SCHWARTZS HOUR

PANCREAS AND
SPLEEN
RAISA L. POCAIS
3RD YEAR RESIDENT
 PANCREAS
ANATOMY
ARTERIES

• Celiac and SMA

• Celiac: Splenic, Left Gastric and Common
Hepatic Artery
• Splenic: superior Pancreaticoduodenal
artery
• Common Hepatic-> Gastroduodenal
Artery-> Right Gastroepiploic artery->
Anterior Superior PD Artery
• SMA: inferior pancreaticoduodenal artery
VENOUS

• Superior veins- portal vein

• Inferior veins- IMV
 VARIATIONS OF PORTAL VENOUS ANATOMY
ANATOMY
LYMPHATICS AND NEUROANATOMY
 PANCREATIC DUCT ANATOMY

Ventral duct-Wirsung-Main Pancreatic Duct- Common Channel (bile duct and pancreatic duct joins)
Ventral Anlage- Rotates to the right and goes postero-inferior- Pancreatic head and uncinate process

Dorsal-Santorini- Lesser Pancreatic Duct- lesser papilla- Duodenum 30% ends blindly
Dorsal Anlage- Body and Tail of the pancreas

10% Pancreas Divisum- failure of Santorini and Wirsung to fuse

 PANCREATIC DUCT ANATOMY
Variations of the common channel length:
1/3: bile duct and pancreatic duct remain distinct to the end of the
papilla
1/3: 2 ducts merge at the end of the papilla
1/3: true common channel is present for a distance of several
millimeters

Pancreatic duct: 2x more pressure than CBD

Ampulla of Vater: 2nd portion of the duodenum

Lesser duct: 2cm proximal to the ampulla of vater

HISTOLOGY AND PHYSIOLOGY

• Exocrine Pancreas-85% of pancreatic mass

• Extracellular Matrix- 10%
• Blood vessels and Major ducts-4%
• Endocrine Tissue 2%
• 20% of normal pancreas is required to prevent
insufficiency
 HISTOLOGY AND PHYSIOLOGY

• A. Exocrine Pancreas-85%
• 500-800ml of colorless, odorless, alkaline, isosomotic pancreatic juice
(acinar and ductal secretions)
Acinar cells secretes Amylase, protease and lipases
Amylase- secreted in active form
- Hydrolyzes starch and glycogen to glucose, maltose, maltotriose and
dextrins

• Protease- require activation

• Trypsinogen-eneterokinase->Trypsin then activates elastatse,
Carboxypeptidase A and B and phospholipase
• Chymotrypsinogen->Chymotrypsin

• Lipase-secreted in active form

• hydrolyzes triglycerides to 2-monoglyceride and fatty acid
 HISTOLOGY AND PHYSIOLOGY

• Ductal cells (Centroacinar and intercalated duct cells)

• Secrete water and electrolytes in the pancreatic juice
• Acinus-40 acinar cells arranged as a spherical unit
• Centoracinar cells- located near the center of the Acinus responsible
for the fluid and electrolyte secretion
• contains carbonic anhydrase, needed for bicarbonate secretion

• Chloride is secreted inversely to bicarbonate secretion such that the

sum of the two becomes constant
• Stimulants of Bicarbonate secretion: Secretin (major stimulant),
CCK, Gastrin and acetylcholine
• Inhibitors: Truncal Vagotomy, Somatostatin, pancreatic polypeptide
and glucagon
• B. Endocrine Pancreas 2%
• 1Million islets of Langerhans: larger islets are located close to major arterioles with smaller islets located within the
parenchyma
• 5 major types: of Islet cells:
 PHYSIOLOGY (INSULIN)

• 2 phases of insulin release: first phase: stored insulin 2nd phase: new insulin synthesis (longer)
• Beta cell synthesis of insulin is regulated by: glucose levels, neural signals, paracrine influence of other islet
cells
• Incretins: augment insulin secretion eg. GIP, GLP-1 and CCK
• OGTT: overnight fasting, baseline glucose is taken
• 75g of glucose is taken with blood sample taken every 30 mins
Normal: <200mg/dl on all values and the 120min value <140mg/dl
Stimulants: Arginine, Lysine Leucine, FFA, cholinergic and beta sympathetic fibers
Inhibitors: Somatostatin, amylin, pancreastatin, alpha sympathetic fibers
 ACUTE PANCREATITIS

• Hallmark: Acute Pancreatic Inflammation with little

or no fibrosis
• Etiology: MC: gallstones (60 y/o; Females)and
Alcohol (30-40 y/o; Males)(80% cases)
GALLSTONES

• 3 theories: “common channel hypothesis”

1. Gallstone transiently lodged in the distal common channel of the ampulla of Vater
allowed bile to reflux into the pancreatic duct,
2. Transient incompetence caused by the passage of a stone through the sphincter might
allow duodenal fluid and bile to reflux into the pancreatic duct,
3. gallstone obstructing the pancreatic duct, leads to ductal hypertension.

• minor ductal disruption, extravasation of pancreatic juice into the less alkaline
interstitium of the pancreas, and promotion of enzyme activation
 ALCOHOL

• sustained alcohol ingestion is associated with recurrent acute pancreatitis and development of chronic
pancreatitis in drinkers for a decade
• Amount is more important than the type of alcohol consumed typically (100-150g/day) and the pattern
of drinking
• Mechanisms:
• metabolic toxin to pancreatic acinar cells
• Secretory burst coupled with ethanol induced spasm of the sphincter of Oddi
• Induces ductal permeability allowing prematurely activated enzymes to cause damage to the pancreatic
parenchyma
• Increases the protein content of pancreatic juice, decreases bicarbonate levels, and trypsin inhibitor
concentration.
• formation of protein plugs may also contribute by causing an obstructive element to pancreatic outflow
ACUTE PANCREATITIS
 DIAGNOSIS
ACUTE PANCREATITIS

• Symptoms: acute onset of constant epigastric pain

radiating to the back
• Signs: Cullen’s, Grey Turner’s sign
• Serum amylase/lipase: >3x upper limit of normal
• Amylase: increases immediately with the onset of
disease and remains elevated for 3-5 days
• Lipase: increases within 4-8 hours, peaks at 24 hours
and remains elevated for 1-2 weeks

