B.

Thoracic and abdominal surgery

1. Inguinal and femoral hernia

Inguinal hernia:
Definition: Protrusion of abdominal cavity contents through inguinal canal. MC type of hernia (more in men).
Classification
1) Indirect (MC): lateral to inf. Epig Artery, protrude through deep ingl ring + superf inguinal ring.
- congenital, Narrow-necked; offer surgical repair.
2) Direct: medial to inf. Epigastric art. Through inguinal ring.
-chronic straining/coughing/obese/old people=weakening of tissues. Wide-necked; not well controlled by pressure!
ClassF: Reducible: can be pushed back in. Incarcerated: can’t be reduced.
Strangulated: compromise blood= infarction.
Form: Inguinoscrotal: Descends via ingl canal (indirect) Sliding: sac partly by retroperit. Pantaloon: mix
(in/direct).
Exam: bulge medially over ingl canal (direct), descend to scortum (indirect), below/lateral pubic tubercle (Fem. hernia).
Diagnosis: Clinically, CT or rarely herniography (intraperitoneal contrast injection).
Tx: - Uncomplicated: Children (excision of sac+apply deep ingl ring). Adults (Herniotomy/herniorrhaphy)
- Strangulated/obstructed: Emergency surgery (resection + surgery repair).

Herniotomy: hernia sac is freed, its neck ligated, and the sac reduced.
Herniorrhaphy: returning the displaced tissues to their proper position.
Hernioplasty: mesh patch is sewn over the weakened region of tissue.
Complications: Infection, recurrence, nerve entrapment, scrotal hematoma.
-Extra: Avoid heavy lifting / straining for 2w post-opert. Truss belt: pressure prevent hernia protrusion (if surgery is
contraindicated)
-Extra: Hesselbachs triangle: ingl lig (inf), inf epigast (lat), rectus abdomin (med).

Femoral hernia: Through tissues of the femoral canal, more in women.

Clinical: below & lateral to pubic tubercle. Flattening & loss of the inguinal skin crease (in distinction to inguinal hernias). If
obstructed= vomit/constip. If strangulated= severe pain/shock. Swelling below the inguinal lig.
Diagnosis: Clinical presentation.
Differential: Low presentation of inguinal hernia. Femoral canal lipoma/lymph node/artery aneurysm.

High approach (emergency): Cut above ingl lig. - dissecting through posterior wall of the inguinal canal.
Low approach: Cut below ingl lig, don’t interfere with inguinal struct- small range for resecting compromise small bowel.

2. Umbilical, epigastric and incisional hernia

Umbilical hernia “anterior hernia” (congenital)

- Risk factor= acquired due to Increased abd pressure (ascites, pregnancy, obesity)
- Treatment: Close spontaneously by age 3. Pure tissue repair (if <3 cm) or Mesh repair (if > 3cm)
Extra: Paraumbilical hernia=acquired, through periumbulical tissue.

Epigastric hernias: Defects in the midline tissues of the linea alba (umbilicus to xyphoid).
- Male > Female
- Typically pain out of proportion to the size of hernia
- Treatment: Pure tissue repair – open approach. (small defects: overlapping suture. Large defects: require mesh)
Incisional hernias: Protrusion through a surgical scar/cut insufficient healing (loose suture).
- High reoccurrence (15-30%)
- Risk factors: suture under tension, ↑ [Link] pressure, inadequate healing, infections, wound complications.
- Treatment: pure tissue repair – open (if <3cm) – mesh (if >3cm – inlay or underlay)
3. Diaphragmatic and other rare types of hernia

Diaphragmatic hernias:
- Hiatal hernia -> sliding, rolling or mixed through oesophageal hiatus.
Clinical: reflux symptoms, obstruction possible
Treatment: hiatoplasty – repositioning of contents and approximating the hiatal curs on left and right side

Posttraumatic -> when traumatic rupture of diaphragm was not detected

Obturator hernia: due to weakening of the obturator membrane which can lead to compression of the obturator nerve
(Howship-Romberg sign – pain in medial aspect of thigh that is relieved with flexion of thigh) – mesh repair (laparoscopic is
ideal).

Sciatic hernia: through greater sciatic foramen – usually asymptomatic until strangulation.
Mesh repair is superior to pure tissue repair.

Perineal hernia
Lumbar hernia
Parastomal hernia

4. Strangulated hernia

A strangulated hernia is life-threatening.

Fatty tissue or a section of the small intestines pushes through a weakened area of the abdominal muscle. The surrounding
muscle then clamps down around the tissue, cutting off the blood supply to the small intestine. This strangulation of the small
intestine can lead to intestinal perforation, shock, or gangrene (death) of the protruding tissue, which can lead to death
Clinical features: Sudden/severe acute pain, Bulge (has aching sensation) bloody stools, inflm, tenderness, nau/vom. Dark/red
skin over hernia.
Cause: Increased abd pressure. Pregnancy, chronic cough, straining abd muscles, history of abd surgeries (e.g. cesarean section).
RF: Male (8x more), old, family, chronic cough/constip, pregnancy, previous hernia.
Complication: Cuts off blood flow to intestines (infarction). Can be gangrenous within hours. SepsisàSepticemia à Death.
Prevention: Healthy weight, diet (fiber), avoid heavy lifting, stop smoking (chronic cough).
Surgery:
- Open hernia repair: incision in groin & push back into abdomen. Reinforce with hernioplasty (mesh) & close by
stiches/staples.
- Laparoscopic (minimally invasive) hernia repair use: inserted through a small incision at the umbilicus (belly button).

Recovery: You should be able to return to your regular routine within a week or two
5. Acute abdomen – definition, classification and role of general practitioner in diagnostic process

+ Traumatic: perforation, intraabdominal bleeding.

+ Non- traumatic: Inflammatory diseases, Ileus, bleeding from GIT. dark sticky faeces containing partly digested blood

↑
vomiting of blood.

I
Symptoms: Pain, nausea, vomiting, damaged bowel passages, tension of abd wall, hematemesis, melena.
Differential: Pneumonia, pleuritis, pneumothorax, MI, aortic aneurysm, pyelitis, urolithiasis.
Diagnosis: Pain (start, duration, character, spasm),
- Exam: look, palpate, percussion, auscultation, per rectum – Lab: blood exam, haemogram, coagulation, biochemical.
- Imaging: X-ray, USG, CT, MRI
1) Epigastric acute abdomen: 30-40% biliary/gallstone colic, 20-30% acute cholecystitis, perforated peptic ulcer, acute
pancreatitis,
2) Right meso + hypogastrium: acute appendicitis/adnexitis/ectopic preg/crohns/mekel’s diverticulum or hernia.
Left meso + hypogastrium: diverticulitis/tumors of sigma /urethrolithiasis/nephrolithiasis/adnexitis/ectopic, scrotal hernia

Stones (kidney
Mesogastrium: acute obstruction of mesenteric vessel, necrotizing enteritis, rupture of abd aorta, urinary retention.
crethon stone
Role of GP of first contact in diagnosis:
- The initial approach: assess for life-threatening causes (e.g. ruptured abdominal aortic aneurysm, bowel perforation).
CHECK: vital signs, quick physical examination, and appropriate diagnostic tests (e.g. abdominal ultrasound, abdominal x-
ray).
- Once emergency causes ruled out à thorough history + physical examination. Narrow the diagnoses + diagnostic workup.

Sometimes can be due to faces (stone) Leadthatgrowth.

stuck.

The most specific physical findings in appendicitis are rebound tenderness, pain on percussion, rigidity, and guarding. Although RLQ tenderness is present in 96% of patients

e
6. Acute appendicitis excessive discharge or build-up of mucu

*
MC cause of acute abdomen –always be considered as differential in acute abdomen.
Pathophysiology: not understood – due to obstruction of lumen with subsequent bacterial overgrowth.
Classification: catarrhal, phlegmonous, gangrenous or perforated (perforation often occurs within 48 hours); if perforation
occurs peri-appendiceal abscesses or diffuse peritonitis can occur – Subacute appendicitis (if inflammatory processes develop
slower than normal, associated w/ inflamm pseudotumor – palpable mass).
Types: retrocecal (10% - in retroperitoneal space – mild pain in right iliac region), pelvic (similar symptoms to gynecological
diseases, also diarrhea may be symptom), mediocecal (may present with small bowel obstruction), Subhepatic (dislocated
cranially due to imperfect bowel rotation or pregnancy), Left sided (situs viscerum inversus).
tenderness
Diagnosis: history, physical exam, fever, RLQ pain, Mcburney’s sign, dunphey’s sign (any movement causes
pain), Rovsing’s sign (RLQ pain when palpating LLQ), Blumberg’s sign, Plenies’s sign (painful percussion), obturator sign, iliopsoas
pain upon removal of pressure

sign – Lab: non specific, increased WBC, CRP usually normal.

USG (thick walled, non-compressible, diameter of >7mm) CT in dubious cases.
Treatment: appendectomy – open or laparoscopic (diagnostic laparoscopy).
7. Specific aspects of acute appendicitis in children, geriatric patients and pregnancy

Children: > 90% of acute abdomen in children are due to appendicitis

Presents with diarrhea, fever, vomiting, RLQ pain (pain only minor symptom).
Perforation occurs quickly (due to short omentum, decreased inflammatory response of the peritoneum and limited systemic
resistance against infections).

Geriatric: rare and has only mild symptomatology -> subacute appendicitis and peri appendiceal abscesses
are more common findings, also intestinal obstruction. Appendicitis develops relatively slow, it becomes fibrotic with age and
the area is more readily walled off by omentum and adherent small bowel; often it resolves spontaneously. Clinical
presentation: obstruction, vomitus, colic pain, obstructed bowel sounds. Potentially a mass may be palpable if patient is relaxed.
X-ray may show fluid levels in RLQ.
Necessary to differentiate from e.g. colon cancer

Pregnancy: seldom, prevails around 3rd month of pregnancy and threatens both mother and fetus. Mortality up to 9% for mum
and 20% for fetus. Diagnosis is difficult because appendix is dislocated by enlarged uterus
Many symptoms of appendicitis mimic symptoms of pregnancy (vomiting, nausea, tachycardia)

8. Subacute appendicitis

Inflammatory processes happen slower than in acute appendicitis – is defined by inflammatory pseudotumor
that involves appendix and surrounding organs/tissues (omentum, coecum, ileum, right ureter, retroperitoneum). Clinical: RLQ
pain lasting more than 48 hours, fever, palpable mass in right iliac region which is visible in CT or USG, ↑ CRP.
Treatment: Conservative treatment with ATBs and bowel rest (appendectomy impossible due to pseudotumor formation).
9. Examination of patient with acute abdomen – history taking, physical examination, clinical and paraclinical investigations

History: Exact time of onset; localization of pain (which quadrant), Radiation of pain (biliary colic, acute pancreatitis, renal colic);
Type of pain (colic (intermittent), inflammatory (constant), Ischemic (severe, sudden)), Triggering or relieving factors; Similar
pain in past? Nausea? Vomiting? If yes was vomiting before pain onset (gastritis) or after onset of pain (acute abdomen). Does
vomiting relieve pain?
Stool + Flatulence status: character (normal, diarrhea, constipation), color (brown, black, red, green, pale), frequency, change in
stool pattern? Urination: changes in normal pattern?
Previous surgeries or concomitant diseases
Physical exam: must be meticulous and complete – adequate exposure of the abdomen, rectal examination.
Para- clinical exam: laboratory test: blood count, natrium, potassium, urea, creatinine, glycemia, liver test (ALT, AST. ALP, GMT),
Bilirubin (total and conjugated), amylase, CRP; urine analysis.
ECG, abdominal USG, abdominal and chest X-ray
Diseases mimicking AA: porphyria, hyperglycemia in diabetes, uremia in renal failure.

o
a rare hereditary disease in which there is abnormal metabolism of
the blood pigment haemoglobin. Porphyrins are excreted in the
urine, which becomes dark; other symptoms include mental
disturbances and extreme sensitivity of the skin to light.

10. Acute cholecystitis swelling (inflammation) of the gallbladder

Classification:
- Calculous: associated with cholecystolithiasis – 90-95%
- Acalculous: without gallstone disease
Clinical: RUQ pain, worsened by movement//relieved by when still (relaxed abd wall; nas/vom & fever.
If jaundiced: suspect cholangitis or Mirizzi syndrome (obstruction of gallbladder neck by stone with additional inflammation and
obstruction of common bile duct) Positive Murphy’s sign, guarding, tenderness.
Diagnosis: USG: thickened gallbladder wall (>4mm), pericholecystic fluid +/- gallstones Increased CRP and leukocytes
Treatment: conservative with IV ATBs or surgically – total or subtotal cholecystectomy -surgical removal of the gall bladder.

Cholecystectomy: laparoscopic is preferred

Subtotal cholecystectomy: distal part of gallbladder is left in situ to prevent bile duct injury (if inflammatory changes prevent
safe standard procedure).
In patients unable to undergo anesthesia – transhepatic cholecystostomy to drain bile.
11. Subacute cholecystitis
prolonged, subacute condition caused by the mechanical or functional dysfunction of the emptying of the gallbladder
If adjacent organs and tissues such as the omentum or duodenum or transverse colon cover the gallbladder to localized the
inflammatory process and form an inflammatory pseudotumor.
Also called peri-cholecystitis
Clinical: painful mass in right hypochondrium may be palpated, increased leukocytes and CRP
Diagnosis: increased leukocytes and CRP, final diagnosis by abdominal USG.
USG: thickened gallbladder wall (>4mm), pericholecystic fluid +/- gallstones
Treatment: If surgery is impossible à conservative treatment with ATBs.
Surgery: cholecystectomy (laparoscopic).

Porcelain = inner gallbladder wall is encrusted with calcium.

