains the left hepatic vein. This fissure divides the left lobe
into
Anterior sector
Segment IV (Quadrate lobe)
Segment III
Posterior sector
Segment II
Segment I (caudate lobe) is an autonomous segment.
Pathology
Highly vascular tumor
Histological variants
Fibrolamellar
Mixed hepatocellular cholangiocarcinoma cellular
Clear cell variant
Giant cell variant
Childhood HCC
Carcinosarcoma
Pathological types
Hanging type: It is attached to the liver by a small stalk—easily resected.
Pushing type: A tumor pushing the blood vessels. It is also resectable.
Infiltrative type: Difficult to resect because of infiltration into surrounding structures
Clinical features
Age group: Highest incidence is found after 50 years
Sex: Male alcoholics
Hepatomegaly is the most common feature
Liver is hard on palpation
Weight loss
Weakness
Paraneoplastic syndromes - Hypoglycemia, hypercholesterolemia
Investigations
Complete blood picture → Hb is usually low
LFTs → High bilirubin, low albumin and high globulin levels
Chest X-ray → CT chest pulmonary metastasis
Abdominal USG
Diffuse distortion of hepatic parenchyma and a well-circumscribed hyperechogenic
mass suggests HCC
Mosaic pattern of tumor with thin halo and lateral shadows, nodule in nodular patter
with separating fibrous septa and posterior echo nehancement
Tumor thrombi in portal vein, hepatic vein or IVC
Triple Phase CT is the investigation of choice. It helps differentiate HCC from
metastasis
Non contrast phase → Both appear hypodense
Arterial phase
HCC appears hyperdense
Metastasis appears hypodense
Washout (Venous) phase
Rapid washout in HCC
Metastasis appear hypodense
Tumor markers
Alpha-fetoprotein
PIVKA 2 (Protein induced Vitamin K antagonism)
Glycipan
HepPar - 1
Neurotensin-B raised in fibrolamellar variant
MRI
Liver biopsy - Done for unresectable cases or metastatic disease before starting
chemotherapy.
Treatment
Resection → It is the best possible treatment for hepatocellular carcinoma. Up to 3
segments of the liver can be resected. Rest of the liver will be enough to maintain life
provided remaining liver is healthy/noncirrhotic
Functional liver remnant (FLR) should be >20% of standardised total liver volume
after resection.
The remnant liver should have vascular inflow, venous outflow, biliary drainage.
Two contiguous liver segments must be left behind
Transcatheter arterial chemoembolization
By introducing gel foam into the branches of hepatic artery some amount of tumor
necrosis occurs.
This arterial embolization combined with chemotherapeutic agents such as
doxorubicin, results are better because the tumor has prolonged exposure to the
drug. This is called transarterial chemoembolisation (TACE).
This method is followed only as a palliative procedure
Trans-arterial radioembolization
Another option for unresectable HCC
Also called internal radiation
Most commonly used radioactive material is Yttrium-90 (90Y).
It emits β-radiation.
It is delivered through feeding vessels of the tumour.
Thus, any tumor, any size, any nodules can be irradiated.
Survival is prolonged with this treatment.
Can be used in cirrhotic patients of poor liver function
It is indicated in advanced disease, portal vein thrombosis
Percutaneous ethanol ablation
Tumor necrosis occurs as a result of cellular dehydration denaturation of proteins
and occlusion of small tumor vessels.
It is cheaper and is a palliative treatment. Tumor less than 3 cm and nodules not
more than 3 are candidates. It reduces the tumor size and decreases pain
Radiofrequency ablation (RFA)
It is now being tried for inoperable tumours or patients who are not ideal candidates
for surgery, as per Milan’s criteria -
Single tumor < 5 cm
1-3 tumors < 3 cm with no distant metastasis/vascular invasion
Electrical energy (500 kHz) is delivered through a 18 G needle inserted under US or
CT guidance through the skin into the tumor. In the following few months, the tumor
is destroyed and the cells are killed
Injection octreotide
Sorafenib
Drug of choice in advanced liver disease with good liver function
Multi-tyrosine kinase inhibitor
Promotes apoptosis and inhibits angiogenesis
Side effects: Fatigue, skin rashes, hand-foot syndrome, hypertension
Hydatid cyst liver - etiopathogenesis and treatment // Management of Hydatid cyst
of Liver // Discuss the management and complications of Hydatid cyst of liver.
Etiopathogenesis
The disease is caused by Echinococcus granulosus, transmitted by dogs which are the
chief mediators (host) and man is the intermediate host.
After swallowing the ova, they penetrate gastric mucosa, reach retroperitoneal
structures, penetrate portal vein directly and then enter into liver.
Having reached liver, the organisms grow and develop their own protective layer and
form hydatid cyst.
Investigations
USG can detect the cyst, localize it and used for aspiration purposes.
Plain X-ray abdomen - speckled calcification
CT scan
ERCP if there is obstructive jaundice. A wide sphincterectomy should be given so as
to allow the drainage of hydatid contents into the duodenum.
Casoni’s intradermal test
ELISA and electrophoresis
Treatment
All interventions are done under the cover of Albendazole for at least 7-10 days
PAIR
The first line treatment is percutaneous aspiration, injection and re-aspiration (PAIR)
The procedure is done under USG guidance
A needle is introduced into the cyst and the hydatid fluid is aspirated
A scolicidal agent is then injected into the cyst to kill the organism. Scolicidal agents
used are
Ethanol
Absolute alcohol
Cetrimide solution
Mebendazole solution
The scolicidal agent is then re-aspirated
Surgical procedures
Cystopericystectomy (Cyst along with pericyst)
Liver resection : If multiple cysts in one lobe
Capitonage : The cyst is removed and the cavity is spirally sutured
Complications
Rupture → Can lead to
Anaphylactic shock
Implantation of cysts within peritoneal cavity
Obstructive jaundice (Rupture into biliary radicles)
Jaundice due to cysts within biliary tree or due to large cyst compressing biliary ducts
Suppuration
Calcification
Management of amoebic liver abscess
Investigations
Total WBC count - increased
Stool examination - Ova and cysts
Serological testing - Indirect hemagglutination test is positive
Sigmoidoscopy - large, deep amoebic ulcers - flask shaped
Abdominal USG
Locate the site of abscess
USG guided aspiration can be done - anchovy sauce pus devoid of neutrophils
CECT can demonstrate the abscess cavity and is the investigation of choice.
Treatment
Double strength metronidazole (800 mg TID) is started. If the patient is responding it
is continued for 2-3 weeks
A 10 day course of diloxanide furoate (luminal amebicide) is given after the
metronidazole course.
Chloroquine (tissue amebicide) can be added if there is no response to
metronidazole.