• Contrast Enhanced abdominal CT Scan

 MANAGEMENT
ACUTE PANCREATITIS

Anlagesics:
• nonsteroidal anti-inflammatory
drug (e.g., metamizole 2g/8h IV)
• more severe pain are best
managed with opioid analgesia
(e.g., buprenorphine 0.3mg/4h IV)
• Morphine is to be avoided, due to
its potential to cause sphincter of
Oddi spasm
 MANAGEMENT
ACUTE PANCREATITIS

• Determining the etiology:

• History of alcohol ingestion, drug use, trauma, ERCP, infection
• Gallstones: ALP (>300IU/L), ALT (>100IU/L), Amylase (>4000 IU/L)
• Ultrasound evidence of gallstones

• Fluid Resuscitation- Lactated Ringer’s Solution

• Nutritional Support-commenced after initial resuscitation within 24 hours of admission
• ERCP
• Antibiotics-not necessary
• Local Complications: CT scan, CRP, Close monitoring, Delayed Intervention: allows the lesion
to be more walled off and safer to treat
• Cholecystectomy-prevent gallstone pancreatitis
CHRONIC PANCREATITIS

Prognosis: 5 YSR:70%
20 YSR:45%

Mortality risk: 1.6 fold

higher

Increased risk for

pancreatic cancer by
1.5-6%
CHRONIC PANCREATITIS

ALCOHOL
CHRONIC PANCREATITIS
OTHER ETIOLOGIES
 PRESENTATION
CHRONIC PANCREATITIS

• MC: persistent boring pain at mid epigastric

may involve LUQ or RUQ of the abdomen, may
penetrate through the back that lasts for hours or
days exacerbated by eating or drinking alcohol
• Cause: Ductal hypertension (strictures/stones),
parenchymal disease or retroperitoneal
inflammation (fibrosis>obstruction)

• Associated with anorexia, nausea and vomiting

*Burned out Pancreatitis- absence of pain with
presence of exocrine/endocrine deficiency
 PRESENTATION
CHRONIC PANCREATITIS

• Diarrhea, Steatorrhea, weight loss- when exocrine capacity

falls below 10%
• Pale, greasy, foul smelling, oil slick, floating stool

• Duodenal acidity secondary to decreased bicarbonate

secretion from exocrine function deterioration
• Pancreatogenic Diabetes (Type 3c DM)- 20% of cases with
chronic pancreatitis, also seen in cystic fibrosis and pancreatic
cancer
• Global deficiency of all three glucoregulatory islet cell
hormones occur: insulin, glucagon, and PP
• patients are hyperglycemic when insulin replacement is
insufficient and hypoglycemic when insulin replacement is
barely excessive
CHRONIC PANCREATITIS
 DIAGNOSTICS
CHRONIC PANCREATITIS

• Radiology: (a) diagnosis, (b) the evaluation of severity of disease, (c) detection of
complications, and (d) assistance in determining treatment options
• Transabdominal Ultrasonography: Sensitivity: 48%-96% usually used for periodic
reexamination to determine efficacy of treatment
• EUS: able to obtain fluid and tissue samples, can evaluate subtle changes in 2-3mm structures
within the pancreas and indolent neoplasms
• CT scan: able to visualize relationships of structures and lesions, cannot detect small neoplasms
• MRI/MRCP: non invasive screening for ductal abnormalities
• ERCP: gold standard for diagnosis and staging of Chronic Pancreatitis
 COMPLICATIONS
CHRONIC PANCREATITIS

• Pseudocyst: MC complication of Chronic Pancreatitis

• s/sx: may be asymptomatic or with pain, fullness, early
satiety

• Treatment: CT or Utz guided FNA, percutaneous drain

placement (if infected), if symptoms persist, internal
drainage may be done to avoid pancreaticocutaneous
fistula
Endoluminal
Cystogastrostomy: Transpapillary
a. EUS transgastric drainage of
puncture of pancreatic
pseudocyst pseudocyst
b. Transgastric stent
placement on
posterior wall of
stomach and anterior
wall of pseudocyst
 COMPLICATIONS
CHRONIC PANCREATITIS
Cystogastrostomy drainage of a
retrogastric pancreatic pseudocyst
Pancreatic Ascites: free drain of
fluid extravasation into the peritoneal
cavity
Paracentesis: >25g/L protein level,
elevated amylase and low serum
albumin
ERCP: delineates location of
pancreatic duct leak and underlying
anatomy
Octreotide acetate, Bowel rest and Central: Roux-en-Y
Parenteral Nutrition pancreaticojejunostomy
Surgery: for failed medical treatment
COMPLICATIONS

• Head of Pancreas Mass: 30% of cases

• s/sx: severe pain, cholestasis, duodenal stenosis, compression of portal vein, stenosis of the proximal
main duct
• 3.7% risk of ductular carcinoma

• Splenic and Portal Vein Thrombosis

• Infrequent, usually secondary to pancreatic head mass
• Left sided or sinistral portal hypertension- splenic venous thrombosis with gastric variceal formation
• Portal Vein thrombosis with risk for bleeding (>20% mortality risk)
• When GE varices are caused by splenic vein thrombosis (+) splenectomy is warranted to prevent
variceal hemorrhage
 MANAGEMENT

• Pain relief: 3 approaches: a) reducing secretion

and/or decompress the secretory compartment, (b)
resecting the focus of chronic inflammatory
change, or (c) interrupting the transmission of
afferent neural impulses through neural ablative
procedures
• Analgesics same as acute pancreatitis

• Abstinence from alcohol-reduces pain by 60-75%

• Somatostatin analogue- 200mcg SQ 3x a day
• Endoscopic Management: stent, drainage,
sphincterotomy and endoscopic stone removal
 SURGICAL MANAGEMENT

• Sphincteroplasty- incision of the septum

Duval’s Caudal Puestow and Gillesby’s
between the pancreatic duct and Pancreaticojejunostomy longitudinal
common bile duct
pancreaticojejunostomy
 SURGICAL MANAGEMENT

Partial Distal Radical distal Proximal Pancreatectomy/ Total Pancreatectomy

Pancreatectomy (40-80%) pancreatectomy (95%) Whipple’s

Focal inflammatory changes For patients with sclerotic Preferred for cases of For refractory chronic
localized in body/tail, (-) disease chronic pancreatitis pancreatitis
ductal dilatation

60% pain relief->completion 60-77% pain relief 71-89% of pain relief 80-85% pain relief
pancreatectomy in 13%

With risk of recurrence With risk of brittle diabetes, 1.5-3% mortality risk Brittle diabetes,
hypoglycemic coma and 25-38% major complications hypoglycemic coma/death
malnutrition
HYBRID RESECTION