T

12. Cholecystolithiasis

Presence of gallstones in the gallbladder – mostly cholesterol but may be pigmented (due to hemolysis or
infection).
Etiology: Imbalance in bile salts, lecithin, cholesterol, calcium carbonate and bilirubin + BILIARY STASIS (Impaired gallbladder
emptying) – Risk: obesity, female, multiparity or pregnancy, >40 years, family history – for black stones: chronic hemolytic
anemia, cirrhosis, crohn, >age, parenteral.
Clinical: most asymptomatic; biliary colic: dull RUQ pain (<6 hours) especially postprandial (vagal stimulation causing gallbladder
contraction), may radiate to epigastrium, right shoulder and back; nausea, vomiting, early satiety, bloating, dyspepsia.
Gallbladder cancer risk: gallbladder polyps,O porcelain gallbladder or gallstones >3cm.
Diagnosis: In suspected symptomatic: Imaging: USG of RUQ (strong posterior acoustic shadow, echogenic
foci intraluminal); MRCP (magnetic resonance cholangiopancreatography); CT (if MRI is not available and USG was inconclusive)
– Lab: usually normal in cholelithiasis.
Treatment: Provide supportive care; asymptomatic can consider elective cholecystectomy if there is risk for
gallbladder cancer or complications.
Symptomatic uncomplicated: elective cholecystectomy is mainstay; symptomatic complicated cholelithiasis (acute cholecystitis,
choledocholithiasis, acute cholangitis): cholecystectomy, initial ATB.
13. Complications of cholecystolithiasis Presence of gallstones in the gallbladder – mostly cholesterol but may be pigmented (due to hemolysis or infection).

the collection of pus in a cavity in the body,

Acute and chronic cholecystitis ↑especially in the pleural cavity

- Acute cholecystitis — gallbladder empyema, gallbladder perforation

- Chronic cholecystitis — porcelain gallbladder, gallbladder cancer
▪--Fibrotic and calcified gallbladder due to chronic inflammation
Hydrops of the gallbladder (permanent obstruction of the cystic duct by the stone)
Migration of the stone into common bile duct causing obstructive jaundice
- Biliary pancreatitis
- Obstructive cholangitis
Biliary fistula: type of fistula in which bile flows along an abnormal connection from the bile ducts into nearby hollow structure.
Types of biliary fistula include:
- Bilioenteric fistula: abnormal connection to small bowel, usually duo- denum.
- Thoracobiliary fistula: abnormal connection to pleural space or bronchus (rare).
Mirizzi’s syndrome: gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the

C
common hepatic duct, resulting in obstruction and jaundice. Can lead to gallbladder cancer.

14. Complications of cholecystectomy

1) Injury of common bile duct (including accidental clipping)à Bile leakage/bleeding.

2) Perforation of adjacent organs
3) Bleeding
4) Infections
5) Post cholecystectomy syndrome:
- Persistent abd pain or new sypmt after gallbladder removal.
- Etiology: Biliary injury.
- Clinical: Abd pain + upper/lower GI tract (dyspepsia/diarrhea)
- Diagnosis: USG/CT
- Dyspepsia=PPI //For bile acid diarrhea=Loperamide.
 15. Diseases of common hepatic duct, common bile duct and papila of Vater

Choledochal cysts - congenital dilations of the biliary tree with risk of malignant transformation and
recurrent cholangitis – risk of developing cholangiocarcinoma
Symptoms: classic triad: abdominal pain, jaundice and abdominal mass
Diagnosis: USG and CT
Treatment: Surgical excision and biliary-enteric anastomosis.
Common bile duct stone, also known as choledocholithiasis

Choledocholithiasis: stones in CBD – usually cholesterol formed in gallbladder migrate through cystic duct
Symptoms: asymptomatic; biliary colic – sharp RUQ pain radiating to scapula and back O
Diagnosis: USG, hyperbilirubinemia, increased ALP
Treatment: remove stone with ERCP.

Cholangitis - inflammation of bile duct with at least partial obstruction of bile flow and bacterial growth
Symptoms: Charcot triad: pain, jaundice and fever with chills
Treatment: ATBs and removal of obstruction (ERCP) or cholecystectomy.

Carcinoma of ampulla of Vater - adenocarcinoma 2cm distal to CBD, common metastasis to liver
Symptoms: obstructive jaundice, epigastric pain, pruritus, nonspecific: weight loss, fatigue
Diagnosis: USG, MRCP
Treatment: Whipple (pancreaticoduodenectomy).

16. Surgical procedures on bile ducts

Cholecystectomy: laparoscopic or open – dissection of. The cystic duct and cystic artery with clipping and
dissection of the gallbladder from the liver bed (retrograde – preferred first dissection of structures; antegrade -first dissection
from liver bed).
Acute or elective

Choledochotomy: incision of common bile duct – usually in supraduodenal part in order to explore biliary
Tree by traditional (forceps, probe, balloon) or by flexible endoscope (choledochoscopy),
Suturing of the choledochotomy by absorbable suture – either primary or by suture over a T-tube
of Water

hole-Papil a Papillotomy: incision of the fibrous

This

(Papilla
part of the papilla of Vater

Papillosphincterotomy: incision of the sphincter of Odi - both can be performed by endoscopy during ERCP
Or open surgery via duodenectomy

Bilio-digestive anastomosis: connection btw biliary system and digestive system either for drainage of bile.
(palliative procedure) or as reconstruction after resection of extrahepatic biliary
tree – gallbladder, common bile duct or common hepatic duct may be connected to duodenum, stomach or Roux limb of
jejunum.
O
O O

O O
17. Hydrops and empyema of gallbladder
- *
Hydrops: marked distension of the gallbladder with sterile mucinous content due to chronic biliary outflow obstruction.
Etiology: impacted gallstones at the gallbladder neck (most common), tumors at gallbladder neck or CBD (GB polyps,
cholangiocarcinoma, carcinoma of pancreatic head), acute inflammatory conditions (Kawasaki disease), extrinsic compression of
outflow tract (lymphadenopathy, adhesions, strictures).
Symptoms: abdominal pain, RUQ mass, jaundice.
Treatment: ATBs, analgesia and hydration – Cholecystectomy.

Empyema: distended, pus-filled gallbladder (suppurative cholecystitis)

Symptoms: similar to uncomplicated acute cholecystitis (RUQ pain >6 hours, postprandial, radiation to right scapula, positive
murphy’s sign – pausing during inspiration upon deep palpation of the RUQ due to pain; fever, guarding, nausea, vomiting).
Dg: Imaging: gallbladder distension with hyperechoic (USG) or hyperintense (CT with contrast) in the lumen.
Treatment: Empiric ATBs for biliary infection, emergency source control procedure.
Low surgical risk: laparoscopic cholecystectomy
High surgical risk: imaging-guided percutaneous drainage of empyema.

↑Hydrops

Empyema
*

18. Acute cholangitis

Also called ascending cholangitis is a bacterial infection of the biliary tract often secondary to biliary obstruction and stasis
(biliary structure or choledocholithiasis).
Symptoms: Charcot triad: 20-75% of patients have this – Abdominal pain (RUQ), high fever and jaundice; Reynold’s pentad:
Charcot triad PLUS hypotension and metal status changes; Features of sepsis, septic shock and multiorgan dysfunction may be
present.
Diagnosis: based on systemic signs of inflammation (fever, leukocytosis, increased CRP) in combination with signs of cholestasis
(jaundice, increased GGT, ALP).
Imaging: USG – dilated common bile duct, dilated intrahepatic bile ducts, thickened bile duct walls, choledocholithiasis –
evaluate for biliary obstruction CT with contrast – if USG is inconclusive.
Treatment: Empiric ATB treatment and urgent biliary drainage are mainstays of treatment.
Therapeutic ERCP-guided transpapillary biliary drainage (ERCP w/ papillotomy OR w/ temporary biliary stenting).
EUS-guided biliary drainage (second line procedure – fistula is created and stent placed between stomach/duodenum and the
CBD).
Underlying cause should be treated: removal of stone, cholecystectomy, stenting for stricture.
Complications: sepsis, septic shock, MODS, pyogenic liver abscess, pericholecystic abscess, biliary stricture.
 Cholelithiasis or gallstones are hardened deposits of digestive fluid that can form in your gallbladder.
·

19. Gallbladder cancer

malignant (cancer) cells form in the tissues of the gallbladder. condition in which the inner gallbladder wall is encrusted with calcium.
Originate within the mucosal lining of the gallbladder. &

Etiology: Cholelithiasis with chronic inflammation (most common), porcelain gallbladder, liver fluke infection,
choledocholithiasis, chronic cholecystitis, chronic cholangitis, gallbladder hydrops.
Symptoms: symptomatic in early stages; often diagnosed accidentally; symptoms of biliary colic or chronic cholecystitis.
Advanced disease: non-specific (weight loss, nausea, weakness, fatigue), abdominal mass, RUQ or epigastric pain, Courvoisier
sign (enlarged, non-tender gallbladder and painless jaundice).
Diagnosis: Lab: liver function test may show increased levels; possible elevated levels indicating cholestasis (ALP, GGT, total
bilirubin) Tumor markers: increased AFP, increased CA19-9 and CEA.
Imaging: USG; MRCP (for definitive diagnosis), endoscopic USG, chest CT for staging.
Magnetic resonance cholangiopancreatography

X
Biopsy is unnecessary in gallbladder cancer – immediate surgical exploration.
Treatment: Cholecystectomy and resection of hepatic segments IVb and V, lymphadenectomy, with or
without bile duct excision.
Contraindications for surgery: distant metastases, spread to adjacent organs, involvement of hepatic artery or vein,
retropancreatic/paraceliac or porta hepatis node involvement, jaundice.
Unresectable: palliative chemo, biliary stenting.

-
20. Mechanical jaundice

Def: Also called obstructive or post-hepatic icterus. Bilirubin deposition most commonly occurs in the skin and sclerae. It results
from elevated bilirubin, starting at levels > 2mg/dL (34µmol/L).
Causes: Biliary tract disorders: choledocholithiasis, cholangitis, postoperative bile leaks or biliary strictures, malformations of
bile ducts or mirizzi syndrome.
Tumors: Pancreatic, cholangocellular, hepatic, intrahepatic metastases, gallbladder Inflammatory: primary sclerosing cholangitis,
primary biliary cholangitis, acute and chronic pancreatitis Infectious diseases: Liver flukes, Weil disease, Yellow fever
Clinical: jaundice, pale, clay-colored stool, darkening urine, pruritis, fat malabsorption, pain
Diagnosis: Liver parameters: increased ALP,GGT, bilirubin, transaminases (ALT,AST), hepatitis, albumin
levels, inflammatory markers – normal indirect bilirubin, high direct bilirubin , decreased
urinary urobilinogen. USG: extrahepatic obstruction (dilated common bile duct – double duct sign)
Treatment: manage underlying condition – surgical excision of obstruction, cholecystectomy if stones.
 the
~
Between 3
types
T
21. Differential diagnosis of jaundice

Def: Jaundice is the yellow discolouration of the skin, mucous membrane and sclera due to ↑ (50µmol/L (3mg/dL) levels of
bilirubin in the blood.
Classification: Prehepatic, hepatocellular, Posthepatic
1) Prehepatic: Hemolytic jaundice (excessive extrahepatic formation of bilirubin due to increased break-down of RBC).
Causes: Hemolytic anemia, sickle cell anemia. Pathogenesis: bilirubin is unconjugated and not water soluble. Cant be
excreted in urine. Mild: 70-100 µmol/L. Clinical: Dark feces because of unconjugated hyperbilirubinemia.
2) Hepatocellular jaundice: from damaged hepatocytes. Pathogenesis: Hemochromatosis, amyloidosis, Wilson’s disease,
viral hepatitis, drug-induced (rifampicin), cirrhosis.
3) Posthepatic jaundice: impaired bile flow due to large obstruction. Causes: common bile duct stones, biliary strictures.

⑧ Cholestatic jaundice: Common bile duct stone, cholangitis, hepatitis A (cholestatic type), EBV/CMV hepatitis, primary biliary
cirrhosis, sickle cell disease, periampullary cancer (pancreatic, cholangiocarcinoma), AID cholangiopathy, parasites.

⑧ Isolated jaundice: hereditary spherocytosis, hematoma, immune hemolysis, thalassemia, G6PD deficiency.

D Other: postoperative, drugs (niacin, acetaminophen), excessive ingestion of beta-carotene (squash, carrot, melon – doesn’t
cause scleral jaundice).
Diagnosis: Phys: Hepato/splenomegaly, ascites. Viral markers: Hep A/B/C. US: tumor, stones, size of ducts. CT/Biopsy.

· Gilbert Syndrome:
People with the syndrome have a faulty gene which causes the liver to have problems removing bilirubin from the blood.

In Gilbert’s syndrome, the faulty gene means that bilirubin isn't passed into bile (a fluid produced by the liver to help with digestion) at
the normal rate. Instead, it builds up in the bloodstream, giving the skin and white of the eyes a yellowish tinge.

⑥C

22. Acute pancreatitis

Def: Inflamt of pancreas by prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion.
Etiology: associated with biliary stones or ethanol abuse – 10-15% idiopathic
Clinical:
- Abdomen: Severe pain radiating to the back, Tenderness, Guarding. Ascites.
- Dyspnea, signs of shock (tachy, hypot, oliguria)
- Skin changes (rare): Cullens sign (discoloration of umbilicus)
Diagnosis:
Blood test: serum amylase/lipase up 3x normal value, WBC, kidney/liver function/enzymes.
CT/US: Gallstones or assess extent of inflm.
MRI: Abnormalities of duct, bladder, pancreas.
Treatment: 80% of episodes are mild & self-limiting (3-5 days)
Moderate/severe signs must be monitored closely (to detect complications); IV fluids, ATBs (can cause candida superinfection)
Surgical: patients w/ necrosis: necrosectomy is gold standard - removal of necrotic tissue & pancreatic ascite.
Complications: pancreatic necrosis, abscesses, pseudocysts, renal failure, Sepsis, Shock, DIC.
23. Chronic pancreatitis

Caused by progressive inflm and irreversible damage to structure/function (endo/exocrine) of the pancreas.
Risk factors: alcohol abuse (MC=70%), Idopathic (20%), ductal obstruction, hereditary.
Clinical: Persistent epigastric abd pain (radiates to back, ↑ after meal + nau/vom), steatorrhea (malabsorption of fats), diabetes.
Diagnosis: Secretin test: measures levels of pancreatic enzyme; serum amylase/lipase↑; fecal elastase measurement in stool.
Imaging: Abdominal CT(best), USG, EUS, MRI, ERCP –X-ray (calcification).
Look after duct abnormalities (obstruction, calcification, dilation/narrowing, enlargement)
Treatment:
General: alcohol abstinence, small/regular meals (↓fat, ↑carbs), Insulin therapy (if endocrine insuff.), fat-vitamin (ADEK) if
required.
Pain: NSAIDS, Opioids (severe pain). Celiac plexus block: pain relief by injection to block nerve.
Surgical
- 80% Resection: Remove the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and
bile duct.
- 20% Ductal drainage: Lateral pancreaticoje-junostomy, incision of abdomen from the lower breastbone to the belly
button. Pancreas exposed, main pancreatic duct is opened from the head to the tail of the pancreas.
Complication: Splenic vein thrombosis, Pancreatic Ascites/abscess/cancer/pseudocysts.