Aspiration and pig-tail catheter insertion can be done in following cases
No response to medical therapy
Secondary infection
Abscess cavity > 5 cm
Pregnant patient
Impending rupture
Left lobe liver abscess : Slim chance of rupture into pericardium
Transjugular intrahepatic portosystemic stent shunts: procedure and complication
Used for the treatment of massive bleeding varices in portal hypertension
Consists of vascular placement of expandable metal stent across the tract between
hepatic vein and major branch of portal system
TIPSS helps a small group of patients
Low morbidity and mortality
Incidence of encephalopathy is similar to surgical shunts
Enumerate Liver Function tests and significance of Alkaline phosphatase
Serum proteins - Total protein, albumin and albumin globulin ratio
Enzymes - SGOT and SGPT
Serum bilirubin - direct, indirect and total
Prothrombin time, bleeding time and clotting time
Gamma glutamyl transferase
Alkaline phosphatase
It is the product of epithelial cells of cholangioles—↑ levels are due to increased
enzyme production.
Intrahepatic cholestasis, cholangitis, and extrahepatic obstruction are the chief
factors causing elevation.
Focal lesions in the liver—single hepatic metastasis or liver abscess or a tumour can
cause increased levels without jaundice.
In cholangitis, bilirubin may be normal but alkaline phosphatase may be very high.
Gross elevation - Obstructive jaundice, biliary cirrhosis, bone disease
Mild elevation - Metastasis in the liver, hepatic abscess, hepatitis

25. Gall Bladder and Pancreas

Enumerate causes of obstructive jaundice

Enumerate the causes of obstructive jaundice. Describe the clinical features,

investigations and treatment of a suspected case of jaundice due to CBD stones.
Causes
Causes in the Lumen
Stones in the common bile duct
Ova, cysts, ascaris worms
Hydatid cyst of the biliary tree
Stone in the pancreatic duct/CBD junction
Causes in the Wall
Periampullary carcinoma
Bile duct stricture
Stenosis of sphincter of Oddi (papillary stenosis)
Klatskin’s tumour—carcinoma of the bile duct where right and left ducts join
Choledochal cyst
Post-laparoscopic cholecystectomy
Causes from Outside (due to Pressure)
Carcinoma head of pancreas
Chronic pancreatitis
Lymph nodes at the porta hepatis obstructing the biliary tree
Clinical features
Asymptomatic
More common in females
Age: 30-50 years
Symptoms
Obstructive jaundice
Charcot’s triad : Intermittent pain, intermittent fever and intermittent jaundice
Reynold’s pentad : Charcot’s triad + Shock + Altered mental status
Pruritus
Signs
Deep yellow jaundice
Per abdomen : Liver enlarged due to back pressure. It is smooth with round border
and firm in consistency
Gall bladder : Not palpable
Investigations
Hb% is low in malignancy
Total count and differential count are increased in case of infections
Bleeding time, clotting time and prothrombin time are altered in case of obstructive
jaundice
Urine for urobilinogen is negative in obstructive jaundice
Serum ALP : Normal is 60-300 units/L. More than 500 units is suggestive of
obstructive jaundice.
GGT
Abdominal USG → Stones can be diagnosed with their posterior acoustic shadow
ERCP → Stones appear as filling defects in the CBD or in the common hepatic duct
(CHD)
MRCP → Investigation of choice in cases of obstructive jaundice due to high
strictures or cholangiocarcinoma
Endosonography → To detect missed stones in CBD.
Treatment of CBD stones
Depends on the scenario
CBD stone and GB stone detected before surgery
ERCP, sphincterectomy → Few days → Laparoscopic cholecystectomy
CBD stone detected during laparoscopic cholecystectomy
Indicators for CBD stone
Increased ALP
History of jaundice
USG : CBD > 10 mm in diameter
If indicators for CBD stone present then confirmation has to be done.
Do laparoscopic cholecystectomy + exploration of CBD
If laparoscopic exploration of CBD not possible do open exploration
Make a longitudinal cut in CBD.
Insert a T-tube in CBD
Inject dye after 7-10 days
If no residual stone → Remove T-tube
Stones present → Remove stones through tract
CBD stone detected after surgery
Could be residual stone (< 2 years) or recurrent stone (> 2 years)
ERCP sphincterectomy (1.5 cm in size)
If fails do transduodenal sphincterectomy
If fails or stone impacted higher up → Supraduodenal choledocholithotomy
A 65 year old patient presents with progressive jaundice, weight loss and loss of
appetite. His reports are negative for viral markers. Discuss the differential
diagnosis, investigation and treatment of the patient.
Differential diagnosis : Obstructive jaundice due to
Carcinoma periampullary/head of pancreas.
CBD stones : Presents without loss of appetite or weight.
Investigations -
Hb% is low in malignancy
Total count and differential count are increased in case of infections
Bleeding time, clotting time and prothrombin time are altered in case of obstructive
jaundice
Urine for urobilinogen is negative in obstructive jaundice
Serum ALP : Normal is 60-300 units/L. More than 500 units is suggestive of
obstructive jaundice.
GGT
Abdominal USG
Mass lesion in the head region can be seen in cases of chronic pancreatitis or
carcinoma head of the pancreas causing obstructive jaundice
Ultrasound can detect multiple secondaries in the liver, thus, favouring the diagnosis
of malignancy
CECT
A head mass of even 2–3 cm in size and portal vein infiltration can be demonstrated
by CT scan.
Obliteration of fat plane between the mass and superior mesenteric vessels can be
demonstrated by CT scan which decides the operability of periampullary carcinoma
or carcinoma head of the pancreas
Endoscopy
Useful to diagnose a periampullary carcinoma which may be seen as an ulcerative
lesion in the second part of the duodenum.
Biopsy can also be taken which shows adenocarcinoma
Barium meal
Periampullary carcinoma - Distortion of medial border of the duodenum (Inverted 3
sign)
In carcinoma head of pancreas - Widening of C-loop of duodenum (Pad sign)
ERCP
A periampullary carcinoma gives rise to an irregular filling defect or there may be
total cut off in the flow of dye.
Chronic pancreatitis may show the dilated duct and stones in the pancreatic duct—
‘chain of lakes’ appearance.
MRCP
Investigation of choice in cases of obstructive jaundice due to high strictures or
cholangiocarcinoma
Endosonography → To detect missed stones in CBD. It can also detect pancreatic
head mass, lymph nodes.
Diagnostic laparoscopy
CA 19-9 → Carcinoma pancreas / Chronic pancreatitis
Treatment
Resectable tumors
Head of pancreas → Whipple’s surgery / Pancreaticoduodenectomy
Body and tail of pancreas → Distal pancreatectomy
Unresectable tumor → palliative management
Modified Whipple’s / Longmire and Traverso procedure
Incision : Chevron or rooftop incision
The vessels lie in the groove of pancreas
To carry out a pancreaticoduodenectomy the pancreas has to be resected around the
vessel
This is possible with the help of a plane which is present in between the vessel and
the pancreas called the tunnel of love
Structures cut
Transected at the pylorus
CBD is resected and a cholecystectomy is done
Head and neck with part of body and pancreas.