• excavation of the
Duodenum pancreatic head,
Preserving including the ductal
Pancreatic Head structures in
resection (DPPHR) continuity with a
long dichotomy of
• Dissection of the the dorsal duct
gastroduodenal Frey Procedure/
artery and creation • preservation of the
Longitudinal
of 2 anastomoses Pancreaticojejunostomy pancreatic neck as
(LR-LPJ) well as the capsule
of the posterior
pancreatic head
 HYBRID RESECTION (LR-LPJ MODIFICATIONS)

• Hamburg Modification: Berne Modification:

• wider excavation of the pancreatic head is excavation of the
central portion of the
created in continuity with the dorsal
pancreatic head without
dochotomy, and is followed by a single, any effort to include the
side-to-side pancreaticojejunostomy duct of the body in the
lateral
pancreaticojejunostomy
PANCREATIC NEOPLASMS
(ENDOCRINE)
• 5/1million cases
• MEN 1 syndrome: pituitary tumors, parathyroid hyperplasia, and pancreatic neoplasms.
• Functional vs non functional neoplasms
• Immunohistochemistry: confirms peptides produced by the neoplasms
• Histopathologic characteristics does not predict clinical behavior
• Malignancy: presence of local invasion and lymph node or hepatic metastases
• Course of the disease more favorable than Exocrine tumors
• Diagnostic imaging of choice: Ct Scan pancreatic protocol: four phases of contrast and fine
cuts through pancreas and liver
 PANCREATIC NEOPLASMS
(ENDOCRINE)
• Insulinoma: MC functional endocrine pancreatic neoplasm
• Benign and solitary, 10% malignant; 90% sporadic, 10% associated with MEN 1 syndrome (higher
recurrence)
• Whipple’s Triad: symptomatic fasting hypoglycemia, <50mg/dl serum glucose, relief of symptoms with
glucose administration
• palpitations, trembling, diaphoresis, confusion or obtundation, and seizure, and family members may
report that the patient has undergone a personality change
• May have profound syncopal episodes averted by frequent eating
• Labs: Elevated serum insulin, C-peptide levels
• Imaging: CT scanning and EUS: localize insulinomas (evenly distributed in head, body and tail of
pancreas)
• TTT: enuclation unless >2cm, close to main pancreatic duct warranting distal pancreatectomy or
Whipple’s
PANCREATIC NEOPLASMS
(ENDOCRINE)
• Noninsulinoma, Hyperinsulinemia, Hypoglycemia Syndrome
• Beta-cell hypertrophy, islet hyperplasia and beta-cell mass.
• Nesideoblastosis: ectopic islet cell tissue, multilobulated islet and ductulo-insular complexes
• Associated patients post subtotal or total pancreatectomy, roux en y gastric bypass

• Gastrinoma
• Usually solitary
• Gastric secreting tumor leading to acid hypersecretion, diarrhea (21%), ZES (abdominal pain,
peptic ulcer disease, severe esophagitis)
• Serum gastrin level measurement: >10000 pg/ml if equivocal secretin stimulation test
 PANCREATIC NEOPLASMS
(ENDOCRINE)
• Gastrinoma: (15 YSR: 80% (if no metz) 5YSR: 20-50% (with metz)
• Passaro’s triangle (70-90%)- junction of the cystic duct and common bile duct, the second and third
portion of the duodenum, and the neck and body of the pancreas
• Imaging of choice: SSTR (octreotide) scintigraphy + CT scan
• EUS: may be used in mass <1cm located at the pancreatic head/ duodenal wall
• Rule out MEN 1 syndrome- check serum calcium levels before surgery (1/4 th cases)
• 50% metastasize to LN or liver
• Surgery: duodenal gastrinoma: full thickness duodenal wall excision
• Excision of all lymph nodes in Passaro’s triangle
• Enucleation: if main pancreatic duct is not involved
• Resection: solitary gastrinoma with no metastases
• Highly Selective Vagotomy- if unresectable or gastrinoma cannot be localized
VIP secreting Tumor/ VIPoma
• Commonly located in distal
pancreas, metastases is
common
• WDHA syndrome: massive
Intermittent watery diarrhea
(5L/day), hypokalemia,
achlorhydria
• Serum VIP levels must be
monitored on multiple
occasions due to episodic
excess secretion of VIP; Serum
Electrolytes
• Imaging: CT scan; EUS (most
sensitive)
• Palliative Surgery may
improve symptoms for a period
with octreotide
Glucagonoma
• MC seen at body and tail, mets is
common
• Mild Diabetes + dermatitis
• Cyclic migration of lesions with
spreading margins and healing
centers probably from low levels of
amino acids
• Usually located at abdomen,
perineum, perioral area and feet
• Enlarged sensitive tongue
• Labs: Serum Glucagon (500pg/ml)
• Debulking operation may relieve
symptoms
Somatostatinoma
• Ampulla and periampullary area
(60%), metastatic
• Somatostatin- inhibits pancreatic
and biliary secretion
• Bile stasis, diabetes and steatorrhea
• Abdominal pain (25%),
jaundice(25%) and cholelithiasis
(19%)
• Labs: Elevated Somatostatin
(>10ng/ml)
 NON FUNCTIONING PANCREATIC ENDOCRINE
TUMORS
• Pancreatic Neuroendocrine Tumors (PNET)
• Majority are malignant and discovered incidentally.
• Sometimes present with vague pain, or weight loss
• CT scan with contrast: presents with cystic component due to central necrosis
• Octreoscan can be helpful to stage the disease
• Surgery: may be done in absence of metastases; however whipples with wedge resection of the liver
may be done in fit patients to avoid GI bleeding, biliary and Gastric outlet obstruction
• Adjuvant chemotherapy after resection: done only if with evidence of metastases by radiology
• Temozoamide and Sunitinib
Pancreatic neuroendocrine tumor (PNET)
demonstrating enhancement during arterial
phase of CTscan. Pancreatic head PNET
seen in (left) sagital, (middle) coronal, and
(right) lateral views of the abdomen.
PANCREATIC NEOPLASMS
(EXOCRINE)
• Worst prognosis of all malignancies with 5YSR of 6%
• Exact cause is unknown
• MC in elderly, male, African Americans
• 2-3X risk if parents or sibling had the disease
• Cigarette Smoking, Type 2 diabetes- 2x risk; Chronic Pancreatitis-20x risk
• Coffee, alcohol, high fat, low fiber, fruits and vegetable diet may be associated with
increased risk of pancreatic cancer
• 80% have glucose intolerance, 50% have overt diabetes
• Genetics: Kras mutation(90%), Her 2-neu overexpression, deletion or mutation of
p53,p16, DPC4, BRCA 2
 PANCREATIC NEOPLASMS
(EXOCRINE)
• Pancreatic Intraepithelial Neoplasia- pre cursor lesions of the pancreas
• 3 stages