2.
24. Pancreatic tumors – surgical treatment

Def: Asympt in early stage, then presents with belt-like epigastric pain (radiates to back).
- 95% is ductal adenocarcinoma (located in pancreatic head). Epid: Extremely poor prognosis, >60+.
RF: Smoking, alcohol, chronic pancreatitis.
Clinical: belt-like abd pain (radiate to back), big gallbladder + jaundice, pale stools+dark urine, pruritis, ↓appetite/weight, clots.
Diagnosis: Phys ex: Jaundice (skin, tounge, eyes) & Abd palpation (ascites). Blood test: ↑ Lipase, CA19-9 (tumor marker).
Imaging: Abd CT (ducts). Endosc-US - (location/size). Needle biopsy/excision, Staging by CT. Cancer antigen = <A

Treatment: 20% have localized disease and therefore suitable for Surgery.
(most commonà Whipple: pancreaticoduodenectomy)
1) Pancreatic head carcinoma=Whipple, resect pancreatic head + duodenum + gallbladder + bile duct. Remaining organs are
reattached to allow digesion of food.
Food bypass: stomach-jejunum (gastrojejunostomy) + drain bile: loop of jejunum to cystic duct (cholecystoje- junostomy).
2) Distal pancreatectomy - resection of tail of pancreas.
3) Adjuvant chemotherapy (gemcitabine) should be offered.
4) In inoperable patients with lots of pain: celiac plexus block (no more pain transmission), palliative chemotherapy.
 Both cysts and pseudocysts are collections of fluid.
A true cyst is a closed structure. It has a lining of cells that separates it from the nearby tissue.
A pseudocyst isn't closed and doesn't have a lining of epithelial cells separating it from the nearby tissue. #

25. Pancreatic cysts and pseudocysts

is
cyst
Cyst

·
Complicationretreatito types #docyst

Pancreatic cyst: Pancreatic cysts are saclike pockets of fluid on/in pancreas. Epith, lining
↓ Retention
situat
Clinical features: Abd/back pain, nau/vom, weight loss, Jaundice Neoplast
↓
Jermoid
Diagnosis: CT scan — hyperdense mass. Cancer: hypodense.
Real cyst: decreased amylase, may contain mucin, high levels of tumor markers (CEA, CA-15-3), epithelial cells. Treatment:
Asymp — no surgical treatment.
Symptomatic — CT-guided, endoscopic or surgical drainage.

Pancreatic pseudocyst: Pseudocyst are collections of leaked pancreatic fluid, develops after acute/traumatic attack of pancreas.
Clinical: Often asympt. Painless abd mass. Pressure effects: Gastric/distal duodenum; obstruction, Steatorrhea.
Diagnosis: CT—> appears as a fluid filled mass. Needle aspiration. Transabdominal USG.
Pseudocyst: often adherent to surrounding structures, histo: inflammatory cells.
Treatment: 3 drainage methods: Endoscopic drainage. Percutaneous catheter. Open surgery.
Complications: Obstruction. Haemorrhage. Rupture. Infection.

Goal is to create pathway from pseudocyst to stomach or small bowel.

Pseudocytogastrostomy (cyst in lesser sac) or pseudocystojejunostomy (large cysts).

26. Gastroduodenal peptic ulcer – indications for surgery

Peptic ulcers result from corrosive action of acidic gastric juice on the vulnerable epithelium and can occur in the esophagus,
stomach and duodenum (also ileum or jejunum)
Clinical: Pain (most common), bleeding, perforation, obstruction due to inflammatory swelling, scaring Duodenal: most common
20-45 years old - men > women – 95% in duodenal bulb
Clinical: epigastric pain (relieved by food, antacids), tenderness, normal or increased gastric acid production, possibly H. pylori
infection positive
Diagnosis: Endoscopy; Diagnostic testing: gastric acid production by unstimulated stomach (BAO) and during stimulation with
histamine or pentagastrin (MAO)
Radiography: upper gastrointestinal series (inflammatory changes, deformities, niche)
Differential: chronic cholecystitis , chronic pancreatitis
Treatment: acid suppression, H. pylori eradication – surgical treatment if complications arise (bleeding, perforation, obstruction)
– PPI + H2 receptor agonist (ranitidine),
Gastric: peak is 40-60 years – 95% on lesser curvature
Clinical: epigastric pain relieved by food and antacids (same as duodenal), pain appears earlier after eating (often within 3o
minutes), vomiting, anorexia
Diagnosis: gastroscopy and biopsy (preferably 6 specimens from edge of lesion) Imaging: upper GIT X-ray can show ulcer –
meniscus sign (rim of translucency around ulcer)
Differential: uncomplicated hiatal hernia, atrophic gastritis, chornic cholecystitis, irritable colon Syndrome
Treatment: same as duodenal – eradication of H. pylori
Treat: Angioembl
Indication: if failed endoscopic therapy, continuous bleeding, haemodynamic instability despite volume resuscitation.
27. Perforated gastroduodenal ulcer

Most perforated peptic ulcers are on anterior - Death risk 15% - increased with increasing age, female, and gastric perforation –
5% of patients with perforation are overlooked.
Anterior ulcers tend to perforate instead of bleed due to absent protective viscera Shortly after perforation contents reach
cavity causing chemical peritonitis.
Etiology: NSAIDS, Corticost, smoking, acidic food.
Clinical: shallow breathing (-Escaped air from stomachàabdominal distention à tympanic percussion - Decreased bowel
sounds). Initial reaction is chemical peritonitis where the patient symptoms may improve -> progresses to bacterial peritonitis.
Doctors shouldn’t misjudge this improvement.
Diagnosis
- Clinical: sudden/severe pain+rigid abd + tachycardia (even slight movement), tenderness, ↓ bowel sounds. Shallow
breathing.
- History: NSAIDS, pain before/after meal, acidic food, smoking, alcohol, H-Pylori infection.
- Lab: early stages: Mild ↑ serum amylase. Mild leukocytosis – 12.000/L.
After 24 hours: leukocytosis – 20.000/L.
- Imaging: CT (contrast)- Abdomen. Endoscopy. US (if radiation is contraind). X-ray show free air under the diaphragm.
Differential: acute pancreatitis/cholecystitis + perforated gallbladder; acute appendicitis, diverticulitis.
Treatment: Nasogastric tube to empty contents; IV ATBs (cefazolin); laparoscopy/laparotomy – closure of perforation by usage
of omentum (Graham-Steele closure), lavage. Gastric lavage involves placing a tube through the mouth (orogastric) or through

o solutions into the stomach, followed by suction of gastric contents.

the nose (nasogastric) into the stomach. Toxicants are removed by flushing saline

Surgical management:
- Laparoscopy/laparotomy and suture closure of the perforation + followed by intra-abdominal lavage and aspiration.
- Haemorrhage and perforation together cannot be treated by suture alone; vagotomy plus gastroenterostomy or
pyloroplasty should be performed.
I
&
1
-

28. Ulcerogenous pylorostenosis can(Pyloric sphincterins

In pyloric stenosis, the pylorus muscles thicken, blocking food from entering the baby's small intestine.
Gastric Outlet Obstruction (GOO)– due to cycle of inflam & repair – scarring, muscle spasm, edema – more common in duodenal
ulcers.

Etiology: Peptic ulcer, malignancy most common, acute/chronic peptic ulcer disease.
- Acute peptic ulcer disease — inflammation and oedema — GOO
- Chronic peptic ulcer disease — scarring and fibrosis — GOO

Clinical: history of peptic ulcer, increasing pains of weeks or months, anorexia, vomiting, failure of antacids, weight loss,
dehydration, malnutrition, upper GI tenderness

Laboratory: 25% have anemia, metabolic alkalosis with dehydration (due to vomiting), hypochloremia, hyponatremia,
hypokalemia, increase bicarbonate.
Imaging: X-ray may show larger gastric fluid level; endoscopy (rule out neoplasm)
Treatment: emptying stomach, lavaged until clear, tube for some days to allow edema/spasm to subside. PPI. Parenteral
nutrition.
I washing out an organ (such as the stomach or colon), a body cavity, or a wound by flushing it with a fluid.

Surgical treatment if no result after 5-7 days of gastric aspiration- then do vagotomy, gastrojejunostomy.
29. Congenital pylorostenosis

Infantile Hypertrophic pyloric stenosis - HPS is MC cause of gastric outlet obstruction in infants.
Characterized by hypertrophy & hyperplasia of the pyloric sphincter during first 3-6w of birth.
–near complete obstruction.

Epid: 1 in 300 living infants – MC cause of vomiting in infancy.

Etiology: Genetic, Macrolide ATB, nicotine during pregnancy.
Clinical: Frequent regurgitation, forceful vomiting in young infants. Dehydration, depletion of potassium and chloride.
Diagnosis: palpation of typical “olive” in right upper quadrant – + USG. Endoscopy.
Treatment: not surgical emergency, fluid resuscitation and correction of electrolyte abnormalities
General anesthesia – Fredet-Ramstedt extra mucosal pyloromyotomy.

30. Complications of gastroduodenal ulcer – surgical treatment – procedures on gastroduodenum

+ Perforation (question 27)

Hemorrhage - 20% of patients experience bleeding episode - MC cause of massive upper GI bleed. Posterior bleeding more
often than anterior. Bleeding is more severe in duodenal ulcers on posterior wall ( massive bleeding -> erosion of
gastroduodenal artery). Perforated gastric ulcers of the lesser curvature may cause hemorrhage of the left gastric artery.
Clinical: bleeding, hematemesis, shock, or chronic anemia, weakness are only findings
Diagnosis: endoscopy
Treatment: administration of epinephrine or ethanol into the ulcer, electro cauterization (all
endoscopic) – emergency surgery (laparotomy – suture ligation of the vessel).
Obstruction – due to cycle of inflammation and repair – scarring, muscle spasm, edema – more common
in duodenal ulcers.
Clinical: history of peptic ulcer, increasing pains of weeks or months, anorexia, vomiting, failure of antacids, weight loss,
dehydration, malnutrition, upper GI tenderness.
Laboratory: 25% have anemia, metabolic alkalosis with dehydration (due to vomiting), hypochloremia, hyponatremia,
hypokalemia, increase bicarbonate.
Imaging: X-ray may show larger gastric fluid level; endoscopy (rule out neoplasm)
Treatment: emptying stomach, lavaged until clear, tube for several days to allow swelling to subside.
Surgical treatment if no result after 5-7 days - vagotomy, gastrojejunostomy.
Gastric/duodenal perforation — secondary peritonitis. Duodenal ulcers of ant. wall=perforate into abd cavity
àpneumoperitoneum & irritation of phrenic n. shoulder pain).
presence of air or gas in the abdominal (peritoneal) cavity.

Fistula formation
Malignant transformation: -Gastric ulcers – high malignant potential. -Duodenal ulcers, usually benign.
Surgical procedures on gastro-duodenum:
1) Peptic ulcer — surgical treatment: The surgical procedures that can cure peptic ulcer are aimed at reduction of gastric acid
secretion or by reducing gastrin section. Methods= vagotomy and antretomy plus vagotomy.
a. Vagotomy — consists of resection of 1 or 2 cm of each vagal trunk as it enters the abdomen on the distal
oesophagus — vagal denervation results in delayed emptying of the stomach. Drainage procedure may also be
performed (pyloroplasty (Heineke-Mikulicz procedure) as well as parietal cell vagotomy or proximal gastric
vagotomy.
b. Antrectomy — distal gastrectomy of 50% of stomach. According Billroth 1 resection (proximal remnant may be
reanastomosed to the duodenum) or Billroth 2 resection (to the side of the proximal jejunum. Preferred
reconstruction is Roux-en-Y gastrojejunostomy. Another surgical procedure is partial gastrectomy (Billroth)
2) Perforated ulcer: Laparoscopy/laparotomy & suture closure of perforation. Done via a Graham Steele closure using
omentum sutured into place rather than sutured apposition closure of the defect. Followed by intra-abdominal lavage &
aspiration.
31. Gastric cancer

Epidemiology – more men, 70y.

Pathology: 95% Adenocarcinomas from mucus-producing cells of gastric mucosa (early metastasis) 5% GIST, gastric lymphoma,
carcinoid, squamous cell carcinoma
Risk factors: diet – high salt, smoked foods, low fresh fruit/ vegetables; smoking, alcohol – male gender, low
socioeconomic levels, occupation (rubber workers, miners), EBV, H. pylori, atrophic gastritis
Clinical: often non-specific – abdominal pain, weight loss, anemia (chronic blood loss), dysphagia, nausea,
vomiting, gastric outlet obstruction – advanced: signs of metastasis, palpable mass
Diagnosis: history, physical exam, laboratory, CT, USG, esophagogastroduodenoscopy with biopsy
Treatment
Surgical: in absence of disseminated disease: radical surgical approach – gastrectomy, lymph node resection.
Endoscopic mucosal resection – for early cancers.
Lymphadenectomy – according to the staging of the cancer.
Reconstruction – Roux-en-Y esophagojejunostomy (gastric bypass), pouch construction, jejunal interposition.