Duodenum
Parts left after resection
Cut end of CBD
Cut end of GB
Cut end of pancreas
Jejunum
Jejunum is anastomosed with pancreas, stomach and CBD - Hepatico-choledocho-
jejunostomy, gastro-jejunostomy, pancreatico-jejunostomy
Steps :
The plane “tunnel of love” is formed
Body is resected
Retroperitoneal mobilization of pancreas
Cupping of pancreatic head, proximal jejunum and duodenum
Ligation of inferior pancreaticoduodenal vessel
The ligament of Trietze is cut
Mobilization of jejunum through the transverse mesocolon window
Uncinate is dissected under the confluence of the superior mesenteric vein and
portal vein lateral to SMA
Stomach is dissected and stapled
Cholecystectomy is done (fundus first method)
CBD is clamped (using Bulldog clamp) and resected
Head of pancreas tumor is sent to pathologist
The three anastomosis are done.
Discuss the clinical presentation, complications, diagnosis and treatment of gall
stone disease
In the GB
Silent stones : Accidentally discovered by a USG.
Rarely causes problem hence left without treatment
Flatulent dyspepsia
Fatty, fertile, flatulent female in fourties
Gaseous distension, intolerance to fatty food and discomfort in the abdomen
Treatment: Cholecystectomy
Gall stone colic
Usually occurs at night
Severe colicky upper abdominal pain felt in right hypochondrium, may shoot to the
back or in between shoulder blades
Acute cholecystitis
Symptoms : RUQ colicky pain, nausea and vomiting, low fever
Signs :
Murphy’s sign : Patient catches his/her breath when pressed in right hypochondrium
Boa’s sign : Hyperesthesia in the region of 12th rib
Guarding and rigidity of upper abdomen
Management : Cholecystectomy
Chronic cholecystitis : Multiple episodes of acute cholecystitis
Symptoms : Dyspepsia, upper abdominal discomfort. Murphy’s sign is positive.
Management : USG to confirm diagnosis followed by cholecystectomy
Mucocele : Stone blocks the cystic duct. No infection of bile. Due to obstruction the
bile is absorbed and is replaced by the mucus secreted from gall bladder epithelium
Soft fluctuant globular mass in right hypochondrium which moves with respiration
Needs cholecystectomy
Empyema and Perforation
High grade fever with chills and rigors, toxicity, high leucocyte count
Perforation in the general peritoneal cavity can cause diffuse biliary peritonitis
Management : Urgent laparotomy, aggressive resuscitation, good antibiotic cover
may help in reducing mortality.
Carcinoma gall bladder
In the bile duct :
Obstructive jaundice
Clinical features
Asymptomatic
More common in females
Age: 30-50 years
Symptoms
Obstructive jaundice
Charcot’s triad : Intermittent pain, intermittent fever and intermittent jaundice
Reynold’s pentad : Charcot’s triad + Shock + Altered mental status
Pruritus
Signs
Deep yellow jaundice
Per abdomen : Liver enlarged due to back pressure. It is smooth with round border
and firm in consistency
Gall bladder : Not palpable
Treatment
Depends on the scenario
CBD stone and GB stone detected before surgery
ERCP, sphincterectomy → Few days → Laparoscopic cholecystectomy
CBD stone detected during laparoscopic cholecystectomy
Indicators for CBD stone
Increased ALP
History of jaundice
USG : CBD > 10 mm in diameter
If indicators for CBD stone present then confirmation has to be done.
Do laparoscopic cholecystectomy + exploration of CBD
If laparoscopic exploration of CBD not possible do open exploration
Make a longitudinal cut in CBD.
Insert a T-tube in CBD
Inject dye after 7-10 days
If no residual stone → Remove T-tube
Stones present → Remove stones through tract
CBD stone detected after surgery
Could be residual stone (< 2 years) or recurrent stone (> 2 years)
ERCP sphincterectomy (1.5 cm in size)
If fails do transduodenal sphincterectomy
If fails or stone impacted higher up → Supraduodenal choledocholithotomy
Acute pancreatitis
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
Treatment
Nil per oral (Bowel rest) + Aspiration with Ryle’s tube
IV fluids - Ringer lactate (preferred)
Analgesic to control pain
No role of empirical antibiotics (given if severe pancreatitis / infected necrosis /
necrosis > 50%)
Antibiotic of choice : Meropenem
Nutrition
Early phase : Total Parenteral nutrition
Start enteral nutrition early (reduces infections)
Nasojejunal feeding is preferred
ERCP : No routine use. Indications -
Biliary pancreatitis
Pain > 48 hours
Features of obstruction / jaundice
Patients with documented stones in CBD
Cholecystectomy
Done in all patients with gallstones before discharge
In the intestine
Gallstone ileus : Dynamic bowel obstruction secondary to cholecysto-duodenal
fistula most commonly at terminal two feet of ileum.
Medical Treatment of Gall Stones
Indicated for pure cholesterol stones only
Patient selection
Patients with functioning GB proven by OCG or scintigraphy
Young, thin, female patients
Tiny (< 5mm), translucent, floating stone
Types
Oral dissolution treatment
Drugs used → CDCA—chenodeoxycholic acid, UDCA—ursodeoxycholic acid
MOA: They inhibit HMG-CoA, a rate limiting step in the synthesis of cholesterol,
thereby increasing the bile salt pool
Direct contact dissolution
MTBE—methyl tert-butyl ether is the drug which is given through a catheter placed
in gall bladder percutaneously
Enumerate the etiopathogenesis of cholecystitis. Detail briefly the effects and
complications of Gall Stones. Add a note on management of acute calculous
Cholecystitis
Etiopathogenesis of cholecystitis
Acute calculous cholecystitis
Due to obstruction to bile flow from gall bladder by stone or edema formed as a
result of local mucosal erosion and inflammation caused by stone.
Once mucosa is eroded, the exposed tissue planes are destroyed by the action of bile
salts leading to necrosis and perforation of gall bladder.
Acute acalculous cholecystitis
Caused due to prolonged TPN, burns, prolonged ICU stay etc.
Acute emphysematous cholecystitis
Caused due to Clostridium infection in immunocompromised patients
Effects and complications of gall stones
In the GB
Silent stones : Accidentally discovered by a USG.
Rarely causes problem hence left without treatment
Flatulent dyspepsia
Fatty, fertile, flatulent female in fourties
Gaseous distension, intolerance to fatty food and discomfort in the abdomen
Gall stone colic
Usually occurs at night
Severe colicky upper abdominal pain felt in right hypochondrium, may shoot to the
back or in between shoulder blades
Acute cholecystitis
Symptoms : RUQ colicky pain, nausea and vomiting, low fever
Signs :
Murphy’s sign : Patient catches his/her breath when pressed in right hypochondrium
Boa’s sign : Hyperesthesia in the region of 12th rib
Guarding and rigidity of upper abdomen
Chronic cholecystitis : Multiple episodes of acute cholecystitis
Symptoms : Dyspepsia, upper abdominal discomfort. Murphy’s sign is positive.