• Pancreatic Adenocarcinoma
• Location: 2/3rds head/uncinate process, 15% body, 10% tail or may be diffuse involvement throughout the
gland
• Tumors in the body or tail are larger and usually non resectable at time of diagnosis
• Tumors at the head are diagnosed early due to presence of obstructive jaundice

• Ductal Adenocarcinoma (75% non endocrine cancers)

• Adenosquamous carcinoma- glandular and squamous differentiation
• Acinar Cell Carcinoma- uncommon, >10cm diameter, better prognosis than ductal adenocarcinoma
PANCREATIC NEOPLASMS
(EXOCRINE)
• Pancreatic Intraepithelial Neoplasia- pre cursor
lesions of the pancreas
• Step wise progression of cellular changes
• 3 stages have been defined
• Demonstration of oncogenic mutation and loss of
tumor suppressor genes found in invasive cancers
• Increase in genetic mutation coincide with
increase in cellular atypia and architectural
disarrat
STAGING
PRESENTATION

• 5YSR: 5.8% due to vague symptoms

• Majority: pain (prolonged pain for months located at the epigastrium radiating to the
back) and jaundice, icteric sclera, distended gallbladder
• Some are undiagnosed until weight loss occurs which is a sign of advanced disease
• elderly patients with unexplained, persistent, although vague, abdominal pain or with new
onset diabetes -> Pancreatic Protocol CT scan
 DIAGNOSTICS

• Serum Markers: Ca 19-9: 75% elevated in pancreatic cancer 10% in benign cases of
pancreas, liver and bile duct
Jaundice

HBT Ultrasound

Ductal Dilatation -
+

+ cholelithiasis - Hepatocellular
Disease
choledocholithiasis Pancreatic head
mass
ERCP
CT Scan
DIAGNOSTICS

• CT scan: 90-95% accuracy on unresectable disease

• Unresectable:
• >180 degrees of the celiac axis
• Hepatic or superior mesenteric artery
• Enlarged lymphatic nodes outside the boundaries of resection
• Distant metastases (eg. Liver)

• Borderline Resectable:
• <180 degrees of the SMA, celiac axis or hepatic artery
• short segment of vein occlusion
• Suspicious metastases too small to characterize or biopsy
• Multiple co morbidities or marginal performance status
DIAGNOSTICS

• EUS- detects small pancreatic masses that can be missed by CT scanning and is commonly used
when there is high suspicion for pancreatic cancer with no mass identified in CT scan.
• Provides opportunity for transluminal biopsy of pancreatic mass
• Diagnostic laparoscopy with ultrasound (98% accuracy)
• Peritoneal exploration, ligament of Treitz, base of transverse mesocolon, lesser sac examination
• Utz probe examines liver, porta hepatis, portal vein, superior mesenteric artery
• *if proven unresectable, or delayed resection, biliary obstruction can be relieved with endoscopic approach
in most cases, 10F plastic stents are used and for replacement in 3 months, metallic stets 5 months.
• Higher yield: >4cm tumors, located in body or tail, equivocal findings of metastasis or ascites on CT scan,
marked weight loss, elevated Ca 19-9 >1000 U/ml
 PALLIATIVE SURGERY AND ENDOSCOPY

• Because of poor prognosis, toxic regimens are not encouraged

• Clinical trials may be done of those who prefer chemotherapy
• 3 clinical problems to address: Pain, Jaundice and Duodenal
obstruction
• Pain: Oral narcotics (morphine sulfate) or Celiac Plexus nerve
block in severe cases
• Jaundice: Biliary stenting/ Choledochojejunostomy
• Duodenal Obstruction: Gastrojejunostomy
PALLIATIVE CHEMOTHERAPY AND RADIATION

• Locally Advanced and unresectable: chemotherapy + radiation

• Stage IV: Chemotherapy
• Gemcitabine: improved pain control, performance status and weight gain
• Erlotinib-minimal improvement
• 5FU and Capecitabine: radiosensitizers
• FOLFIRINOX (5 FU, leucovorin, irinotecan, oxaliplatin)- 9-32% response rate with median
survival of 7-11 months

• Neoadjuvant Treatment:
• Decrease tumor burden, increase rate of resectability, kill some tumor cells
• Lower rate of lymph node positivity
 SURGERY

• Pancreaticoduodenectomy:
• If with appropriate clinical and imaging indications, biopsy is not necessary prior to surgery
• Risks during biopsy: hemorrhage, pancreatitis, fistula, abscess, and even death can occur, tumor
seeding is uncommon
• many pancreatic cancers are not very cellular and contain a significant amount of fibrous tissue, so a
biopsy may be misinterpreted as showing chronic pancreatitis if it does not contain malignant glandular
cells
• In patients who are not candidates for resection because of metastatic disease, biopsy for a tissue
diagnosis becomes important because these patients may be candidates for palliative chemotherapy
trials
SURGERY
 SURGERY

• Complications of pancreaticoduodenectomy
• Mortality rate may be <5% in high volume center
• Median survival rate after surgery:22 months
• MC causes of mortality: sepsis, hemorrhage and Cardiovascular events
• Post op complications: delayed gastric emptying, pancreatic fistula and hemorrhage
• Delayed gastric emptying: may be conservatized if outlet obstruction is ruled out or if not combined with biliary leak
• Pancreatic leak: modification of anastomosis (end to side, end to end, duct to mucosa, invaginated), duct stents,
Octreotide
• Hemorrhage MC occurs due to a dissection of the portal vein

• Post op monitoring: CA 19-9 q 3 mos for 2 years

 PANCREATIC NEOPLASMS
(EXOCRINE)
• Ampulla: junction of the biliary and pancreatic ducts within the duodenum
• Usually detected early due to presence of jaundice
• May have intestinal and/or pancreaticobiliary histologic morphology
• Intestinal: better prognosis