32. Peritonitis – classification, symptoms, most common causes

1) Spontaneous bacterial peritonitis - infection of ascitic fluid in the absence of any focal intraabdominal, surgically
treatable source of infection – liver disease, kidney disease.
2) Secondary bacterial peritonitis - inflammation of peritoneum due to bacterial infection from a surgically treatable
intraabdominal source (perforation, complications).
Etiology: Spontaneous most often in patients with ascites and cirrhosis; additional risk factors are upper
GI bleeding, prior SBP usually monomicrobial in Spontaneous peritonitis; multimicrobial in Secondary – most common by E. coli
and Klebsiella (gram -), also gram + Strep, Staph., Enterococcus.
Medical: ruptured appendix, stomach ulcer or perforated colon; pancreatitis, diverticulitis, Trauma, peritoneal dialysis,
complication of surgery (anastomosis insufficiency).
Symptoms: Diffuse abdominal tenderness, fever and chills, worsening of ascites, new-onset or worsening
encephalopathy, nausea, vomiting, constipation, diarrhea, abdominal pain, bloating or fullness, loss of appetite, low urine
output, confusion.
33. Peritonitis – diagnosis and treatment

Diagnosis: spontaneous: Ascites fluid >250/mm3 neutrophils with or without positive ascites fluid bacterial.
Culture in absence of other intraabdominal infection source.
Laboratory: Blood culture, inflammatory markers (CRP, ESR) may be elevated, CBC (potential leukocytosis), Liver can show signs
of cirrhosis, metabolite panel to rule out kidney and hepatorenal injuries or hyponatremia; coagulation panel.
Imaging: X-ray to check for perforations and free air, also USG, CT can replace X-ray
Paracentesis: sample of fluid can be cultured
Treatment: Spontaneous: can be life-threatening
ATBs: type and duration depend on the severity and agent causing the peritonitis
Cephalosporins, pip-Taz (if low prevalence of multidrug-resistant pathogens)
Surgery: remove infected tissue, treat underlying cause and prevent spreading
Other: pain medication, fluids, oxygen.

34. Special types of peritonitis

Localized: Sterile abdominal surgery causes localized peritonitis, which may leave behind a foreign body reaction and fibrotic
adhesions.
Symptoms: localized tenderness, guarding, positive sign of peritoneal irritation (Blumberg’s, Plenie’s and Rowsing’s sign). May
progress into abscess or diffuse peritonitis
Treatment: conservative (ATBs), surgery if there is abscess.

Diffuse peritonitis: Defined as generalized infection of the peritoneum and abdominal cavity.
Signs/Symptoms: seriously/rapidly ill. Hypovolaemia, toxaemia , if infection is present, systemic sepsis.
Abdomen is rigid and tender and bowel sounds are absent

Infectious peritonitis
- Perforation of GIT: stomach (peptic ulcer, gastric carcinoma), duodenum (peptic ulcer), intestine (appendicitis),
gallbladder (cholecystitis).
- Disruption of the peritoneum: trauma, surgical wound.
- Spontaneous bacterial peritonitis: in patients with ascites.
o Ascites can be caused by NS, CHF, most commonly chronic liver disease!
o Caused by aerobic intestinal flora (usually monobacterial) – E. coli, Klebsi- ella, Strep pneumoniae, Staph
- Intra-peritoneal dialysis (due to [Link])– Tx / cephalosporins(cephalexin)
- Systemic infections (tuberculosis) :rarely

Non-infectious peritonitis:
Leakage of sterile body fluids into - peritoneum (chemical peritonitis): blood (endometriosis), gastric juice (peptic ulcer), bile
(liver biopsy).
35. Acute abdomen – ileus

Acute abdomen: sudden, severe abdominal pain that requires hospitalization and immediate medical intervention. Etiology:
acute appendicitis/peritonitis/pancreatitis, peptic ulcer perforation, intestinal obstruction, infection. Ectopic rupt.
Pain can be:
- Constant (inflam.) - Colic pain (obstruction) - back pain (acute pancreatitis, ulcer perforation, aortic rupture).
- Gradual onset (appendicitis) - Sudden onset (perforate ulcer, acute pancreatitis & rupture of ectopic pregn).
Other symptoms: constipation, vomiting, changes in urinary frequency.

Diagnosis
Physical ex: scars, distensions, masses, Cullen’s sign, blunt trauma. Guarding. Spasm.
Palpation
- Blumberg’s sign (pain after releasing pressure),
- McBurney’s sign (deep pain after pressure, in appendicitis),
- Murphey’s sign (palpation of gallbladder makes patient unable to breathe, in cholecystitis),
- Rovsing’s sign (pressure on lower left quadrant increases pain in the LRQ, in appendicitis),
Auscultation: ↑sounds=fluid obstruction or absent sounds due to Ileus/Ischemia/peritonitis.
Vaginal & Rectal examination.
CBC= increase WBC in inflammations, increased CRP, ESR and serum electrolytes in inflammations, or increased serum amylase,
bilirubin, aminotransferases and ALP in acute cholecystitis for example.
Imaging: Abd X-rays=air under diaphragm. USG=cholang/cholecyst/appendicitis.
CT/Laparoscopy investigation.

Treatment: Resuscitation. Symptom control: I.V / I.M opiate analgesics. Antiemetic tx. NG tube if vomiting.
Nonsurgical: I.V gentamicin, amoxycillin (suspected perforated peptic ulcer, mesenteric ischemia).
Surgical: appendicitis - appendicectomy, ureteric colic - analgesia & initial observation, acute peritonitis – peritoneal lavage,
intestinal obstruction – laparotomy, bowel resection if necrosis.

Ileus: lack of movements in intestines leading to build-up and blockage of contents.

Mechanical (dynamic): peristalsis is working against obstruction.
Subtypes
- Obstructive (WITHOUT blood vessels obstruction): Intramural/intraluminal/extramural.
- Strangulation (WITH obstruction): adhesive/incarcerated/invaginate/volvulus due to adhesions, hernia.
Treatment: urgent operation, avoid perforation of bowel!

36. Mechanical and paralytic ileus

Ileus: lack of movements in intestines leading to build-up and blockage of contents.

Mechanical (dynamic): peristalsis is working against obstruction. Subtypes:
- Obstructive (WITHOUT blood vessels obstruction): Intramural/intraluminal/extramural.
- Strangulation (WITH obstruction): adhesive/incarcerated/invaginate/volvulus due to adhesions, hernia, calculus, internal
hernia (diaphragm).
Treatment: urgent operation, avoid perforation of bowel!

Paralytic (adynamic): peristalsis is absent or inadequate, obstruction is absent.

Etiology: recent surgery, hypokalemia, mesenteric ischemia due to embolism/trombosis, long time
mechanical ileus, breackdown coordination btw symp & parasymp. Ogilvie syndrome: acute
pseudoobstruction & dilation of colon.
Clinical presentation: Abdominal bloating, nausea, vomiting, severe constipation, loss of appetite & cramps.
DG: Few / Absent bowel sounds - "peristalsis". X-ray of abd (bulging loops of intestine & air /fluid levels). CT.
Treatment: absolute diet, enteral feeding tube I.V Fluids & electrolytes (sodium, chloride & potassium).

Surgical: exploratory laparotomy – management of etiology – adhesiolysis, hernia reduction, tumor resection; resection of
gangrenous bowel conservative: bowel rest, IV fluids, electrolyte, parenteral analgesics, parenteral antiemetic, nasogastric tube
(bowel decompression – if persistent vomiting, significant GI distension, complete obstruction, volvulus); stool evacuation
(sometimes enough for simple obstructions).
37. Strangulative ileus

Def: defined by the obstruction of both lumen of GIT and principal feeding vessels. Its associated with ischemia of the intestines
that cause necrosis and possible perforation/ peritonitis if untreated – Gangrene can develop in as few as 6 hours.

Subclassified as:
- Strangulation by bands (fixed Meckel’s diverticulum, omental band)
- Volvulus (rotation of stomach or some part of bowel around its axis)
- Intussusception (one segment of intestine "telescopes" inside of another— mc are ileocolic.
- Strangulated hernia
Clinical: sudden symptoms, pain, vomiting, shock. Necrosis of strangulated tissue. Signs of irritation of peritoneum.
Diagnosis: Depend on location and stage of disease. CT angiography useful for making early diagnosis. Xray or USG of abdomen.
Treatment: If detected before necrosis is present – simple releasing of strangulation is enough.
Otherwise: Remove adhesions, de-rotation of volvulus, fixation of intussusception, repair hernias, if necrotic bowel→ resect and
anastomose!

38. Vascular ileus – mesenteric thrombosis, abdominal angina

Thrombosis: arterial: atherosclerosis, arteritis, AA or dissection- Venous: uncommon; infection, malignancy

- both cause intestinal hypoxia (acute) – infarction and necrosis of small bowel.
Most common vessel are superior and inferior mesenteric and celiac artery.
Clinical: pain, nausea, vomiting, diarrhea (can become bloody), rectal bleeding, sepsis, hypotension – arterial more severe
(embolism is most severe).
Diagnosis: increased lactate, increased LDH, increased creatine kinase; leukocytosis, metabolic acidosis; imaging: CT angiography
(confirmatory); MR angiography, USG doppler.
Treatment: nasogastric tube, IV fluids, ATBs. Emergency exploratory laparotomy: mesenteric artery bypass and resection of
necrotic bowel; endovascular revascularization: balloon angioplasty and stenting can be done in stable patients.
[Link]. Arteries
Abdominal angina: chronic ischemia – slowly progressing stenosis of two or more main arteries (SMA and IMA are most
common, celiac artery).
Etiology: atherosclerosis – hypertension, diet, smoking, DM, increased cholesterol
Clinical: often asymptomatic - postprandial abdominal pain within 1 hour of eating; can cause fear
of eating (weight loss), bloating, nausea, abdominal bruit (turbulent flow)
Diagnosis: nonspecific labs; USG-doppler – CT (identifies atherosclerotic disease) – CT-angiography
(stenosis of 2 or more main vessels)
Treatment: nutritional changes, anticoagulation, angioplasty and stenting or bypass grafting.
39. Upper GI-tract bleeding

Upper GI bleeding accounts for 70-80% of GI bleeding – bleeding proximal to ligament of Treitz (suspensory
muscle of duodenum).
Etiology: peptic ulcer disease, esophagitis, erosive gastritis, esophageal varices, gastric antral vascular ectasia, Angiodysplasia,
esophageal cancer, gastric carcinoma, hiatal hernia, Mallory-Weiss syndrome, Boerhaave syndrome, after endoscopic surgery,
portal hypertensive gastropathy, coagulopathies.
Symptoms: Anemia due to chronic blood loss, acute hemorrhage can show shock symptoms (tachycardia, hypotension, altered
mental status), Hematemesis (coffee-ground or red), Melena.
Diagnosis: symptoms are indicative – first line is EGD, if negative do colonoscopy.
If the colonoscopy is negative – bleeding from small bowel should be ruled out.
If unstable patient with negative EGD do angiography.
Laboratory studies: Hb, Hct, platelet count, coagulation panel, blood type and cross match.
Treatment: Endoscopic hemostasis – indicated in active bleeding – can be done by injection (diluted epinephrine), cauterization
(electro, heat), mechanical therapy (band ligation or clips), polypectomy if there is bleeding polyp, Interventional radiology
(angiography) – ongoing GI bleed and hemodynamic instability, Angioembolization, intraatrial vasopressin. Surgery: if
therapeutic options have failed, unstable patients with ongoing bleeding. Exploratory laparotomy and surgical hemostasis.

40. Lower GI-tract bleeding

Lower GI bleeding accounts for 20-30% of all GI bleeding and is distal to ligament of Treitz (usually in colon)
Etiology: Diverticulosis, IBD, invasive or inflammatory diarrhea, hemorrhoids, ischemia, arteriovenous malformation, rectal
varices, angiodysplasia, colorectal cancer, colonic polyps, lower abdominal trauma, anorectal trauma, anal fissures
Symptoms: Anemia due to chronic blood loss, acute hemorrhage can show shock symptoms (tachycardia, hypotension, altered
mental status), Hematochezia – bright red blood with or without stool – colonic bleeding (jelly-like, maroon) Melena can also
occur when there is small bowel or right colon bleeding.
Diagnosis: symptoms are indicative – first line is colonoscopy after bowel preparation, if its negative do EGD. If both negative
esophagogastroduodenoscopy

rule out small bowel bleeding.

Laboratory studies: Hb, Hct, platelet count, coagulation panel, blood type and cross match
Treatment: Endoscopic hemostasis – indicated in active bleeding – can be done by injection (diluted epinephrine), cauterization
(electro, heat), mechanical therapy (band ligation or clips), polypectomy if there is bleeding polyp Interventional radiology
(angiography) – ongoing GI bleed and hemodynamic instability, Angioembolization, intraatrial vasopressin
Surgery: if therapeutic options have failed, unstable patients with ongoing bleeding
Exploratory laparotomy and surgical hemostasis.
41. Injuries and caustic damage of the esophagus

Causes: due to objects (endoscope or swallowed foreign objects) or stabbing injuries from thorax traumas or by burns w/ acid or
dye. Rarely due to Boerhaave syndrome (violent vomiting after extensive eating cause perforation).
Symptoms: chest pain, upper abdominal/ back pain, vomiting blood, swallowing disturbances, shortness of
breath, fever. Cyanosis, subcutaneous emphysema in the neck region, pneumothorax, pleural effusion
depending on type of injury.
Diagnosis: Chest X-ray: air or fluid in pleural cavity and mediastinal emphysema – Contrast-Swallow
Treatment: small injuries treated conservatively (no oral intake allowed) with IV ATBs.
If due to acid or dye: esophageal/stomach flushing, steroids prevent excessive swelling of mucus membranes.
Large injuries: surgical – if perforation with leakage of acid into abdominal cavity = acute Abdomen
If inflammation to high, temporary feeding tube, surgery after 3-6 months.