Mucocele : Stone blocks the cystic duct. No infection of bile. Due to obstruction the
bile is absorbed and is replaced by the mucus secreted from gall bladder epithelium
Soft fluctuant globular mass in right hypochondrium which moves with respiration
Empyema and Perforation
High grade fever with chills and rigors, toxicity, high leucocyte count
Perforation in the general peritoneal cavity can cause diffuse biliary peritonitis
Carcinoma gall bladder
In the bile duct :
Obstructive jaundice
Clinical features
Asymptomatic
More common in females
Age: 30-50 years
Symptoms
Obstructive jaundice
Charcot’s triad : Intermittent pain, intermittent fever and intermittent jaundice
Reynold’s pentad : Charcot’s triad + Shock + Altered mental status
Pruritus
Signs
Deep yellow jaundice
Per abdomen : Liver enlarged due to back pressure. It is smooth with round border
and firm in consistency
Gall bladder : Not palpable
Acute pancreatitis
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
In the intestine
Gallstone ileus : Dynamic bowel obstruction secondary to cholecysto-duodenal
fistula most commonly at terminal two feet of ileum.
Management of acute calculous cholecystitis
Investigations
USG is the investigation of choice
Stones cast posterior acoustic shadow
Inflamed, thickened organ
HIDA scan : Hepatobiliary iminodiacetic acid
Non-visualization of GB in acute cholecystitis
Total WBC count : Raised
Blood and urine sugar : To rule out diabetes mellitus
Plain X-ray abdomen
Gallstones can be demonstrated in 10% cases
To rule out causes such as perforated peptic ulcer (air under the diaphragm sign)
Treatment
Nil per oral + Aspiration with Ryle’s tube
IV fluids
IV antibiotics : Broad spectrum antibiotics
Analgesic : Injection morphine 8–10 mg IM
Antispasmodic : injection atropine 0.6 mg
If patient presents
within 2-3 days of onset of symptoms
Emergency cholecystectomy (can be done by laparoscopic route)
presents after 3 days of onset of symptoms
Conservative management as above
After symptoms relieve the patient is allowed to have clear oral fluids followed by
soft diet
Discharged
Interval cholecystectomy after 6 weeks
Cholelithiasis - types and complications
Types
Cholesterol stones
10% of the gall stones
Pigment stones
Brown : Rare in GB, occurs in bile duct
Composition : Calcium bilirubinate, calcium palmitate and calcium stearate +
cholesterol
Cause : Bile stasis by foreign bodies, endoprosthesis, Clonorchis sinensis and Ascaris
lumbricoides
Black
Composition : Calcium bilirubinate
Cause : Hemolysis - G6PD deficiency, Hereditary spherocytosis, Sickle cell aemia
Mixed stones (80% of all gallstones)
Composition : alternating layers of cholesterol and pigment with epithelial debris or
vegetation from infective organisms
Clinical presentation and Complications
In the GB
Silent stones : Accidentally discovered by a USG.
Flatulent dyspepsia
Gall stone colic
Acute cholecystitis
Chronic cholecystitis : Multiple episodes of acute cholecystitis
Mucocele : Stone blocks the cystic duct. No infection of bile. Due to obstruction the
bile is absorbed and is replaced by the mucus secreted from gall bladder epithelium
Empyema and Perforation
Carcinoma gall bladder
In the bile duct :
Obstructive jaundice
Cholangitis
Acute pancreatitis
In the intestine
Gallstone ileus
Clinical features of cholelithiasis
In the GB
Silent stones : Accidentally discovered by a USG.
Rarely causes problem hence left without treatment
Flatulent dyspepsia
Fatty, fertile, flatulent female in fourties
Gaseous distension, intolerance to fatty food and discomfort in the abdomen
Gall stone colic
Usually occurs at night
Severe colicky upper abdominal pain felt in right hypochondrium, may shoot to the
back or in between shoulder blades
Acute cholecystitis
Symptoms : RUQ colicky pain, nausea and vomiting, low fever
Signs :
Murphy’s sign : Patient catches his/her breath when pressed in right hypochondrium
Boa’s sign : Hyperesthesia in the region of 12th rib
Guarding and rigidity of upper abdomen
Chronic cholecystitis : Multiple episodes of acute cholecystitis
Symptoms : Dyspepsia, upper abdominal discomfort. Murphy’s sign is positive.
Mucocele : Stone blocks the cystic duct. No infection of bile. Due to obstruction the
bile is absorbed and is replaced by the mucus secreted from gall bladder epithelium
Soft fluctuant globular mass in right hypochondrium which moves with respiration
Empyema and Perforation
High grade fever with chills and rigors, toxicity, high leucocyte count
Perforation in the general peritoneal cavity can cause diffuse biliary peritonitis
Carcinoma gall bladder
In the bile duct :
Obstructive jaundice
Clinical features
Asymptomatic
More common in females
Age: 30-50 years
Symptoms
Obstructive jaundice
Charcot’s triad : Intermittent pain, intermittent fever and intermittent jaundice
Reynold’s pentad : Charcot’s triad + Shock + Altered mental status
Pruritus
Signs
Deep yellow jaundice
Per abdomen : Liver enlarged due to back pressure. It is smooth with round border
and firm in consistency
Gall bladder : Not palpable
Acute pancreatitis
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
In the intestine
Gallstone ileus : Dynamic bowel obstruction secondary to cholecysto-duodenal
fistula most commonly at terminal two feet of ileum.
Management of choledocholithiasis.
Investigations
Hb% is low in malignancy
Total count and differential count are increased in case of infections
Bleeding time, clotting time and prothrombin time are altered in case of obstructive
jaundice
Urine for urobilinogen is negative in obstructive jaundice
Serum ALP : Normal is 60-300 units/L. More than 500 units is suggestive of
obstructive jaundice.
GGT
Abdominal USG → Stones can be diagnosed with their posterior acoustic shadow
ERCP → Stones appear as filling defects in the CBD or in the common hepatic duct
(CHD)
MRCP → Investigation of choice in cases of obstructive jaundice due to high
strictures or cholangiocarcinoma
Endosonography → To detect missed stones in CBD.
Treatment of CBD stones
Depends on the scenario
CBD stone and GB stone detected before surgery
ERCP, sphincterectomy → Few days → Laparoscopic cholecystectomy
CBD stone detected during laparoscopic cholecystectomy
Indicators for CBD stone
Increased ALP
History of jaundice
USG : CBD > 10 mm in diameter
If indicators for CBD stone present then confirmation has to be done.
Do laparoscopic cholecystectomy + exploration of CBD
If laparoscopic exploration of CBD not possible do open exploration
Make a longitudinal cut in CBD.