• Periampullary: from the distal bile duct, duodenal mucosa and pancreas adjacent to the
ampulla
• 10 YSR: 35% higher than pancreatic adenocarcinoma due to not only early detection but
also lower incidence of p53 and K-ras mutations
 PANCREATIC NEOPLASMS
(EXOCRINE)
• Endoscopic biopsy: 25-56% false negative rates
• Benign,<2cm, no duodenal wall invasion: endoscopic / transduodenal local excision (2-
3mm margin)-> if diagnosed as invasive cancer post op-> whipples
• Cancer or patient with FAP: standard Whipples
CYSTIC NEOPLASMS

• Identified as fluid filled lesion by CT scan

• Benign and slow growing, however may undergo malignant transformation
• Surgical cure is possible however with dilemma on resection vs observation
• Consider: size, growth rate, density, nodules, septations, calcifications and relationship of
lesion to pancreatic duct.
• FNA and analysis of fluid: thick mucinous fluid/ elevated CEA or presence of atypical
cells must be treated as potentially malignant
 CYSTS

• Pseudocysts
• MC cystic lesion of the pancreas with no epithelial lining, non neoplastic
• Biopsy of the pseudocyst wall is necessary to differentiate from a cystic pancreatic neoplasm vs pseudocyst

• Cystadenoma
• 1) Serous Cystadenoma
• Benign tumors without malignant potential
• <1% of cases; Older women, 50% head/uncinate process; 50% body/tail
• May be observed in absence of symptoms due to mass effect or rapid growth (>0.45cm/year)
• 50% are asymptomatic and detected incidentally as microcystic, spongy lesions, fluid close to water
density, central scar with calcification
• (-) mucin stain, Low CEA (<200ng/ml)
• s/sx: abdominal pain, epigastric fullness, weight loss, may grow to a size causing jaundice or GI
obstruction
• Surgery: may be done if symptomatic, splenectomy is not necessary; laparoscopy may be done
CYSTS

• 2) Mucinous Cystadenoma
• Benign with potential for malignancy
• Common in perimenopausal women, 2/3rd at body/tail
• Usually asymptomatic or may cause upper abdominal discomfort or pain, weight loss, early satiety
• Thick walled cysts, no communication with main pancreatic duct, (+) nodules/calcifications in wall of cyst.
• Histopath: tall columnar epithelium theat fills the cyst with vicuous mucin, elongated nuclei at submucosal
area
• Malignant: Elevated CEA >200ng/ml; atypical cells or invasive cancer in solid areas; relative risk if larger
tumor, older patients
• Surgery: resection (distal oancreatectomy) may be done with splenectomy to ensure removal of lymph
node basin
OTHER NEOPLASMS

Intraductal Papillary Mucinous Neoplasm

• Head of pancreas within the main pancreatic ducts
• Mucin production causing dilatation of pancreatic ducts, atrophy of parenchyma (-)calcification or
beaded ducts seen in chronic pancreatitis
• ERCP: “fish eye lesion”- mucin extruding from ampulla of vater; diagnostic of IPMN
• MC: 70-80 y/o, male
• Management: asymptomatic <1cm-observed; 1-2 cm- EUS FNA: (mural nodules, dilated main duct,
cystology, CEA) serial imaging; >3cm resection
• Surgery: Resection with RFS until normal duct
• 5-10 YSR: 50-60%
SPLEEN

A: Hilar Region: 54%

• Encapsulated Mass of Vascular and Lymphoid B: Pedicle: 25%
tissue C: Tail 6%
D: splenocolic
• Largest reticuloendothelial organ in the body ligament 2%
E: Greater Omentum
• Evident at 5th week AOG 12%
• Until 5th month AOG becomes source of F: Mesentery 0.5%
G left Ovary: 0.5%
hematopoiesis
• MC anomaly of splenic embryology:
Accessory spleen (20% of population)
SPLEEN

• 7-11 cm in length
• 150 g (70-250g)
• Splenic ligaments:
• Colon: splenocolic
• Stomach: gastrosplenic: contains short gastric vessels
• Diaphragm: phrenosplenic
• Kidney, adrenal gland, tail of the pancreas: splenorenal
 SPLEEN
Blood supply: splenic artery
Pattern:
a) Distributed type (70%)
Short trunk with many long branches
b) Magistral type (30%)
Long main trunk with short terminal branches
Others: short gastric vessels from left GE artery
Portal Vein: splenic vein + SMV

Splenic Parenchyma:
b) Red Pulp (75% of splenic volume)
c) White Pulp- site of lymph proliferation
c)Narrow marginal zone: interface b/w red and white- lymphocytes
are loosely aggregated
1. marginal zone macrophages- bacteria
2. marginal zone metallophilic macrophages: IF A and B (viral)
 PHYSIOLOGY AND PATHOPHYSIOLOGY

• Splenic inflow of blood: 250-300ml/min

sequestering 2/120 day life cycle of RBC
• Fast/Closed circulation: blood flowing from
arterioles into venous sinuses
• Slow/Open circulation: blood flow from splenic
cords to venous sinuses through endothelial
slits/gaps exposing the blood to extensive contact
with splenic macrophages occurring in the marginal
zone
 PHYSIOLOGY

• Major site of clearance from the blood of damaged or aged red blood cells.
• 2 days in the 120 day cycle of RBCs are spent sequestered in the spleen
• Daily: 20ml of aged RBC are removed

• Extramedullary site for hematopoiesis

• Recycles iron
• Released hemoglobin from damaged erythrocytes are carried by haptoglobins to the spleen

• Site of Innate (red pulp) and Adaptive immune responses(white pulp) (cell mediated and humoral
immunity)
• Marginal zone B cells- detect pathogens and differentiate into IgM or APCs which the latter enters the
white pulp initiating adaptive immune response
 PHYSIOLOGY AND PATHOPHYSIOLOGY

• Major source of Properdin: initiates the alternate pathway of complement activation

• Splenic reticuloendothelial system: able to clear bacterial that are poorly or inadequately opsonized from the
circulation (encapsulated Bacteria); Site of antigen presentation and initiation of B and T lymphocyte activities
• Chronic hemolytic disorders: hypertrophy: reticular spaces of the red pulp become distended with macrophages
engorged with the products of erythrocyte breakdown and splenomegaly can result