42. Esophageal diverticula and strictures

Are located either above the upper esophageal or lower esophageal sphincter – due to abnormalities in resting pressure,
relaxation in response to swallowing and coordination w/ the segment above the sphincter.
Esophageal diverticulum – Zenker diverticulum
Etiology: more common in men, >60 years old, originates in posterior wall of esophagus (killian triangle)
Symptoms: dysphagia, regurgitation of undigested food (Aspiration risk),Halitosis, 30% have associated GERD
Diagnosis: barium swallow (position and size of diverticulum), esophageal manometry (lack of + coordination, hypertensive UES,
hypotensive LES)
Treatment: excision of the diverticulum and myotomy of the cricopharyngeus muscle and the upper 3cm of the posterior
esophageal wall; for small diverticula (<2cm) only myotomy
Epiphrenic diverticulum
Cause: due to underlying motility disorders (achalasia most common), causes an outflow obstruction at the level of the
gastroesophageal junction. Symptoms: dysphagia, regurgitation, can be asymptomatic
Diagnosis: barium swallow, esophageal manometry – located just above diaphragm, Chest X-ray: air-fluid level in the posterior
mediastinum
Treatment: surgical: laparoscopic preferred – resection of the diverticulum, long myotomy on the side opposite to where the
diverticulum is located; partial fundoplication to prevent GERD
Midesophageal diverticulum - commonly 5cm above or below the level of the carnia
Causes: previously due to TBC, histoplasmosis, mediastinal granulomatous diseases
Symptoms: usually asymptomatic because their small
Treatment: no surgical treatment necessary
 With Barium

43. Achalasia

Primary esophageal motility disorder – unknown cause men > women

Symptoms: dysphagia for solids and liquids common, regurgitation of undigested food, heartburn (40%) due
to stasis and fermentation of food not reflux; chestpain. hypertensive lower esophageal sphincter (LES)

Diagnosis: barium swallow X-ray: distal esophageal narrowing, absence of esophageal peristalsis, hypertensive LES; endoscopy
to rule out tumor of gastroesophageal junction. Esophageal manometry is key test for diagnosis: absence of peristalsis,
hypertensive LES that only partially relaxes when swallowing occurs.
Differential: GERD, esophageal carcinoma
Treatment: Calcium-channel blockers: to decrease pressure of LES (10% benefit)
Endoscopic injection of botulinum toxin at level of LES (not all benefit, reoccurrence)
Pneumatic dilatation: balloon inflated at level of GE-junction to rupture the muscle fibers
Surgical: laparoscopic Heller myotomy and partial fundoplication – myotomy of lower 6 cm of muscles of esophagus and upper
2cm of stomach + partial fundoplication.

44. GERD – pathology and surgical treatment

Chronic syndrome caused by an abnormal retrograde flow of gastric contents into the esophagus resulting in mucosal damage.
Etiology: defective LES, Hiatal hernia, obesity, pregnancy. Cirrhosis and increased levels of [Link].
Symptoms: heartburn, belching, oversalivation, odynophagia, regurgitation. It is relieved by antacids and made worse by lying
down. Can also cause atypical sy: cough, chest pain, hoarseness and dental erosions.
Complications: Barret’s esophagus (pre-cancerous), esophagitis, nocturnal asthma, chronic cough, laryngitis, esophageal
stricture, adenocarcinoma.
Dx: trial therapy, if required – endoscopy or pH monitoring; barium swallow is useful to detect a possible hiatal hernia;
esophageal manometry.
Tx: Lifestyle changes – quit alcohol and smoke, weight loss diet, avoid spicy foods, fatty foods and chocolate. Medical – antacids,
H2-blockers (ranitidine), PPI.
Surgical – if persistent symptoms, respiratory complications, vocal cord damage or Barret’s esophagus – partial or total
fundoplication, gastroplasty.
45. Crohn´s disease and surgical treatment

A type of inflammatory bowel disease (IBD) may affect any part of GIT but mainly ileus + ascending colon.
Chronic inflammatory disorder, the immune system attacks the GIT tract.
Etiology: interaction between environmental, immunological & bacterial factors in a genetically susceptible individual.
Clinical presentation:
- Constitutional – N/V, malaise, lethargy, low fever
- Major sy – diarrhea, abdominal pain, weight loss
- Can lead to malabsorption, bloody diarrhea, sideropenic anemia
- Extra-GI sy – arthropathy, uveitis, erythema nodosum, liver disease, venous thrombosis, nephrolithiasis
Diagnosis: Colonoscopy: Patchy distribution of lesions, “Skip lesions”. Deep, trans mural involvement. CT
with oral contrast. Sideropenic anemia; increased ESR, CRP; hypoalbuminemia
Treatment:
- Stop smoking, use loperamide for diarrhea, B12, iron supplements
- Induce remission by CS, azathioprine, and methotrexate
Corticosteroids

- In resistant px – infliximab, adalimumab, pegFab, 80% will require surgery

- Surgical – surgery is not curative, it is used to solve complications (intestinal obstruction, perforation with fistulas or
abscesses, malignant changes). Intestine sparing surgery is preferred taking as little intestine as possible (resection of
bowel).
Complication: short bowel disease.
46. Inflammatory disease of mammary gland

MASTITIS: Inflammation of the breast tissue. Etiology: S. Aureus, S. epidermis & streptococci.
Classification: milk stasis, noninfectious / infectious inflammation & abscess.
Clinical presentation: Early states present with local pain, redness, swelling & warmth. Later stages present with systemic
symptoms like fever & flu-like symptoms. In rare cases abscess may develop. Types:
- Puerperal: Inflammation of breast connected with pregnancy, breastfeeding / weaning. Though to be caused by blocked
milk ducts / milk excess. Light cases are called breast engorgement.
- Non puerperal mastitis: Inflammatory lesion of breast unrelated to pregnancy & breastfeeding. Includes mastitis as well as
various kinds of mammary abscesses.
Treatment: Frequent emptying of breast by breastfeeding is essential! Maintain adequate fluids.
Usually ATB's are not needed, only used if there is bacterial infection (dicloxacillin / cephalexin).
Complications: Recurrence, milk stasis & abscess (requires surgical drainage).

INFLAMMATORY BREAST CANCER: rare & very aggressive, in which cancer cells block lymph vessels in the skin of the breast.
Detected usually in late stages.
Clinical presentation: Quick onset of symptoms, breast often looks swollen/red, easily confused w/ mastitis. Nipple retraction /
discharge. Pain, Itching breast. Swelling of lymph nodes under the arm / neck. Consistency of breast tissue changes.
Diagnosis: Only reliable method is biopsy (cancer cells in sub dermal lymphatic on skin biopsy). MRI, mammography / USG may
show “suspicious” signs.
Staging:
- IIIA: less than one complete breast is affected.
- IIIV: Whole breast is affected, may have spread to adjacent tissues.
- IV: Metastasis (Bones, lungs, liver and / or brain).
Treatment: Chemotherapy. Radiation. Hormonal therapy. Estrogen & progesterone receptor positive, have better prognosis.
Surgery in some cases (Mastectomy / lumpectomy).

47. Diverticulosis and diverticulitis of the colon

DIVERTICULOSIS: Presence of diverticula (out pocketing of the colonic mucosa through weakness of muscle layers in the colon
wall). More common in the sigmoid colon (high pressure) & age > 40.
Symptoms: painless rectal bleeding (bright red blood).Cramps & tenderness.
1) Uncomplicated diverticulosis: Cramping, bloating, flatulence, irregular defecation. Not clear if these symptoms are due
to diverticulosis / coexisting IBS.
2) Complicated diverticulosis: Very uncommon but highly dangerous. Diverticula may bleed, become infected & develop
abscesses. A SERIOUS MEDICAL EMERGENCY!
Risk factors: Increasing age. Constipation. Low dietary fiber (controversial). Connective tissue disorders
(Marfan). Hereditary & genetic predisposition.
Diagnosis: X-ray: Thickened wall. Ileus, constipation, small bowel obstruction & free air (Pneumoperitoneum) in case of
perforation. Contrast CT is the investigation of choice. Colonoscopy. Barium enema. MRI.
Treatment: High diet fiber to prevent constipation.

DIVERTICULITIS: “Complicated diverticulosis”.

Symptoms: Triad of left lower quadrant pain, fever & leukocytosis. Also nausea / diarrhea / constipation. Less
common, right sided abdominal pain.
Differential diagnosis: colon cancer, IBD, ischemic colitis.

Treatment:
-If bacterial infection is suspected ATB's.
-Recurrent attacks / complications, such as peritonitis, abscess, fistulas are treated surgically.
-Surgical procedures, depends on severity: Resection & primary anastomosis. Resection with colostomy
(AKA Hartmann’s operation).
48. Colon cancer

Colorectal cancer is a cancer from uncontrolled cell growth in the colon / rectum / appendix. The most common type is
adenocarcinoma - 95% of cases. Other, rarer types - lymphoma & squamous cell carcinoma.
Etiology: polyps can change into cancer over time (usually many years), but not all polyps become cancer.
The 2 main types of polyps are:
- Adenomatous polyps (adenomas): These polyps sometimes change into cancer. Because of this, adenomas are called a
pre-cancerous condition.
- Hyperplastic polyps and inflammatory polyps: These polyps are more common, but in general they are not pre-cancerous.
Clinical: Depend on the location of tumor & if metastasis. Classic warning signs: worsening constipation, blood in the stool,
decrease in stool calibre, loss of appetite/weight, nausea/vomiting in someone > 50 y.o.
Risk factors: Older age, male gender, high intake of fat, alcohol / red meat, obesity, smoking & lack of physical exercise. ~ 10%
linked to insufficient activity. Inflammatory bowel disease (ulcerative colitis & Crohn's disease): prevention with aspirin & regular
colonoscopies.
Genetics: most common is hereditary nonpolyposis colorectal cancer (HNPCC / Lynch syndrome).
Other syndromes: Gardner syndrome & familial adenomatous polyposis (FAP) in which cancer almost, always occurs! APC gene
mutation almost in all colorectal cancers.
Diagnosis: biopsy (typically done during colonoscopy / sigmoidoscopy). CT for staging. PET, MRI. Colon cancer staging is done
next, based on the TNM system (size, positive lymph nodes & metastasis).
Treatment: early diagnosis, surgery may be curative. later stages (metastasis), usually treatment is palliative.
Surgery: localized cancer, the preferred treatment is complete resection with adequate margins,
attempting to achieving a cure. Done by laparotomy / laparoscopically. If there are only few
metastases in the liver / lungs they may also be removed.
Chemotherapy: used before surgery to shrink cancer. As neoadjuvant therapy. If wide metastasis palliative. (fluorouracil /
capecitabine, epidermal growth factor receptor inhibitors).
Radiation: used for rectal cancer. Neoadjuvant/adjuvant.
Palliative care: improving quality of life. Surgical removal of cancer tissue, bypassing part of the intestines / stent placement.
radiation therapy to decrease tumor size as well as pain medications.
Prognosis: Europe 5y survival < 60%.

49. Anorectal fistulas and abscesses, pilonidal sinus

Anal fistula: small tunnel that develops between the end of the bowel and the skin near the anus.
Patophysiology: Anal fistula develops from infection of anal crypts gland. The initial infection occurs in the ducts of the anal
glands and the spread of infection results in the formation of the abscess. If the abscess is ruptured, a fistula is formed. RF:
Constipation, diarrhea, IBD, immunocompromised, recent surgery/trauma.
Classification:
- Intersphincteric – 70%, usually results from perianal abscess. External opening, if present, in anal canal.
- Transsphincteric – 25%, usually arise from an ischioanal abscess.
- Suprasphincteric – 5%, results from a supralevator abscess.
- Extrasphincteric – passes from rectum above levators and to the perianal skin Rarest type.
Clinical: Recurrent perianal drainage, painful when one of the tract gets occluded. Redness/swelling/irritation in perianal area.
Diagnosis: Clinical, Bidigital rectal exam, Anoscopy. USG, CT / MRI for deeper abscesses.
Treatment: Surgical drainage of abscess. Fistulostomy- incision in skin near the anus to drain the infection.
With local/deeper anesthesia. In some cases ATB's are indicated (compromised / altered immunity)
Pilonidal cyst / abscess / sinus / sacrococcygeal fistula:
A cyst / abscess near / on the cleft of the buttocks that often contains hair & skin debris.
A sinus tract / small channel, may originate from the source of infection and open to the surface of the skin.
Material from the cyst may drain through the pilonidal sinus.
Clinical presentation: very painful, ages 15 - 35. Usually located in coccyx, may also affect the navel, armpit / genital region
(much rarer). May be asymptomatic.
Etiology: ingrown hair. Excessive sitting, trauma, excessive sweating. Anaerobic bacteria.
Treatment: ATB's, hot compresses, creams.
Surgical excision. Post-surgical wound packing replaced 2/day for 4 - 8w.
- In some cases, 2 years may be required for complete granulation to occur.
- Sometimes the cyst is resolved via surgical marsupialization.
- Surgeons may also excise the sinus and repair with a reconstructive flap technique, such as a "cleft lift" procedure
usually done under general anesthesia.
50. Hemorrhoids and anal fissure

Anal / rectal fissure is a break / tear in the skin of the anal canal.
Symptoms: bright red anal bleeding. If acute they may cause pain after defecation. May become chronic.
Etiology: MC by stretching of anal mucosa. Constipation, hard stool/prolonged diarrhea. ↓blood flow. STD. Trauma. Hygiene.

Lateral fissure: tuberculosis, occult abscesses, leukemic infiltrates, carcinoma, acquired immunodeficiency syndrome (AIDS) /
inflammatory bowel disease (IBD).
Non-healing: spasming internal anal sphincter muscle, by impaired blood supply to anal mucosa. Can lead to ulcer/infection.
Prevention: Prevent constipation: eat fiber, drink water & avoiding constipating agents. Improve anal hygiene.
Treatment: Topical nitroglycerin / calcium channel blockers / injection of botulinum toxin into the anal sphincter. Warm sits
baths, topical anesthetics, high-fiber diet & stool softeners.
Surgery: if medical theryap not helped in 1 - 3 months - lateral internal sphincterotomy(LIS): internal anal sphincter muscle is
incised. Aim to decrease sphincter spasming. It will heal in 6weeks to restore normal blood supply to the anal mucosa.