Insert a T-tube in CBD
Inject dye after 7-10 days
If no residual stone → Remove T-tube
Stones present → Remove stones through tract
CBD stone detected after surgery
Could be residual stone (< 2 years) or recurrent stone (> 2 years)
ERCP sphincterectomy (1.5 cm in size)
If fails do transduodenal sphincterectomy
If fails or stone impacted higher up → Supraduodenal choledocholithotomy
Choledochal cyst (x2) // Types of choledochal cysts // Choledochal cyst clinical
features and investigations
Choledochal cyst is a congenital cyst occurring in the CBD due to partial or complete
weakness of the wall of CBD
Clinical features
Age : Majority of cases manifest in children within 1-2 years of age
Sex : More common in females 4:1
Abdominal distension can be due to large cyst
Slow progressive jaundice, recurrent attacks with abdominal pain and pyrexia
Investigations
USG : Confirm the presence
MRC : Relation between lower end of bile duct and pancreatic duct to know basic
anatomy
CT : To know intrahepatic and extrahepatic dilatation
Types and Treatment : Todani / Modified Alonso-Lej classification
Type I : Cystic dilatation of CBD
Treatment : Roux-en-Y hepaticojejunostomy
Type II : Diverticulum of CBD
Treatment : Cut diverticulum and repair CBD (Roux-en-Y hepaticojejunostomy)
Type III : Dilatation of intraduodenal portion of CBD (choledochocele)
Treatment : ERCP + Sphincterectomy
Type IV :
IVa : Intrahepatic + Extrahepatic biliary tree dilated
Treatment : Liver transplant
IVb : Only extrahepatic biliary tree dilated
Treatment : Kasai procedure (Portoenterostomy)
Type V : Only intrahepatic biliary tree dilated (Caroli’s disease)
Treatment : Liver transplant
Type VI : Cystic dilatation of cystic duct

Classify choledochocoel. Add a note on its management

Laparoscopic cholecystectomy (x2)
Surgeon stands on the left side of the operating table
Assistant stands on the left side of the operating table
Position of patient
Reverse Trendelenburg position
Head end up, foot end down and right side up
Ports
Traditional laparoscopic cholecystectomy

Single incision laparoscopic surgery

Single infraumbilical port
Very high rate of umbilical hernia through the incision
Procedure
Done under general anesthesia
Pneumoperitoneum is maintained through the infraumbilical incision
Cystic duct and cystic artery are clipped and gallbladder is removed using
gallbladder holding forceps and is brought outside through epigastric port
Bleeding from liver is controlled using lasers/cautery
Complications
Hemorrhage
Injury to bile ducts
Right shoulder tip pain (most common) : Retained CO2 under right dome of
diaphragm
Conversion to open surgery
Residual CBD stones
Strictures in CBD or biliary tree
Post-cholecystectomy syndrome: Due to
Retained CBD stones
Biliary dyskinesia
Sphincter of Oddi dysfunction
Acalculous Cholecystitis // Management of acalculous cholecystitis
Nonobstructive cholecystitis
Seen in patients recovering from major illness
Risk factors
Prolonged TPN
Post burns
ICU patients
Post CABG
Prolonged fasting
Clinical features
Right upper quadrant pain
Nausea and vomiting
Investigation of choice : Ultrasound (Thickening of the gallbladder wall)
Treatment
Nil per oral
IV fluids
IV antibiotics
Analgesics
Cholecystectomy
Percutaneous/Tube cholecystostomy (In very sick patients)
Using ultrasound or CT guidance, a pigtail catheter can be inserted into the gall
bladder, ideally transperitoneally
3–4 days later, when sepsis improves, laparoscopic/open cholecystectomy can be
done.
Emergency cholecystectomy
ERCP // ERCP: its role in surgical practice
ERCP (endoscopic retrograde cholangiopancreatography)
With the help of a side viewing endoscope, ampulla of Vater is cannulated and a
radioopaque dye is injected.
It fills up the biliary and pancreatic system.
Interpretation
Stones appear as filling defects in the CBD or in the common hepatic duct (CHD),
which may be mobile (change position, if patient is moved).
A periampullary carcinoma gives rise to an irregular filling defect or there may be
total cut off in the flow of dye. (Done for cholangitis due to carcinoma cases.)
Chronic pancreatitis may show the dilated duct and stones in the pancreatic duct—
‘chain of lakes’ appearance.
Uses
If stones in the CBD are diagnosed, they can be treated in the following ways:
Extraction by using a basket.
Large stone can be crushed by using a lithotripter and can be extracted.
Sphincterotomy (incision of sphincter of Oddi) can be done to facilitate extrusion of
small stones.
In patients with cholangitis with obstructive jaundice, stenting of common bile duct
can be done to relieve obstruction. Stent removal is necessary at a later date.
In selected patients with biliary strictures, stent is placed after ERCP to relieve
obstructive jaundice (sometimes permanent in malignancies).
In selected patients with chronic pancreatitis, pancreatic duct can be stented to
relieve pain.
Complications
Severe infection of biliary tree (cholangitis) and acute pancreatitis can occur in 1–2%
of the patients. Hence, prophylactic antibiotics are given before the procedure
A 45 year old male alcoholic presents with the history of pain in the epigastric
region with early satiety and occasional vomiting. On examination there is a
diffuse mass in the epigastric area. He has had an episode of acute pancreatitis
three months back which had been managed conservatively. A. What is your
diagnosis? B. Enumerate the different causes of acute pancreatitis C. How do
you investigate this patient? D. How do you treat this patient?
Pseudocyst of pancreas as a complication of acute pancreatitis
Causes (I GET PP SMASHED)
I : Idiopathic
G : Gallstones → specifically at Ampulla of Vater
E : Ethanol → alcohol triggers release of pancreatic enzymes
T : Trauma (e.g. seatbelt injury in children)
P : Pancreas divisum
P : Posterior duodenal ulcer rupture
S : Steroids abuse
M : Mumps (other infections are coxsackievirus, mycoplasma pneumoniae)
A : Autoimmune disease (Typically due to IgG4 related disease (+ Riedel's thyroiditis,
retroperitoneal fibrosis, noninfectious aortitis))
S : Scorpion sting
H : Hypertriglyceridemia/Hyperchylomicronemia, Hypercalcemia
E : ERCP
D : Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors, Didanosine, Corticosteroids,
Alcohol, Valproic Acid, Azathioprine, Furosemide, HCTZ, GLP-1 analogs, 6MP)
Investigations
USG : Detect size, location of cyst, and wall thickness
CECT (investigation of choice)
ERCP : May demonstrate communication of cyst with duodenum
Treatment
Conservative
Majority of pseudocysts following acute pancreatitis resolve spontaneously in 3-4
weeks.
Do regular USG for observation
Surgery
Indications :
Increases in size (> 6 cm)
Wall thickness (> 6 mm)
Severe pain
No spontaneous reduction in size (> 6 weeks old)
Procedures
Cystogastrostomy : Opening the cyst to posterior wall of stomach.
Indications : Pseudocyst in relation to head and body of pancreas
Timing : Done after 6 weeks because that is the time required for wall to become
fibrous
Size : Should be less than 6 cm
Distal pancreatectomy
Indications : For cyst confined to tail of pancreas
Cystojejunostomy : Suturing jejunal loop to the cyst in most dependent area
Indication : For large cysts
Endoscopic drainage
Pseudocyst of pancreas (x2) // Management of pseudocyst of pancreas // Pseudocyst
of pancreas clinical features and treatment // Surgical treatment of pseudocyst of
pancreas // Pseudocyst of pancreas: Etiology + clinical features and management.