SPLENOMEGALY HYPERSPLENISM
abnormal enlargement of spleen presence of one or more cytopenias in the context of a
Moderate- >15 cm >500g normally functioning bone marrow
Massive - >22cm > 1kg Categories:
*palpable below left costal margin (x2 in size at a) Increased destruction of abnormal blood cells in a
>750g normal spleen
b) Primary disorders of the spleen resulting in increased
sequestration and destruction of normal blood cells
PHYSIOLOGY AND PATHOPHYSIOLOGY

• Neutropenia: sequestration of normal cells or removal of abnormal cells

• Platelets: 1/3 sequestered in spleen; Thrombocytopenia may result from sequestration of
platelets as well as accelerated platelet destruction in the spleen
• Splenomegaly may occur in sequestration of 80% of platelet pool

• Hematopoiesis may occur in childhood if bone marrow fails to meet hematologic needs,
however in adults, it may occur in myeloproliferative disorders
 IMAGING

• European Association of Endoscopic Surgery: all patients should undergo preoperative imaging
• Indications: surgical planning, trauma, LUQ pain, characterization of splenic tumors, cyst, abscesses,
guidance for percutaneous procedures
• Identify: splenic volume, presence of accessory spleens
• Splenic Volume: Length (cm) x Width x height x 0.52

• Ultrasound- least invasive, least costly, doppler imaging may assess splenic artery and vein, for
biopsy or cyst aspiration, operator dependent
• CT scan-identifies relationship to other structures, splenic trauma scoring, percutaneous guidance,
volume measurement (CT volumetry), red and white pulp (contrast CT scanning: heterogenous
enhancement)
• MRI: no advantage on CT imaging unless for adjunct purposes
 IMAGING

• Angiography with splenic arterial embolization: localization and treatment of hemorrhage, adjunct to
splenectomy for hematologic disorders (ITP/hypersplenism)
• Risk for increased analgesic use, extended hospital stay and risk of pancreatitis

• Nuclear Imaging (Techentium 99)

• Demonstrates splenic location and size. Able to locate accessory spleens
• Indium labeled autologous platelet scanning (ILAPS)- determines if platelet sequestration is predominantly
in the spleen, liver or both
• Diagnosis of NASH revealed by decreased liver to spleen uptake ratio as compared to NAFLD
SPLENECTOMY

• INDICATIONS:
a) Benign Disorders: RBC (Congenital/ Acquired); Platelet
b) Malignant: WBC; Bone Marrow
c) Other: Infection, Abscess, Cyst, Tumors and Metastasis, Storage Diseases
 RED BLOOD CELL
CONGENITAL

1) HEREDITARY SPHEROCYTOSIS
• Inherited deficiency in one of erythrocyte membrane proteins (spectrin, ankyrin, band 3
protein or protein 4.2) -> destabilization of membrane lipid bilayer allowing a spherical less
deformable shape-> sequestration in the spleen-> Hemolytic anemia
• MC hemolytic anemia for splenectomy
BENIGN

• s/sx: mild jaundice, splenomegaly, absence of anemia to severe cases of having hgb as low as
4 g/dl, low MCV, elevated MCHC and EDW, elevated reticulocyte count, LDH, unconjugated
bilirubin, PBS: spherocytes
• Indications for splenectomy in HS: symptomatic hemolytic anemia, growth retardation,
skeletal changes, leg ulcers, and extramedullary hemopoietic tumors in young patients
• Cholecystectomy: if with coexisting gallstones
• *Near total cholecystectomy- children, may be delayed between 4 and 6 years old
 RED BLOOD CELL
CONGENITAL

2) RBC Enzyme Deficiencies

• Pyruvate Kinase Deficiency: MC congenital enzyme deficiency
causing hemolytic anemia
• May cause severe anemia which is transfusion dependent in early
childhood to well compensated mild anemia in adolescents or adults
BENIGN

• Splenectomy may alleviate transfusion requirements

• G6PD: MC RBC enzyme overall
• Presents with moderate health risks with no longevity reduction
• s/sx: Chronic Hemolytic anemia, Acute intermittent hemolytic
episodes, to no hemolysis
• Splenectomy in general is not indicated in cases of G6PD however
with 1 report presenting complete response and partial response in
patients post splenectomy which completely eliminated or decreased
transfusion requirements
 RED BLOOD CELL
ACQUIRED

3) Warm Antibody Autoimmune Hemolytic Anemia

• S/sx: mild jaundice, anemia, splenomegaly (1/3 rd to ½ of cases), reticulocytosis, elevated indirect bilirubin

• + Direct Coomb’s test

• Usual Treatment: Blood transfusion in severe cases, with corticosteroids for 3 weeks until response is noted on rise
of hematocrit and fall in reticulocyte count
BENIGN

• Splenectomy: 1 series presented response to splenectomy in AIHA from CLL with no benefit in patients with SLE or
Inflammatory Bowel Disease

4) Sickle Cell Disease

• HbS gene from mutation of adenine to thymine in the 6 th codon of the Beta Globin gene
• Indications for splenectomy: acute sequestration crises, hypersplenism and splenic abscess
• Hydroxyurea- chemotherapeutic drug elevating fetal hgb intervening sickling process
• Transfusion and hydration
 RED BLOOD CELL
ACQUIRED

5) Thalassemia- MC genetic diseases that arise from an inherited single gene defect
• Absent or reduced production of hemoglobin chains resulting in a) reduced functioning of hemoglobin
resulting in hypochromia and microcytosis b) unbalance of alpha and beta subunits resulting in
insoluble RBC with poor oxygen release
• Thalassemia major usually presents with pallor, growth retardation, jaundice and abdominal swelling at
BENIGN

an early age (before 2 years old)

• Usual treatment: Transfusion, Chelation therapy with deferoxamine
• Splenectomy: indicated for excessive transfusion requirements (>200ml/kg/year) discomfort due to
splenomegaly or painful splenic infarction
• High risk of Post splenectomy infection – due to immune deficiency from iron overload
 PLATELET

• Idiopathic Thrombocytopenic Purpura (ITP)

• s/sx: low platelet count with mucocutaneous and petechial bleeding in the
form of epistaxis, menorrhagia, hematuria or melena; Splenomegaly is
rare, other causes should be sought
• Dx of exclusion; PBS: low platelet count with megakaryocytes
BENIGN

• From premature removal of platelets in liver and spleen from interaction of

autoantibodies with FC receptors of tissue macrophages
• Usual treatment: oral prednisone 1-1.5mg/kg/day responds within 1 st 3
weeks
• Severe cases with <5000 platelet: IV immunoglobulin 1g/kg/d for 2-3 days
• Laparoscopic Splenectomy: failure of medical therapy for prolonged
steroid use (>10-20 mg/d for 3 to 6 months)
 PLATELET