Hemorrhoids: dilated/bulging veins in the rectum, developing due to increased pressure in the rectal veins.
Clinical: Internal hemorrhoids (lie above dentate line) usually present with painless rectal bleeding while external hemorrhoids
(lie below dentate line) may produce pain / if thrombosed significant pain & swelling in the area of the anus.
Etiology: constipation, diarrhea (chronic), obesity, pregnancy, diet low in fiber, carry heavy things, anal sex.
Treatment: Initially for mild - moderate disease consists of increasing fiber intake, oral fluids to maintain
hydration, topical analgesics, proper anal hygiene, stool softener.
Surgery: Rubber band ligation (for internal hemorrhoid, cut off blood supply). Sclerotherapy (injection sclerosing agent).
Coagulation. Electrocautery. Cryotherapy. Laser therapy. Radio wave ablation.

51. Rectal cancer

Colorectal cancer is a cancer from uncontrolled cell growth in the colon / rectum / appendix.
The most common type is adenocarcinoma - 95% of cases. Other, rarer – lymphoma, squamous cell carcinom.
Etiology: polyps can change into cancer over time (usually many years), but not all polyps become cancer. The 2 main types of
polyps are:
- Adenomatous polyps (adenomas): These polyps sometimes change into cancer. Because of this, adenomas are called a
pre-cancerous condition.
- Hyperplastic polyps and inflammatory polyps: These polyps are more common, but in general they are not pre-
cancerous.
Risk factors: Older age, male gender, high intake of fat, alcohol / red meat, obesity, smoking & lack of physical exercise (10%
linked to insufficient activity). Inflammatory bowel disease (ulcerative colitis & Crohn's disease): prevention with aspirin &
regular colonoscopy. Genetics: most common is hereditary nonpolyposis colorectal cancer (HNPCC / Lynch syndrome). Other
syndromes: Gardner syndrome & familial adenomatous polyposis (FAP) in which cancer almost, always occurs! APC gene
mutation almost in all colorectal cancers.
Clinical presentation: Depend on the location of the tumor & if it metastasis. The classic warning signs: worsening constipation,
blood in the stool (hematochezia), decrease in stool calibre, loss of appetite, loss of weight, nausea / vomiting in someone > 50
years old.
Diagnosis: biopsy (typically done during colonoscopy / sigmoidoscopy). CT for staging. PET, MRI. Endorectal USG. Rectal cancer
staging is done next, based on the TNM system (size, positive lymph nodes & metastasis).
Treatment: early diagnosis, surgery may be curative. Later stages (metastasis), usually treatment is palliative.
1) Surgery
- Lower anterior rectum resection (Dixon): complete resection + 1-2 cm margin – proximal colon is prepared for
anastomosis with circular staplers – possible temporary ileostoma to permit healing of the anastomosis in cases of
preoperative chemo/radiation.
- Laparoscopic – proctectomy: actual resection still easily performed in extracorporeal manner.
- Abdominal perineal resection (Miles): removal of the distal sigmoid, rectum and anus perineum closed with suture and
permanent colostomy creation – for very low rectal tumors and tumors of anal canal.
- Hartmann procedure: primary resection with delayed anastomosis – for obstructive or perforated carcinoma – resection
of rectosigmoid, closure of rectal stump and formation of colostomy - later Hartmann reconstruction.
- Local excision of cancer: tumors that don’t penetrate muscularis.
- Transanal endoscopic microsurgery (TEM): T1 tumors
2) Adjuvant and neoadjuvant therapy: chemotherapy has shown efficacy, used before surgery to shrink rectal cancer. High
risk for reoccurrence – 5-Fluorouracil based. If wide metastasis, palliative treatment is needed to improve QoL w/ radiation
therapy and pain medications.
Prognosis: In Europe 5y survival is < 60%.
52. Stool incontinence and its surgical treatment

Fecal incontinence: involuntary loss of gas / liquid stool (called minor incontinence) / solid stool (called major incontinence). Risk
factors: elderly, dementia, physical disability (e.g. pudendal nerve injury).
Etiology: Unknown, but could be associated with…
Damage to the anal sphincters: most commonly occurs during vaginal childbirth & anal surgery. Neurologic causes: diabetes,
multiple sclerosis & spinal cord injury may decrease sensation & control over the lower digestive tract. Nerve damage during
vaginal childbirth.
Decreased distensibility of the rectum: inflammatory bowel disease (Crohn disease & ulcerative colitis) & radiation-induced
inflammation of the rectum (radiation proctitis).
Fecal impaction: When hardened feces accumulates in the rectum, this can cause the anal sphincters to relax & allow liquid
stool to escape around the blockage. A common in older adults. More likely in mental health conditions, immobility & loss of
rectal sensation.
Diarrhea: irritable bowel syndrome, active inflammatory bowel disease / acute gastroenteritis.

Diagnosis: Colonoscopy/ sigmoidoscopy / anoscopy. Anorectal manometry: measures the internal pressure in different areas of
the lower digestive tract under different conditions. Revealing poor tone of the anal sphincters. Determine if rectal sensation &
rectal reflexes are impaired. USG / MRI: of the rectum may reveal abnormalities of the anal sphincters, the rectal wall & the
pelvic muscles that help maintain continence.
Stool tests: infection.
Treatment: Surgical repair particularly in the external anal sphincter injury during childbirth/ due to surgery. Muscle transfer
from other areas of body (leg, buttock).
Synthetic anal cuff: may be inflated to hold back feces & deflated to allow bowel movements.
Colostomy: colon is surgically attached to abdominal wall. Stool is collected in a bag that fits tightly against the skin. This
eliminates leakage of stool from the rectum. Last resort, after other treatments have failed.

53. Abdominal abscesses

An intra-abdominal abscess is a pocket of infected fluid & pus located inside the abdominal cavity. There may be more than one
abscess.
Etiology: Ruptured appendix / intestinal diverticulum, inflammatory bowel disease, parasite infection (E. Coli & Entamoeba
histolytica).
Risk factors: History of appendicitis, diverticulitis, perforated ulcer / surgery that may have infected the abdominal cavity.
Clinical presentation: Abdominal pain & distention. Chills, Diarrhea, Fever, Lack of appetite, Nausea. Rectal tenderness &
fullness. Vomiting, Weakness.
Diagnosis: CBC (leukocytosis, CRP, ESR). Liver, kidney / blood chemistry problems. CT of abdomen will usually reveal an intra-
abdominal abscess. Abdominal x-ray. USG of abdomen. Sometimes laparotomy may be needed to diagnose this condition.
Treatment: I.V ATB & drainage is needed (can be performed percutaneously or surgically)
- Drainage involves placing a needle through the skin in the abscess, usually under x-ray guidance. The catheter is then left
in place for days - weeks until the abscess goes away, to allow continuous draining.
- If abscesses may not be safely drained this way, surgery must be done while the patient is under GA.
- The abscess is drained & cleaned. A drain is left in the abscess cavity & remains in place until the infection goes away.
- It is always important to identify & treat the cause of the abscess.
Complications: Return / Rupture of the abscess. Spread of the infection to the bloodstream. Widespread infection in the
abdomen.
54. Cysts and abscesses of the liver

Abscess is a solitary or multiple collection of pus (thick fluid of blood, dead tissue & germs). Caused by the presence of bacterial,
parasitic / fungal organisms spread from the digestive tract ([Link], strep, Klebsiella).
Cyst is similar to an abscess but without the pus and has an epithelial lining. Types: ‘simple’ cysts & multiple cysts linked to
polycystic liver disease (PCLD). Polycystic cysts & simple cysts are ‘congenital’.
Clinical presentation
Simple cysts: Usually asymptomatic but increased size may cause pain in RUQ.
Polycystic cysts: Abdominal & RUQ pains. May be first noticed, during puberty.
Abscesses: fever, anorexia, sickness, weight-loss, weakness, pain in RUQ & jaundice (late stage).
Diagnosis: Cysts: USG, CT, MRI. Abscesses: Blood tests & analysis of material extracted under USG. CT.
Treatment
Cysts: simple is drained & removed surgically (laparoscopic deroofing – remove part of cystic wall) if produces symptoms (large,
painful).
Polycystic liver disease: Liver has many scattered cysts of various sizes caused by a genetic disease. Often an accidental finding/
during diagnosis of kidney disease. These cysts rarely require treatment, but if they do laparoscopic deroofing.
Abscesses: ATB's as first line but not always sufficiently effective & therefore percutaneous abscess drainage may be needed,
guided by USG / CT. In extreme cases (ruptured abscess) open surgery may be needed.

55. Portal hypertension and possibility of treatment

Portal hypertension
Normal portal vein pressure is 5–10mmHg. Portal hypertension (PH): portal pressure is greater than 12mmHg. Most common
clinical manifestations of liver disease. It results from increased hepatic resistance to blood flow leading to increased pressure
and vasodilation of venous system.
Etiology
- Prehepatic. Congenital portal vein atresia or portal vein thrombosis due to neonatal umbilical sepsis, phlebitis of the
portal vein from abdominal infection (acute appendicitis or diverticulitis), trauma, or a thrombosed portocaval shunt.
- Hepatic. Cirrhosis (e.g. alcoholic most frequently in the UK), chronic active hepatitis, and parasitic diseases
(schistosomiasis).
- Post-hepatic. Budd–Chiari syndrome (hepatic vein thrombosis), constrictive pericarditis, or tricuspid valve incompetence
(rare).
Features and complications: esophageal and gastric varices (can bleed). Rectal varices. ‘Caput medusae’ (Obliterated umbilical
vein). Ascites. Splenomegaly. Liver failure.
The Child–Pugh classification is used to assess the severity of portal hypertension
Diagnosis: CT (visualize portal vein thrombosis). Transabdominal Doppler USG to assess blood flow in the portal vein and hepatic
artery. Gastroscopy (EGD) in acute variceal bleeding. Blood tests (CBC, liver enzymes).
Treatment: focuses on preventing / managing the complications.
Endoscopic therapy: Usually the first line of treatment for varices bleeding and consists of either banding / sclerotherapy (blood
clotting solution injection).
Medications: Nonselective beta blockers (nadolol / propranolol) for varices as prevention to decrease pressure. Drug lactulose
can help treat confusion and other mental changes associated with encephalopathy. Anticoagulation therapy for Budd–Chiari
syndrome.
Surgery – Portosystemic shunts
- Trans jugular intrahepatic portosystemic shunt (TIPS/ TIPSS): Needle catheter inserted via internal jugular vein and
passed along to hepatic vein – there its pierced through liver parenchyma to intrahepatic branch of portal vein where a
metal stent is placed -> side-to-side portocaval shunt.
- Total portosystemic shunts: portal vein is completely shunted to the vena cava, thereby reducing portal pressure.
- Selective portosystemic shunts: portal vein is partially shunted to the vena cava - prevents varices while continuing to
allow portal perfusion.
56. Benign liver tumors

Hepatocellular Adenoma: Relatively rare proliferation of hepatocytes in a normal liver. Typically found in young women and
associated with OCP. Presence of 10 or more adenomas is termed adenomatosis.
Symptoms: upper abdominal pain, due to hemorrhage into tumor/local compressive symptoms. acute intraperitoneal
hemorrhage. may turn into a cancer.
Tx: surgery depending on the size
- < 3 cm, usually not recommend removing.
- 3-5 cm carefully monitor / remove.
- 5 cm usually surgery to remove (risk for bleeding or malignant transformation).
Focal nodular hyperplasia (FNH): 2dmost common benign tumor of the liver and predominantly found in young women. These
masses are found incidentally (imagining/laparotomy), usually small (less than 5 cm) involving left and right liver equally.
Etiology: unknown, related to developmental vascular malformation.
Tx: monitoring using CT / MRI. If it does not grow, no further treatment.

Hemangioma: Most common benign tumor of the liver resulting from malformations of blood vessels. Usually no risk of
bleeding / turning into cancer. Small capillary hemangiomas are of no clinical significance, whereas larger cavernous
hemangiomas have been associated with FNH. Sy: asymptomatic, incidentally found. Only symptomatic tumors (abdominal pain,
nausea) interfering with lifestyle may be recommended for removal. Spontaneous rupture is very rare. Dx: USG, contrast CT,
MRI. Tx: conservative.

Polycystic liver disease: inherited (polycystic kidney). Tx: Most do not require surgery. Massively enlarged and press on adjacent
organs: require surgery to remove / open some of the cysts. May be done laparoscopically / by open approach. In rare cases,
liver transplantation is recommended.
Liver cysts: Usually asymptomatic and only treated if the patient experiences symptoms, related to the cyst. In rare cases (biliary
cystadenomas / choledochal cysts), surgery may be recommended, because they may turn into cancers.

57. Intestinal invagination

Intussusception – invagination of portion of intestine into its lumen. Invagination of the proximal bowel (called the
intussusceptum, e.g. terminal ileum/ileocecal valve) into the distal bowel (called the intussuscepiens, e.g. caecum/ascending
colon). More common in children. Peak age of presentation at 3–10 months (m.c. in boys).
Etiology: Idiopathic. Polyp. Meckel diverticulum. Peyer patches hyperplasia. Tumors. Enteric duplicat cysts.
Clinical features - Classic triad of features is:
- Abdominal pain (associated with pallor, screaming, and restlessness).
- Palpable sausage-shaped mass (mid-abdominal or right upper quadrant).
- Passage of ‘redcurrant jelly’ stool (rectal examination may reveal bloody mucus).
Other: Signs of shock (lethargy, poor feeding, hypotonia). Features of obstruction (distension and vomiting).
Diagnosis
- Ultrasound (diagnostic test of choice). Intussusception in cross-section (‘doughnut’ or ‘target’ sign).
- X-ray. May show soft tissue mass, small bowel obstruction, free air indicating perforation.
- Air contrast enema. Diagnostic + therapeutic.
Treatment
- Immediate IV fluid resuscitation to correct fluid losses, restore fluid, electrolyte, acid/base balance.
- Once fluids are balanced: reduction (Analgesia and sedation (morphine). ATB)
Methods of reduction - resection
Radiological reduction: Air enema/ water soluble enema therapeutic in 75% of cases.
Surgical reduction
- Laparotomy indicated without enema if evidence of peritonitis or perforation.
- Manual reduction by retrograde squeezing and gentle proximal traction.
- Resection and anastomosis if bowel viability is in doubt (70% require resection).
- Post-reduction septic shock may occur with release of bacterial products from viable, but damaged bowel segment.
- Most recover rapidly with resumption of oral feeding in 24–48h and discharge home in 4–5 days.
 58. Malignant liver tumors

May be primary or metastatic (more common) – GIT, breast, bronchus.