Collection of amylase-rich fluid in the lesser sac, due to pancreatic pathology. Fluid
collection in the first 4 weeks is an acute fluid collection. After 4 weeks, it becomes an
acute pseudocyst.
Etiology
Following an attack of acute pancreatitis
Blunt injury of abdomen causing a ductal disruption wherein the pancreatic duct in
the region of body is crushed against vertebral body resulting in pseudocyst
Some cause of chronic pancreatitis may be associated with pseudocyst
Clinical features
Tense cystic mass in the epigastrium, umbilical region or left hypochondrium
Does not move with respiration (retroperitoneal)
Transverse mobility
Does not fall forwards
Percussion : resonant note because of stomach/intestine anterior to it
If Ryle’s tube is passed it can be felt over the swelling (Baid sign)
Investigations
USG : Detect size, location of cyst, and wall thickness
CECT (investigation of choice)
ERCP : May demonstrate communication of cyst with duodenum
Treatment
Conservative
Majority of pseudocysts following acute pancreatitis resolve spontaneously in 3-4
weeks.
Do regular USG for observation
Surgery
Indications :
Increases in size (> 6 cm)
Wall thickness (> 6 mm)
Severe pain
No spontaneous reduction in size (> 6 weeks old)
Procedures
Cystogastrostomy : Opening the cyst to posterior wall of stomach.
Indications : Pseudocyst in relation to head and body of pancreas
Timing : Done after 6 weeks because that is the time required for wall to become
fibrous
Size : Should be less than 6 cm
Distal pancreatectomy
Indications : For cyst confined to tail of pancreas
Cystojejunostomy : Suturing jejunal loop to the cyst in most dependent area
Indication : For large cysts
Endoscopic drainage
A 28 years old male presented to the emergency department with complaints
of abdominal pain radiating to back, on detailed history he revealed the pain
started after a bout of alcohol. What is your probable diagnosis? Discuss the
clinical features, investigations, and management of the patient
Acute Pancreatitis
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
Diagnosis
Abdominal pain consistent with pancreatitis
Serum amylase/lipase > 3 times the upper limit
Characteristic finding on imaging
If any two of the above positive → Pancreatitis
Investigations
CBC → Hb may be low. TLC is raised above 15,000 cells/cu.mm due to inflammation
Blood urea, creatine to rule out renal failure
Serum amylase
Normal → 40-80 Somogyi units
Levels suggestive of acute pancreatitis → >400 units
Levels diagnostic of acute pancreatitis → > 1000 units
Serum lipase - more specific but difficult to measure
Serum calcium levels - Hypocalcemia due to hypoalbuminemia or due to usage of
calcium by the process of saponification
Total proteins are low, especially albumin
Plain X-ray abdomen
Sentinel loop sign - one dilated jejunal loop of intestine which is seen in region of
pancreas
Colon cut-off sign - Mild distension of transverse colon with collapsed descensing
colon
Abdominal ultrasound - Edematous pancreas, fluid in the abdomen
Contrast enhanced CT (CECT)
Done after 3-5 days in patient who fail to respond to conservative treatment
If CT scan demonstrates infected necrosis, an urgent CT guided FNAC is done and
the report is sent for gram staining
If it comes out to be positive the patient has to be treated urgently
Treatment
Nil per oral (Bowel rest) + Aspiration with Ryle’s tube
IV fluids - Ringer lactate (preferred)
Analgesic to control pain
No role of empirical antibiotics (given if severe pancreatitis / infected necrosis /
necrosis > 50%)
Antibiotic of choice : Meropenem
Nutrition
Early phase : Total Parenteral nutrition
Start enteral nutrition early (reduces infections)
Nasojejunal feeding is preferred
ERCP : No routine use. Indications -
Biliary pancreatitis
Pain > 48 hours
Features of obstruction / jaundice
Patients with documented stones in CBD
Cholecystectomy
Done in all patients with gallstones before discharge
Define acute pancreatitis. Enumerate various causes and complications of acute
pancreatitis. Discuss the management of a 32 year old alcoholic presented with
history of abdominal pain 3 months back and symptoms of early satiety with 10
cm epigastric mass.
Definition
It is defined as acute nonbacterial inflammatory condition caused by activation,
interstitial liberation and autodigestion of pancreas presenting as acute abdominal
pain
Causes (I GET PP SMASHED)
I : Idiopathic
G : Gallstones → specifically at Ampulla of Vater
E : Ethanol → alcohol triggers release of pancreatic enzymes
T : Trauma (e.g. seatbelt injury in children)
P : Pancreas divisum
P : Posterior duodenal ulcer rupture
S : Steroids abuse
M : Mumps (other infections are coxsackievirus, mycoplasma pneumoniae)
A : Autoimmune disease (Typically due to IgG4 related disease (+ Riedel's thyroiditis,
retroperitoneal fibrosis, noninfectious aortitis))
S : Scorpion sting
H : Hypertriglyceridemia/Hyperchylomicronemia, Hypercalcemia
E : ERCP
D : Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors, Didanosine, Corticosteroids,
Alcohol, Valproic Acid, Azathioprine, Furosemide, HCTZ, GLP-1 analogs, 6MP)
Complications
Local
Pseudocyst → It represents a localized peripancreatic collection of pancreatic juice
and debris developing in the lesser sac following inflammatory rupture of the
pancreatic duct.
Pancreatic ascites - May develop due to leakage of fluid from disrupted pancreatic
duct into the peritoneal cavity
Leaking pseudocyst
Necrosis → Necrosis may result in an acute necrotic collection that contains a
variable amount of fluid and necrosis or walled-off necrosis which consists of a
mature, encapsulated collection
Abscess
Pancreatic ascites → Localized collection of pus close to the pancreas and containing
little or no pancreatic tissue
Disruption of main pancreatic duct
Bowel infarction
Massive intraperitoneal hemorrhage
Systemic
Systemic Inflammatory Response Syndrome
Pleural effusion
ARDS
Hypotension and shock
Upper GI bleeding
Obstructive jaundice, splenic or portal vein thrombosis
Oliguria, azotemia, renal artery/vein thrombosis
DIC
Diagnosis
Abdominal pain consistent with pancreatitis
Serum amylase/lipase > 3 times the upper limit
Characteristic finding on imaging
If any two of the above positive → Pancreatitis
Investigations
CBC → Hb may be low. TLC is raised above 15,000 cells/cu.mm due to inflammation
Blood urea, creatine to rule out renal failure
Serum amylase
Normal → 40-80 Somogyi units
Levels suggestive of acute pancreatitis → >400 units
Levels diagnostic of acute pancreatitis → > 1000 units
Serum lipase - more specific but difficult to measure
Serum calcium levels - Hypocalcemia due to hypoalbuminemia or due to usage of
calcium by the process of saponification
Total proteins are low, especially albumin
Plain X-ray abdomen
Sentinel loop sign - one dilated jejunal loop of intestine which is seen in region of
pancreas
Colon cut-off sign - Mild distension of transverse colon with collapsed descending
colon
Abdominal ultrasound - Edematous pancreas, fluid in the abdomen
Contrast enhanced CT (CECT)
Done after 3-5 days in patient who fail to respond to conservative treatment
If CT scan demonstrates infected necrosis, an urgent CT guided FNAC is done and
the report is sent for gram staining
If it comes out to be positive the patient has to be treated urgently
Treatment
Nil per oral (Bowel rest) + Aspiration with Ryle’s tube
IV fluids - Ringer lactate (preferred)
Analgesic to control pain
No role of empirical antibiotics (given if severe pancreatitis / infected necrosis /
necrosis > 50%)
Antibiotic of choice : Meropenem
Nutrition
Early phase : Total Parenteral nutrition
Start enteral nutrition early (reduces infections)
Naso-jejunal feeding is preferred
Other drugs : PPIs, glucagon and octreotide
Anticoagulation : With LMWH for prevention of DVT
ERCP : No routine use. Indications -
Biliary pancreatitis
Pain > 48 hours
Features of obstruction / jaundice
Patients with documented stones in CBD
Cholecystectomy
Done in all patients with gallstones before discharge
Enumerate the aetiology, pathophysiolgy, clinical feature of Acute pancreatitis.