• Thrombotic Thrombocytopenic Purpura (TTP)

• Characterized by thrombocytopenia, microangiopathic hemolytic anemia and neurologic
complications
• s/sx: petechiae, fever, neurologic symptoms, renal failure, and, infrequently, cardiac symptoms
such as heart failure or arrhythmia
BENIGN

• Abnormal platelet clumps in arterioles and capillaries from large amounts of Von
Willebrand factor leading to microvascular thrombus which can cause shearing forces
deforming RBCs
• Dx: PBS revealing schistocytes, nucleated RBCs and basophilic stippling and (–) Coomb’s
Test
• Usual Treatment: Plasma exchange
• Splenectomy: for patients who relapse or require multiple exchanges to control symptoms
 WHITE BLOOD CELL

• Hairy Cell Leukemia: splenomegaly, Pancytopenia, elevated lymphocytes in Bone Marrow

• PBS: irregular hairy cytoplasmic projections
• Splenectomy: does not correct underlying disorder but returns cell counts to normal in 40-70% and alleviated symptoms of
MALIGNANT

splenomegaly

• Hodgkin’s Disease
• PBS revealing Reed Sternberg cells
• Spleen is often an occult site of spread, splenomegaly is rare

• Non Hodgkins Lymphoma: may be asymptomatic to presence of pain, swelling, fever and night sweats, splenomegaly
is not common
• Splenectomy is indicated as last resort when diagnosis cannot be established with remaining clinical suspicion
• Splenectomy may improve in up to 75% of patients same as in CLL
 BONE MARROW

• Chronic Myeloid Leukemia:

• disorder of the primitive pluripotent stem cells in the bone marrow that results in a significant increase
in erythroid, megakaryotic, and pluripotent progenitors in the peripheral blood smear
MALIGNANT

• transposition between the bcr gene on chromosome 9 and the abl gene on chromosome 22.
• Splenomegaly is found in ½ of patients with CML with splenectomy done to relieve pain and early
satiety but does not prevent blast crisis

• Acute Myeloid Leukemia/Chronic myelomonocytic leukemia

• Rapid progression as CML
• Splenectomy: for pain relief of LUQ pain
 BONE MARROW

• Essential Thrombocythemia: abnormal growth of megakaryocyte line resulting in Increased levels of

platelets in the bloodstream.
• Diagnosis of exclusion after ruling out CML, polycythemia vera, myelofibrosis
MALIGNANT

• Splenomegaly occurs in 1/3 to ½ of patients

• Splenectomy is reserved in later stages of the disease with risks of heavy bleeding

• Polycythemia Vera
• increase in red blood cell mass, frequently accompanied by leukocytosis, thrombocytosis, and splenomegaly
• Rudy cyanosis, conjunctival plethora, hepatomegaly, splenomegaly and hypertension
• Usual Treatment: phlebotomy to use of chemotherapy
• Splenectomy for later stages on severe splenomegaly symptoms or myeloid metaplasia
 BONE MARROW

• Agnogenic Myeloid Metaplasia

• Nucleated red blood cells and immature myeloid elements in the blood are present in 96% of cases and
strongly suggest the diagnosis. Teardrop poikilocytosis is another frequent finding.
MALIGNANT

• Treatment: allogeneic bone marrow transplantation in younger, high-risk patients.

• Supportive therapy for clinically symptomatic anemia includes steroids, danazol, erythropoietin, or blood
transfusion
• Chemotherapy and low dose radiation: may result in rapid regrowth on discontinuation
• Splenectomy: provides durable, effective palliation for nearly all patients with AMM,
• although postoperative complications are more common in patients with AMM than in those with other
hematologic indications (Thrombosis, Hemorrhage and infection)
INFECTIONS

• Etiologies: Infectious mononucleosis, Malaria, Listeria, Fungal infections, dengue, q

fever
• Infections may cause spontaneous splenic rupture warranting close attention
• Pathophysiology: infiltration of the splenic parenchyma with inflammatory cells, which
distorts the architecture and fibrous support system of the spleen and thins the splenic
capsule
 ABSCESSES
• Uncommon with 0.14-0.7% of cases
• Usually on tropical locations associated with thrombosed splenic vessels and infarction in patients with sickle cell
• 5 mechanism of splenic abscess formation:
• (a) hematogenous infection; (b) contiguous infection; (c) hemoglobinopathy; (d) immunosuppression; e) Trauma

• Presentation: delayed usually endured at 16-22 days before diagnosis

• fever, left upper quadrant pain, leukocytosis, and splenomegaly in about one-third of patients

• Imaging: confirmed by Ultrasound or CT scan with 95% sensitivity and specificity

• MC organisms: aerobes (streptococci and Escherichia coli) others Mycobacterium tuberculosis and salmonella typhi
• Treatment: broad spectrum Antibiotics with adjustment to culture guided results and splenectomy
• percutaneous drainage if splenectomy cannot be tolerated
CYSTS

• Parasitic vs non parasitic

• Parasitic: MC cause majority (Echinococcus species)
symptom: mass lesion in LUQ or impinging lesion on the stomach
Ultrasound: cystic lesion and other asymptomatic lesions
Serologic test: can confirm parasitic etiology
Treatment: Splenectomy- **Avoid spillage of cyst contents to peritoneum to avoid
anaphylactic shock
• Non-parasitic: pseudocysts (trauma), dermoid, epidermoid and epithelial
• Asymptomatic: close follow up by utz, avoid trauma if large
• Small symptomatic: may be excised with splenic preservation
• Large symptomatic: may be unroofed
TUMORS AND METASTASIS