Hepatocellular carcinoma (HCC): most common primary liver malignancy. arising from the hepatocytes. Present as single or
multiple nodules. It can metastasize o LN, lungs, bones.
Etiology: Viral hepatitis (HBV, HCV), liver cirrhosis (fatty liver, alcoholic), hemochromatosis, steroids, OCP.
Clinical presentation: Weight loss, anorexia, RUQ pain, ascites, fever w/ jaundice, hepatomegaly.
Diagnosis: AFP may be raised. USG, CT and MRI (show hypervascularity and metastasis). Biopsy.
Treatment: Surgical resection (hepatectomy), trans arterial embolization (prolongs survival) and anti-angiogenic drugs
(surafenib) in non-resectable cases. Liver transplantation is possible in small tumors (< 3 nodules, < 3 cm / 1 nodule < 5 cm)
without metastasis.

Cholangiocarcinoma: adenocarcinoma that arise from the biliary tree. Extrahepatic or intrahepatic – bile ducts. Very poor
prognosis. Etiology: primary sclerosing cholangitis (autoimmune), liver parasites (mostly Asia), chronic inflammation
(cholangitis), choledochal cysts, Caroli's disease and choledocholithiasis.
Clinical presentation: jaundice, often with pruritus and weight loss. Diagnosis: biopsy, ERCP. USG. MRCP.
Treatment: Resection. Adjuvant radiotherapy/brachytherapy. Chemotherapy (cisplatin).

Angiosarcoma: from endothelial cells occurs due to exposure to vinyl chloride (PVC) and arsenic. Has a very long latency period
and is an extremely rare type of liver cancer.
d Hepatoblastoma: embryonal, most common liver tumor of young childhood (15 months). Rare. Characterized by elevation of
alpha fetoprotein. Treatment: resection and neoadjuvant chemotherapy.

59. Congenital and acquired diseases of the spleen

Spleen is an organ found in vertebrates with similar structure to a large lymph node. It acts like a blood filter. Between 9th and
11th ribs on left side.
Functions: Circulatory filtration; Immune responses – accumulation of lymphoid tissue; Hematopoiesis; Iron reutilization; Blood
and immune cell reservoir.

Diseases associated with spleen

Hematological diseases: e.g. hereditary spherocytosis and hemoglobinopathies (thalassemia, sickle cell).
Tx: Splenectomy relieves excessive degradation of RBC and reduces requirement for blood transfusions.
In terms of malignancies, it is indicated for symptomatic reasons (pain) or to improve hypersplenism associated with an enlarged
organ.
Splenic abscess: uncommon infection that typically results from endocarditis or seeding from other site of infection. Sy:
recurrent or persistent fever, despite antimicrobial therapy, and LUQ pain w/out splenomegaly. May be accompanied by pleural
effusion or by splenic infarction due to septic emboli.
Tx: ATB and splenectomy. CT – guided percutaneous aspiration is occasionally successful.
Splenic infarction: occurs when the splenic artery or one or more of its branches becomes occluded with an embolus or clot. Pt
present with LUQ pain and tenderness, fever, splenomegaly, elevated LDH and WBC.
Etiology: hypercoagulable state, embolic disease, myeloproliferative disorder, essential thrombocytopenia, hemoglobinopathy
(SC). Tx: in complicated cases (hemorrhage, rupture, abscess, aneurysm) splenectomy.
Calcification: may not be detected on conventional imaging techniques and may or may not be associated w/ splenomegaly.
Conditions associated w/ calcifications: phleboliths, splenic artery aneurysm, SCD, tumors (lymphoma, hemangioma,
hemangiosarcoma) and infections (histoplasmosis, brucellosis, candidiasis, TB).
Cysts and pseudocysts: may be noted as incidental findings on conventional imaging, or as result of evaluation of patient w/
LUQ pain, left shoulder pain, abdominal enlargement, or splenomegaly. Usually asymptomatic, but can enlarge slowly to
massive proportions, bleed or become secondarily infected.
Splenic artery aneurysm: 3rd most common aneurysms found within the abdomen. Can rupture and lead to death, especially in
pt w/ portal HTN or during pregnancy. Often calcified, may be mistaken for lesions of the distal pancreas. Tx: surgical resection
w/ vascular reconstruction, stenting or endovascular coiling/ablation.
Rupture: spleen is the most common injured abdominal organ in non-penetrating trauma. Particularly susceptible to external
forces. Patients with ruptured spleen and hemodynamical instability require emergency laparotomy. In some cases, iatrogenic
injuries (laparotomy) or spontaneous rupture may occur.
Neoplastic diseases: primary tumors are rare. Hemangioma is the most common benign neoplasm. Primary mesenchymal
tumors such as lipoma, angiomyolipoma, fibroma and sarcoma have been reported to occur in splenic parenchyma but are quite
rare. Presence of MTS on spleen is a rare occurrence and most commonly due to hematogenous spread of melanoma, gyne
cancer, breast, lung and stomach cancers.
60. Foreign bodies in the respiratory and digestive tract

Most common in children 1-3 years but can affect people of all ages. Accidentally/deliberate ingestion. Patients with mental
illness, intellectual impairment. Most common aspirated objects: food fragments, toys.
Respiratory tract: Most serious is complete airway obstruction. Lower AO more common than UAO. 3 stages:
- Violent paroxysm of coughing, choking, gagging, possibly airway obstruction
- Asymptomatic: lodging of foreign body, reflexes fatigue
- Complications: obstruction, erosions, or infection. Fever, cough, hemoptysis, pneumonia, atelectasis
Dx: history of choking, coughing, wheezing. CXR, PA and lateral neck radiograph (only radiopaque objects are visible).
Bronchoscopy. Most foreign bodies lodge in right main bronchus. Larynx and trachea around 10%.
Treatment: Endoscopic removal (rigid bronchoscopy).
Laryngeal foreign bodies:
- Lodged in supra- or subglottic space.
- Complete obstruction and asphyxia
- Sudden resp. distress, inability to speak or cough
- Tx: Heimlich maneuver, CPR, surgical airway, endoscopic removal
Tracheal foreign bodies: Choking & aspiration (90%), stridor, wheeze (50-60%).
Bronchial FB: Persistent cough w/ sputum production, persistent wheezing, recurrent pneumonia.
Dx: History, Physical findings, XR (CXR: Radiopaque objects. Early: focal air trapping. Late: Atelectasis).

Digestive tract - Location: Esophagus (mc), stomach, intestine, rectum.

Clinical presentation: painful dysphagia, may be asymptomatic, mediastinitis (if esophageal perforation occurs). Abdominal
pain, bloating, blood in stool. Perforation, peritonitis.
Diagnosis: XR may show radio-opaque foreign body. Air in mediastinum (if perforation occur). Barium swallow (Gastrografin if
suspected perforation). Esophagoscopy. Endoscopy.
Treatment
- Esophagoscopy and removal - A flexible endoscope may be used in association with specially designed forceps for
grasping foreign bodies.
- Foreign bodies that pass through the esophagus will normally be passed per rectum.
- Sharp object may perforate the bowel or bowel wall – ENDOSCOPY removal (urgent).

61. Surgical diseases of the retroperitoneum

Primary Retroperitoneal Structures
1) Urinary: adrenal glands, kidneys, ureter.
2) Circulatory: abdominal aorta, Inferior vena cava.
Secondary organs: 1) duodenum – except proximal first segment 2) ascending and descending colon.

Retroperitoneal Hemorrhage
- Vascular: abdominal aorta / renal artery aneurysm rupture (open surgery / endovascular repair), arteriovenous
malformation (embolization, radiation, surgery / or combination of these methods), cystic medial necrosis (excision / graft),
segmental arterial mediolysis (open surgery / endovascular repair).
- Rheumatic: polyarthritis nodosa, Bechet sy.
- Renal tumor: renal cell carcinoma (nephrectomy), angiolipoma (embolization), transitional cell carcinoma / renal
uroepithelial carcinoma (transurethral resection / cystectomy, urinary inversion).
- Adrenal tumor (adrenalectomy, if small laparoscopic invasion): myelolipoma, pheochromocytoma, hemangioma.
- Non-neoplastic renal pathology: nephritis, cystic rupture (laparoscopic), renal calculi (extracorporeal shock wave
lithotripsy, ureteroscopy, percutaneous nephrolithotomy), renal infarct (endovascular - catheter directed thrombolysis).
- Coagulopathy and infectious disease: renal tuberculosis (nephrectomy), renal cortical abscess (percutaneous drainage).
- Acute pancreatitis (sphincterotomy of Oddi sphincter, if stones / cholangitis / jaundice, biliary stenting).
Etiology: Idiopathic, drugs, inflammatory aortic aneurysm. Retroperitoneal fibrosis compresses both ureters bilateral
hydronephrosis and renal failure. May cause inferior vena cava obstruction.
Diagnosis: IVU, increased ESR. USG. CT / MRI.
Treatment: steroids + insertion of double-J stents (pig tail) / dissection of ureters from retroperit (uterolysis).

Retroperitoneal Abscesses: Nonspecific signs and symptoms frequently lead to a delay in diagnosis and treatment. Significant
morbidity and mortality rates approaching 50%.
Clinical presentation: fever, chills, abdominal / flank pain, irritative voiding symptoms, nausea, vomiting, and lethargy / weight
loss. Symptoms are present > 5d in most patients with renal / retroperitoneal abscesses. Diagnosis: Phys exam, lab, radiology.
Treatment: ATB, percutaneous catheter drainage / open surgical drainage.
62. Benign diseases of the mammary gland

Fibroadenoma: benign breast tumor with fibrous and glandular tissue – most common <35 years.
Etio: unknown, hormonal relationship has been established (estrogen) since it increases in size during pregnancy and revert in
menopause. Symptoms: well-defined mass, mostly solitary, non-tender, rubber consistency. Dg: USG – well-defined mass;
Mammography – may have popcorn-like calcifications; Fine-needle aspiration – fibrous and glandular tissue. Tx: regular check-
ups, surgical removal (lumpectomy).
Phyllodes tumor: rare fibroepithelial tumors, similar histology to fibroadenoma – peak incidence 40-50 years old – most
commonly benign. Etio: unkown. Symptoms: painless, smooth, multinodular lump (average 4-7 cm). Dg: USG and mammography
findings similar to fibroadenoma that tends to grow quicker Core-needle biopsy. Tx: surgical excision with wide margin due to
frequent reoccurrence
Intraductal papilloma: solitary or multiple benign lesions that arise from epithelium of lactiferous breast duct Peak incidence 40-
50 years old. Symptoms: solitary lesions (central papilloma) – most common cause of bloody nipple discharge, tumor close to
areola; multiple lesions (peripheral papilloma) – usually asymptomatic. Dg: Core needle biopsy to confirm, ductogram
(mammogram with contrast).
Tx: surgical excision of the affected duct.
Fat necrosis: benign necrosis of adipose tissue. Etio: trauma, surgery. Signs: firm tender mass, nipple retraction. Dg: physical
exam, mammography, needle core biopsy. Tx: conservative or surgical excision.
Lobular carcinoma in situ (LCIS): microcalcifications or production of a mass rare. Usually accidental finding during biopsy, lower
risk of invasiveness than DCIS. Localization: multifocal.

63. Malignant mammary gland tumors

Every by after
I
General: 2nd leading cause of death in women. MTS: bone, liver, lungs. Screening: mammography > 40y.
Risk factors: ↑ exposure to estrogen: Early menarche, Late menopause, Medication contain estrogens;
Gene mutation: BRCA 1, 2, TP53; ↑ expression of receptors: HER2, Estrogen receptors.
Clinical features: firm palpable mass, non-tender, poorly defin, irregular borders, skin retraction, ulceration, orange like nipple
(peau d’orange – obstructed lymphatic channels), bloody discharge. Axillary LPDNT.
Dg: mammography > 30y / US < 30y → calcifications.
Biopsy: fine needle aspiration → cytology. Core biopsy → histology. Tumor markers: CEA, CA15-3, CA27-29.
Tx: Surgery: breast conserving → lumpectomy +/- radiation. Mastectomy +/- radiation.
- Chemotherapy (CMF-DT): Cyclophosphamide. Methotrexate. 5-fluorouracil. Doxorubicin. Taxane (paclitaxel)
- Endocrine therapy: tamoxifen (competitive estrogen receptor). Aromatase inhibitor (letrozole)
- Target therapy: trastuzumab → for HER 2 (+)
Types of cancers
1) Ductal carcinoma in situ: arise from terminal duct, does NOT invade the basement membrane. Most common at 50y.
⑭ Signs: usually without palpable mass. Dg: mammography → micro calcification. Biopsy Tx: lumpectomy + radiation.
2) Invasive ductal carcinoma: mc breast cancer, aggressive. Arise from ducts and INVADE the basement membrane Signs:
painless fixed palpable mass mc → upper outer quadrant +/- skin retraction.
3) Inflammatory breast cancer: orange like skin → secondary to invasion of dermal and lymph nodes Signs: diffuse erythema
X and edema over the breast. Dg: early metastases to lymph nodes.
Tx: chemo + radical mastectomy.
64. Injuries of digestive tube (stomach, small and large intestine)

Gastric injury: stomach is generally well protected by the ribcage, such that penetrating injury is more likely than blunt trauma
to cause damage. Dg: not always obvious; aspiration of blood from a nasogastric tube confirm. Tx: Primary closure of injury may
usually be achieved in layers following local tissue debridement.