Mention in detail the Ranson’s criteria.
Causes (I GET PP SMASHED)
I : Idiopathic
G : Gallstones → specifically at Ampulla of Vater
E : Ethanol → alcohol triggers release of pancreatic enzymes
T : Trauma (e.g. seatbelt injury in children)
P : Pancreas divisum
P : Posterior duodenal ulcer rupture
S : Steroids abuse
M : Mumps (other infections are coxsackievirus, mycoplasma pneumoniae)
A : Autoimmune disease (Typically due to IgG4 related disease (+ Riedel's thyroiditis,
retroperitoneal fibrosis, noninfectious aortitis))
S : Scorpion sting
H : Hypertriglyceridemia/Hyperchylomicronemia, Hypercalcemia
E : ERCP
D : Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors, Didanosine, Corticosteroids,
Alcohol, Valproic Acid, Azathioprine, Furosemide, HCTZ, GLP-1 analogs, 6MP)
Pathophysiology
Causes of autodigestion
Obstruction/Secretion : Recurrent attacks as in chronic cases can lead to multiple
strictures, stasis, resulting in autodigestion
Common channel theory : In 10% cases the bile duct and pancreatic duct have
common channel leading to reflux of bile into pancreases causing gallstone
pancreatitis
Duodenal reflux : Reflux of activated enzymes in the duodenum.
Back diffusion : Back diffusion of pancreatic enzymes through the ductal epithelium
Systemic sepsis : Organ failure - ARDS, renal failure, endotoxins from bacteria
All the above factors can lead to activation of trypsin in the pancreas
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
Ranson’s Criteria (1 point each)
On admission
WBC > 16,000/cu.mm.
Age > 55 years
Glucose > 200 mg/dL
AST > 250 IU/L
LDH > 350 IU/L
Within 48 hours of admission
Hct decrease > 10%
BUN increase > 5 mg/dL
Serum calcium < 8 mg/dL
Fluid needs < 6 L
Arterial pO2 < 60 mmHg
Base deficit > 4 mEq/L
Interpretation
Score < 3 → 0-3% mortality
Score 3-5 → 11-15% mortality
Score > 6 → 50% mortality
Enumerate causes for acute pancreatitis
Causes (I GET PP SMASHED)
I : Idiopathic
G : Gallstones → specifically at Ampulla of Vater
E : Ethanol → alcohol triggers release of pancreatic enzymes
T : Trauma (e.g. seatbelt injury in children)
P : Pancreas divisum
P : Posterior duodenal ulcer rupture
S : Steroids abuse
M : Mumps (other infections are coxsackievirus, mycoplasma pneumoniae)
A : Autoimmune disease (Typically due to IgG4 related disease (+ Riedel's thyroiditis,
retroperitoneal fibrosis, noninfectious aortitis))
S : Scorpion sting
H : Hypertriglyceridemia/Hyperchylomicronemia, Hypercalcemia
E : ERCP
D : Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors, Didanosine, Corticosteroids,
Alcohol, Valproic Acid, Azathioprine, Furosemide, HCTZ, GLP-1 analogs, 6MP)
Causes of Acute Pancreatitis. Enumerate Ranson’s Criteria.
Causes (I GET PP SMASHED)
I : Idiopathic
G : Gallstones → specifically at Ampulla of Vater
E : Ethanol → alcohol triggers release of pancreatic enzymes
T : Trauma (e.g. seatbelt injury in children)
P : Pancreas divisum
P : Posterior duodenal ulcer rupture
S : Steroids abuse
M : Mumps (other infections are coxsackievirus, mycoplasma pneumoniae)
A : Autoimmune disease (Typically due to IgG4 related disease (+ Riedel's thyroiditis,
retroperitoneal fibrosis, noninfectious aortitis))
S : Scorpion sting
H : Hypertriglyceridemia/Hyperchylomicronemia, Hypercalcemia
E : ERCP
D : Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors, Didanosine, Corticosteroids,
Alcohol, Valproic Acid, Azathioprine, Furosemide, HCTZ, GLP-1 analogs, 6MP)
Ranson’s Criteria (1 point each)
On admission
WBC > 16,000/cu.mm.
Age > 55 years
Glucose > 200 mg/dL
AST > 250 IU/L
LDH > 350 IU/L
Within 48 hours of admission
Hct decrease > 10%
BUN increase > 5 mg/dL
Serum calcium < 8 mg/dL
Fluid needs < 6 L
Arterial pO2 < 60 mmHg
Base deficit > 4 mEq/L
Interpretation
Score < 3 → 0-3% mortality
Score 3-5 → 11-15% mortality
Score > 6 → 50% mortality
Clinical features of Acute Pancreatitis. Enumerate Ranson’s Criteria
Clinical features
Symptoms
Severe upper abdominal epigastric pain radiating to the back partially relieved on
stooping and bending forward (Mohammedan Prayer Sign)
Vomiting - frequent and effortless due to reflex pylorospasm
Low grade fever
Hematemesis and malena may occur due to necrosis of duodenum
Signs
Febrile, tachypneic
Cyanosis
Faint jaundice
Features of shock - feeble pulse, tachycardia, hypotension, cold extremities
Abdominal findings
Tenderness in the epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Cullen’s sign - Bluish ecchymotic discoloration seen around umbilicus
Grey turner’s sign - Bluish discoloration in the flanks
Ranson’s Criteria
On admission
WBC > 16,000/cu.mm.