• MC primary tumor: Sarcoma

• 0.6 tumor mets to the spleen MC carcinomas, Lung Cancer
• Infrequent site of metastasis in general and appears if it is widely disseminated
• Metastases from Colorectal, ovary and melanoma may be isolated in the spleen
• Laparoscopic Splenectomy may be done in isolated cases of metastases
 STORAGE DISEASES AND INFILTRATIVE
DISORDERSNiemann-Pick
Gaucher’s Disease Amyloidosis Sarcoidosis
lipid storage disorder with storage of Abnormal lysosomal storage of Abnormal cellular protein Non caseating granuloma
Glucocerebroside in macrophage- sphingomyelin and cholesterol in deposition in affected tissues
monocyte system by deficient macrophage-monocyte system
activity of lysosomal hydrolase Types A and B: deficiency in
lysosomal hydrolase MC presents
with splenomegaly
Splenomegaly: early satiety, Splenomegaly, and its mass Primary amyloidosis- 5% Fatigue and malaise
abdominal discomfort, effects: early satiety, abdominal splenic involvement MC involved organs:
Hypersplenism: thrombocytopenia, discomfort Lung, spleen
thrombocytic anemia, leukopenia, Secondary amyloidosis- (splenomegaly 25% of
bone pain, pathologic fractures, associated with chronic patients)
jaundice inflammatory conditions

Splenectomy- Splenectomy- relieves

splenomegaly symptoms symptoms and corrects
Splenectomy- alleviates hematologic abnormalities but does not correct hematologic abnormalities
underlying abnormalities such as anemia and
thrombocytopenia
 MISCELLANEOUS DISORDERS AND LESIONS

Splenic Artery Aneurysm Portal Hypertension Felty’s Syndrome Wandering Spleen

MC visceral artery aneurysm
Women 4x > Men
MC site: middle to distal
splenic artery
Aneurysm resection/Ligation:
mid-splenic
Splenectomy: Distal to hilum
Splenic artery embolization:
risk for splenic infarction and
abscess
MC from cirrhosis
Accompanied by splenomegaly
and splenic congestion
Splenectomy- indicated in cases
to reduce bleeding from
esophageal varices (cirrhosis)
Treats portal hypertension
(splenic vein thrombosis)
Splenorenal shunt- portal system
decompression
Triad: rheumatoid Floating spleen in the
Arthritis, splenomegaly abdomen due an
and neutropenia embryogenic anomaly
High risk for recurrent May cause splenic
infection torsion and infarction
Splenectomy- >80%
response rate with
resolution of neutropenia
post surgery
PRE OPERATIVE CONSIDERATIONS

• Potential Complications:
• Overwhelming post splenectomy sepsis (MC) Vaccination:
• Splenic Vein thrombosis 1-2 weeks pre op/ 2weeks post op
with PPV, meningococcal,
• Bleeding 2-4 U PRBC Haemophilus vaccine
• Arteriothrombosis
• Deep Vein thrombosis DVT prophylaxis:
• Pulmonary Hypertension Compression stockings
5000 IU SQ Heparin
SPLENECTOMY

• Indications:
• Laparoscopic: Gold standard for normal sized spleen for elective procedures
• Open: Indications: traumatic rupture of spleen, massive splenomegaly, ascites, portal
hypertension, multiple prior operations, extensive splenic irradiation, possible splenic
abscess
OPEN SPLENECTOMY
Incision: Left Subcostal 2 FB below
Midline: ruptured or massively enlarged

• Divide splenocolic ligament and

lateral peritoneal attachments

• Ligate the splenic artery THEN vein

along the superior border of the
pancreas, then short gastric vessels

• Splenic hilar dissection

• Hemostasis

• The splenic bed is not routinely

drained

• Inspect for accessory spleen

 LAPAROSCOPIC SPLENECTOMY

Decreased intraoperative blood

loss, shorter hospital stay, lower
morbidity rate

Right lateral decubitus position

*Mass hilar stapling

Morcellization of spleen with

piecemeal extraction
HAND ASSISTED SPLENECTOMY

• Indication: for spleens greater than 22cm craniocaudal

or 19cm in width
• Shorter operative time
• 7-8 cm incision on the caudal site of inferior pole of
spleen
• The nondominant hand provides medial retraction and
rotation of the spleen through a hand-assist port, while
the dominant hand carries out the dissection using
laparoscopic instruments
 INTRAOPERTIVE SPLENIC INJURY

• MC MECHANISM: Improper traction on the spleen against its

peritoneal attachments
• MC type of injury: Capsular tears; others: parenchymal
lacerations and subcapsular hematomas
• MC site: lower pole due to greater attachments on site
• Hemorrhage: direct spleen compression, compression of vessels at
splenic hilum, pressure on splenic artery and superior pancreatic
margin (splenectomy if hilar injury)
• Capsular Tears: splenorrhaphy: topical hemostatics, suture
plication, omental buttress, bioabsorbable mesh sheets
 SPLENECTOMY OUTCOMES

• Changes in blood composition: presence of Howell-Jolly bodies and

siderocytes; leukocytosis (within the day) and increased platelet counts
(after 2 days), rise in hemoglobin to >10g/dL (chronic hemolytic anemias)
• Complications: pulmonary- left lower lobe atelectasis (MC), pleural
effusion and pneumonia
• Hemorrhagic- present as subphrenic hematoma
• infectious- avoid placement of drains
• Pancreatitis, pseudocyst and pancreatic fistulas- from pancreatic trauma
during dissection
 OVERWHELMING POST SPLENECTOMY
INFECTION (OPSI)
• Asplenic patients- lifelong susceptibility to infection
• Post splenectomy- sepsis is a medical emergency, any note of fever must warrant
suspicion including malaise, myalgias, headache, vomiting, diarrhea, abdominal pain
• Possible progression to fulminant bacteremic septic shock, with hypotension, anuria, and
disseminated intravascular coagulation
• Lifetime risk: <1% - 5%, may take several years to decades post splenectomy to occur
needing lifelong vigilance
• Most influential determinant for OPSI: Indication for splenectomy:
• Hematologic cause- more susceptible than for those from trauma or iatrogenic reasons
• Age- higher susceptibility for <5 years old and >50 y/o.
OVERWHELMING POST SPLENECTOMY
INFECTION (OPSI) PATHOGENESIS
• 3 factors: Loss of splenic macrophages, diminished tuftsin production, loss of
reticuloendothelial screening function
• These three work in concert to eliminate opsonized bacteria from the bloodstream suited
to remove encapsulated bacteria whose polysaccharide coating is a natural defense
against opsonization
• Elimination of these pathogens falls solely to the liver in the absence of spleen
• Antibiotics: Indications: for therapy of established or presumed infections, prophylaxis in
anticipation of invasive procedures, general prophylaxis
• Duration: Pedia: daily dose post splenectomy until 5 years old or 5 years after splenectomy
• With risk of antibiotic resistance, it is now recommended for patients with failure of response
to vaccines, or for asplenic patients to carry at all times antibiotics on first sign of infection
THANK YOU!