Age > 55 years
Glucose > 200 mg/dL
AST > 250 IU/L
LDH > 350 IU/L
Within 48 hours of admission
Hct decrease > 10%
BUN increase > 5 mg/dL
Serum calcium < 8 mg/dL
Fluid needs < 6 L
Arterial pO2 < 60 mmHg
Base deficit > 4 mEq/L
Interpretation
Score < 3 → 0-3% mortality
Score 3-5 → 11-15% mortality
Score > 6 → 50% mortality
Management of gallstone pancreatitis
Investigations
CBC → Hb may be low. TLC is raised above 15,000 cells/cu.mm due to inflammation
Blood urea, creatine to rule out renal failure
Serum amylase
Normal → 40-80 Somogyi units
Levels suggestive of acute pancreatitis → >400 units
Levels diagnostic of acute pancreatitis → > 1000 units
Serum lipase - more specific but difficult to measure
Serum calcium levels - Hypocalcemia due to hypoalbuminemia or due to usage of
calcium by the process of saponification
Total proteins are low, especially albumin
Plain X-ray abdomen
Sentinel loop sign - one dilated jejunal loop of intestine which is seen in region of
pancreas
Colon cut-off sign - Mild distension of transverse colon with collapsed descensing
colon
Abdominal ultrasound -
Edematous pancreas, fluid in the abdomen.
Stone may be visualized in the region of gallbladder
Contrast enhanced CT (CECT)
Done after 3-5 days in patient who fail to respond to conservative treatment
If CT scan demonstrates infected necrosis, an urgent CT guided FNAC is done and
the report is sent for gram staining
If it comes out to be positive the patient has to be treated urgently
Treatment
Nil per oral (Bowel rest) + Aspiration with Ryle’s tube
IV fluids - Ringer lactate (preferred)
Analgesic to control pain
No role of empirical antibiotics (given if severe pancreatitis / infected necrosis /
necrosis > 50%)
Antibiotic of choice : Meropenem
Nutrition
Early phase : Total Parenteral nutrition
Start enteral nutrition early (reduces infections)
Nasojejunal feeding is preferred
ERCP : Endoscopic sphincterectomy is done within days.
Cholecystectomy : After 2-3 weeks, once the jaundice has subsided, cholecystectomy
is recommended
Benign pancreatic tumors
Pseudocyst
Collection of amylase-rich fluid in the lesser sac, due to pancreatic pathology. Fluid
collection in the first 4 weeks is an acute fluid collection. After 4 weeks, it becomes an
acute pseudocyst.
Etiology
Following an attack of acute pancreatitis
Blunt injury of abdomen
Chronic pancreatitis may be associated with pseudocyst
Clinical features : Tense cystic mass in the epigastrium, umbilical region or left
hypochondrium
Investigations
USG : Detect size, location of cyst, and wall thickness
CECT (investigation of choice)
ERCP : May demonstrate communication of cyst with duodenum
Treatment
Conservative : Spontaneous resolution in 80% cases. Monitor using USG.
Surgery : Cystogastrostomy, Distal pancreatectomy, Cystojejunostomy
Endoscopic drainage
Islet cell tumors
Insulinoma
Location : Mostly occur in tail and body of pancreas
Can be a single adenoma, can be due to diffuse hyperplasia or due to carcinoma
Clinical features
Hypoglycemia features
Giddiness, dizziness, syncopal attacks, blurring of vision and diplopia can occur
Late stages : epilepsy, semiconsciousness, and coma
Whipple’s triad
Attack of hypoglycemia in morning hours in the fasting state
Symptoms are relieved on taking glucose
Blood sugar in fasting state is less than 45 mg% during the attack
Investigations
Serum insulin levels are very high. Proinsulin levels and C-peptide levels are also
elevated.
Persistent hypoglycemia less than 40 mg/dL relieved by glucose
Insulin/glucose ratio of > 0.3 is highly suggestive of malignancy
USG and CT of abdomen can demonstrate the tumor if larger than 2 cm
Selective angiography will demonstrate tumor blush (very vascular tumor)
Treatment
< 2 cm : Enucleation
> 2 cm : Suspect malignancy and a wide excision of tumor is done if malignant
Diazoxide to suppress insulin release
For inoperable islet cell carcinoma,
Streptozocin is best chemotherapeutic agent.
Hepatic artery embolization for liver metastasis.
Treatment of biliary atresia
Extrahepatic
IOC → HIDA scan
Gold standard → Intraoperative cholangiogram
Intrahepatic atresia
Liver biopsy (confirmatory) helps in differentiating atresia and neonatal heptitis
Types
I → Atresia of CBD
II → Atresia of common hepatic duct
III → Atresia of right and left ducts
Management
I → Roux-en-Y hepaticojejunostomy
II and III → Protoenterostomy (Kasai Procedure)
Extras
Investigations for obstructive jaundice (CBD stones and periampullary
carcinoma/carcinoma head of pancreas)
Hb% is low in malignancy
Total count and differential count are increased in case of infections
Bleeding time, clotting time and prothrombin time are altered in case of obstructive
jaundice
Urine for urobilinogen is negative in obstructive jaundice
Serum ALP : Normal is 60-300 units/L. More than 500 units is suggestive of
obstructive jaundice.
GGT
Abdominal USG
Stones can be diagnosed with their posterior acoustic shadow
Mass lesion in the head region can be seen in cases of chronic pancreatitis or
carcinoma head of the pancreas causing obstructive jaundice
Ultrasound can detect multiple secondaries in the liver, thus, favouring the diagnosis
of malignancy
CECT
A head mass of even 2–3 cm in size and portal vein infiltration can be demonstrated
by CT scan.
Obliteration of fat plane between the mass and superior mesenteric vessels can be
demonstrated by CT scan which decides the operability of periampullary carcinoma
or carcinoma head of the pancreas
Endoscopy
Useful to diagnose a periampullary carcinoma which may be seen as an ulcerative
lesion in the second part of the duodenum.
Biopsy can also be taken which shows adenocarcinoma
In case of obstructive jaundice due to stones, smooth bulge can be seen in the
second part of the duodenum.
Barium meal
Periampullary carcinoma - Distortion of medial border of the duodenum (Inverted 3
sign)
In carcinoma head of pancreas - Widening of C-loop of duodenum (Pad sign)
ERCP
Stones appear as filling defects in the CBD or in the common hepatic duct (CHD)
A periampullary carcinoma gives rise to an irregular filling defect or there may be
total cut off in the flow of dye.
Chronic pancreatitis may show the dilated duct and stones in the pancreatic duct—
‘chain of lakes’ appearance.
MRCP
Investigation of choice in cases of obstructive jaundice due to high strictures or
cholangiocarcinoma
Endosonography → To detect missed stones in CBD. It can also detect pancreatic
head mass, lymph nodes.
Diagnostic laparoscopy
CA 19-9 → Carcinoma pancreas / Chronic pancreatitis

26. Spleen
Complications of splenectomy (x3)
Early
Pancreatic injury
Vascular injury
Injury to bowel Most common complication - Left lower lobe atelectasis
Diaphragmatic injury Other complications
Splenosis Pulmonary
Pneumonia
Paralytic ileus •
Hematemesis Pleural effusion
Subphrenic abscess Pancreatic
Pancreatitis
Wound problems Pseudocyst pancreas
Thrombocytosis and thrombotic complications
•
Indications for splenectomy (x2) Pancreatic