Small bowel injury: commonly injured in penetrating trauma. Also: deceleration and shearing forces. Indirect injury may occur
from damage to the mesentery and subsequent interruption of blood supply.
Dg: laparotomy for inspection. CT (false negative 15%). Tx: debrided and closed with suturing. Resection. Stoma formation /
restoration of continuity.

Colonic injury: rare, most frequently from penetrating injury. Tx: primary repair (without stoma preferred), resection &
anastomosis, repair w/proximal diversion, exteriorization. Colostomy. Severe injury to right colon may be treated with right
hemicolectomy. Complications: Septic complications are a common, with abdominal abscess.

Rectal injury: blunt / penetrating injury to the abdomen, pelvis / thighs. Dg: digital rectal examination, proctoscopy /
sigmoidoscopy. Tx: Primary repair. Proximal colostomy / loop ileostomy is required to divert fecal contents. In this situation, pre-
sacral drainage should be considered to reduce infective complications.

65. Compartment syndrome – etiology, diagnosis and treatment

Condition caused by an increased pressure within a closed anatomical space, which compromises the circulation and function of
the tissues within that space, leading to impaired tissue perfusion. If it is not treated within 6-8 hours, it may result in temporary
/ permanent damage to muscles and nerves – necrosis.
Sites affected: upper and lower limbs are most affected; also abdominal & gluteal regions.
Forearm: Median and ulnar nerves. Radial and ulnar arteries.
Lower limb: Peroneal nerves and arteries, tibial nerves and vessels.
Gluteal: Uncommon and is often diagnosed late, resulting in muscle necrosis and sciatic nerve palsy.
Abdominal: May occur in any multiple trauma patient who has undergone a period of profound shock. May cause acute renal
failure, cardiac dysfunction and elevated central venous pressure.

Acute compartment syndrome: medical emergency, caused by trauma.

Etiology: Fractures, especially forearm and lower leg that have been internally fixed / infected. Crush injury. Burns. Infection.
Prolonged limb compression (immobilization in a tight plaster cast). Vascular: reperfusion injury, hemorrhage, coagulation
disorders. Iatrogenic: intramuscular injections, vascular puncture in anticoagulated patients. Muscle hypertrophy in athletes.
Clinical Presentation: present within 48h of injury/major trauma. Increasing pain despite immobilization. Sensory deficit. Muscle
tenderness and swelling. Later features = tissue ischemia with pallor, no pulse, paralysis, coolness, and loss of capillary return.
Diagnosis: clinically. Intracompartmental pressure measured by wick catheter, needle manometry. MRI. Treatment: Fasciotomy
(tissue and fascia incisions) to relieve pressure – restoring the perfusion within 6h after onset (otherwise necrosis occurs – need
x Debridement).

Chronic (exertional) compartment syndrome: caused by intense, repetitive exercise, stops with rest.
Risk factors: most often in athletes aged < 40y. Excessive training increases the risk.
Clinical Presentation: severe pain and tightness, with hardness of compartment on examination. Pain resolves with rest. Nerve /
muscle dysfunction within compartment causes muscle weakness, numbness, tingling and abnormal gait. Diagnosis:
Intracompartment pressure testing pre/post exercise is gold standard.
Treatment: Conservative: eliminating offending activity, altering training regimens and deep massage. Surgical treatment:
decompressive fasciotomy (relieves pain and increases exercise tolerance).
66. Traumatic acute abdomen – classification and diagnosis

Abdominal injuries can be particularly dangerous, because it is often difficult to assess intra-abdominal pathology in multiple
injuries victims.
Blunt abdominal trauma: most common.
Etiology: motor vehicle accidents, due to rapid deceleration -> rupture of internal organs from briefly increased intra-abdominal
pressure, dependent on force applied.
Clinical presentation: Pain. Tenderness. GIT hemorrhage. Hypovolemia. Evidence of peritoneal irritation. Diagnosis: x-ray
Pneumoperitoneum. USG: look for free fluid in three areas of abdomen (perihepatic, perisplenic, pelvic). CT and DPL (Diagnostic
peritoneal lavage).
Treatment: I.V solutions / blood to maintain the circulation (minimal systolic BP 90mm hg).
Surgery (open/laparoscopic). Resuscitative thoracotomy in emergency department is only life-saving.

Penetrating abdominal trauma

Etiology: stabs and gunshot wounds. Knife wounds are more common and generally less lethal.
Clinical presentation: Penetrating lacerations of the diaphragm, diaphragmatic herniation may occur. Diagnosis: By clinical
presentation. General physical examination. Blood tests, Urinalysis, Radiological
Studies, (Plain abdominal X-ray, CXR), diagnostic peritoneal lavage (DPL), FAST USG of abdomen, CT.
Treatment: left anterolateral-left thoracotomy: purpose is to relieve cardiac tamponade, control cardiac bleeding, obtain
proximal aortic control and provide open cardiac massage to improve cardiopulmonary cerebral resuscitation efforts.

Organs commonly affected:

- Spleen – most common injured intra-abdominal organ. It must be suspected in any patient with bunt abd trauma. Dg
often suspected on physical examination, confirmed by USG-CT. Splenectomy is the most used surgical option, but due to
post splenectomy sepsis risk, splenic repair is now more used.
- Liver – second most commonly injurie organ after blunt trauma and it is the most injured parenchymal organ follow
penetrating trauma.
The FAST (Focused Assessment with Sonography in Trauma) examination looks for the presence
of fluid—presumed to be blood. Spaces in four areas: Pericardial. Perihepatic. Perisplenic

Heart/lungs

f
Asess RUQ, LUQ, Pelvis

- Gastric injuries – caused by penetrating trauma; rupture secondary to blunt trauma is rare.
+

- Duodenal injuries are relatively rare.

67. Acute abdominal compartment syndrome, damage control surgery

Compartment syndrome occurs when a fixed compartment becomes subject to increased pressure, leading to ischemia and
organ dysfunction.
Abdominal compartment syndrome (ACS) - organ dysfunction caused by intra-abdominal hypertension (IAH). Abd pressure
>20mmHg.
Etiology: Retroperitoneal: edema in necrotizing pancreatitis, pelvic/retroperitoneal hematoma, bleeding after aortic surgery.
Intraperitoneal: hemorrhage, visceral edema, bowel dilatation, pneumoperitoneum, acute ascites, mesenteric venous
obstruction. Other: hemoperitoneum, abd tumors, abscesses, peritonitis.
Rf: massive volume resuscitation, major trauma, obesity, abdominal surgery, severe burns, septic shock.
Symptoms: develops within hours to days in critically ill patients, cardiovascular signs (distended jugular veins, hypotension,
tachycardia), progressive renal failure, tight and distended abdomen, nausea, vomiting, tachypnea, wheezing.
Dg: indirect measure of intra-abdominal pressure (pressure in the bladder via intravesical catheter).
CT-scan: increased abdominal diameter, compression of inferior vena cava, intestinal wall thickening, bilateral inguinal
herniation. X-ray: not useful!
Tx: Conservative: Hemodynamic stabilization, percutaneous drainage of intra-abdominal fluid, ventilation
Surgical - abd decompression is the definitive management (by opening the abdominal wall and abdominal fascia anterior in
order to physically create more space for the abdominal viscera).
Consequences
- Cardiovascular: rise in the intra-abdominal pressure leads to a fall in cardiac output, due mainly to compression of the
inferior vena cava & reduction in venous return to the heart.
- Respiratory: will effectively splint the diaphragm & lead to a rise in peak airway pressure & intra-thoracic pressure &
subsequently a reduced venous return to the heart.
- Renal: leads to oliguria & anuria probably due to compression of the renal vein & renal parenchyma.
- Cerebral: leads to a rise in central venous pressure which prevents adequate venous drainage from the brain & worsing
brain edema.
- Vascular: venous stasis -> DVT.
- Hepatic: decreased blood flow
- GI: bacterial translocation, multiorgan failure
 Direct indirect hiatal
Iso
called
%

68. Hernia in children

Most commonly inguinal hernia – most common in newborns.

Indirect inguinal hernias: protrusion of abdominal-cavity contents through the inguinal canal (internal inguinal ring), sometimes
until the scrotum / labium major with / without intestinal content. Arises lateral to artery. Mainly in boys (only 10% in girls),
common on the right side because of delayed descent of rx testicle.
Etiology: patent processus vaginalis. Dg: by clinical presentation, USG (not for incarcerated type).
Clinical presentation:
1) Reducible hernia: visible swelling / bulge painless, commonly intermittent (appear with crying & often resolves during
night). Palpable smooth mass originating from the external ring, easily reduced.
2) Incarcerated hernia: painful: ± bilious vomiting in case of intestinal content → obstruction → ischemic necrosis
develops → intestinal perforation may result, representing a true medical emergency. Palpable firm mass originating
from the external ring, that cannot be reduced. The skin overlying the bulge may be edematous, erythematous &
discolored.
3) Strangulated: incarcerated with compromise to the blood supply of the contents, which may lead to infarction.
Commonly accompanied by bowel obstruction.
Tx: Surgical repair asap after diagnosis to prevent incarceration with general anesthesia (endotracheal intubation). Repair in
children only involves ligation - excision of the sac & plication of the deep inguinal ring.

Femoral hernia: protrusion of abdominal-cavity contents through femoral canal, below inguinal ligament. Rare in children. May
be strangulated. It must be operated (reduction of hernia & femoral canal narrowing). It cannot be distinguished easily from
inguinal hernia that does not extend to the scrotum, before surgery.

Umbilical hernia: protrusion of the abdominal cavity content through the umbilical ring due to an imperfect closure of umbilical
ring. Common in low birthweight infants. No risk of strangulation.
Dg: by clinical presentation. Clinical presentation: Visible swelling / bulge, painless, commonly intermittent (appearing with
crying / straining). The size from < 1cm - 5cm.
Tx: No treatment needed. Small disappears by 1 year of age, large until 5-6 years of age.

Hiatal hernia: protrusion of part of the stomach into the thoracic cavity through the esophageal hiatus.
Types
Sliding hernia: Results from axial displacement of upper stomach through the esophageal hiatus, usually with stretching of the
phrenic-esophageal membrane. Most common. May result in GERD.
Rolling (paraesophageal) hernia: Results from the displacement of part / all of the fundus & body of the stomach through a
defect in the phrenico-esophageal membrane such that it comes to lie alongside the normal esophagus.
Symptoms: hiccough, pressure in the chest & odynophagia (painful swallowing).
Risk factor for: Volvulus (obstruction caused by twisting of stomach/intestine). Incarceration & obstruction.
Clinical presentation: asympt, symptoms of gastro esophageal reflux (regurgitations, ± esophagitis).
Dg: X-ray - contrast medium meal. Video barium swallow identifies the type & extent. CT in acute presentations. Tx:
Symptomatic of gastro esophageal Reflux: PPI, antacids. Rarely surgery.

69. Congenital diaphragmatic hernia

Diaphragmatic hernia: protrusion of intra-abdominal contents through an abnormal opening in the diaphragm – congenital are
due to the incomplete fusion of embryonic components of the diaphragm (septum transversum). Incidence 1 in 3000. The defect
in the diaphragm causes displacement of abdominal contents into the pleural cavity causing compression of the lung tissue and
pulmonary hypoplasia.
Types
Morgagni hernia - Anterior mediastinum: 2% of all congenital diaphragmatic hernias. Hernia through foramen Morgagni.
Adjacent to xiphoid process. Usually on right side & asymptomatic. Recurrent chest infections & GIT symptoms. Laparoscopic
surgical repair (due to risk of strangulation).
Bochdalek hernia - Posterior mediastinum: 95% of congenital Diaphragmatic Hernias. Usually on left side.
Diaphragmatic eventration: Abnormal displacement (elevation) of a part / all diaphragm which is otherwise intact. Due to
thinning → incomplete muscularization.
Symptoms: depend on the degree of lung hypoplasia and lung hypertension; respiratory distress (nasal flaring, tachypnea,
cyanosis, intercostal retractions, grunting); barrel shaped chest – bowel sounds in chest; absent breath sounds.
Dg: Antenatal USG often reveals it: fluid-filled stomach/bowel seen in thorax, peristalsis may be noted (confirms diagnosis),
esophageal compression can cause polyhydramnios. Chest X-ray: abdominal contents in thorax, poorly aerated lungs.
Tx: assisted ventilation, extracorporeal membrane oxygenation (ECMO), gastric decompression (nasogastric tube), surfactant
administration if preterm. Surgery repair when baby is stable (thoracotomy – laparotomy).
70. Congenital defects of the anterior abdominal wall
& is a birth defect where there is a hole in the abdominal wall beside the belly button. The baby's intestines, and sometimes other organs, are found outside of the baby's body, exiting through the hole.

Gastroschisis: defect in anterior abdominal wall through which the abdominal contents may protrude; intestine lie free outside
the abd cavity, not covered. There is no overlying sac. The abdominal wall defect is located at the junction of the umbilicus and
normal skin and is almost always to the right of the umbilicus.
Dg: Intrauterine: ↑AFP in maternal blood. USG: if serial USG's shows dilatation & thickening of the intestine in a baby with
Alfa feto protein

gastroschisis, delivery should occur as soon as amniocentesis demonstrates lung maturity.

Tx: A surgical emergency! Patients frequently require more than one surgery. Initially placement of a protective "silo" around
the intestine outside the abdomen, then slowly pressuring the herniated intestine into the abdominal cavity (not compressing
vena cava).

Omphalocele: defect in the anterior abdominal wall around the umbilicus through which the abdominal contents may protrude,
covered by peritoneum.
(Diff- Dg from umbilical hernia - abdominal content protrudes covered by skin).
Tx: The baby should be carefully examined to detect any other associate malformations. IV fluids are administered. If there is
vascular compromise because of small abdominal wall opening, the defect should immediately be surgically enlarged. Place the
exposed viscera and entire lower half the baby into a transparent nonadherent plastic bowel cover and wrap to preserve body
heat and moisture.
Closure with no urgency small or moderate-sized omphalocele by excising the omphalocele membrane, reducing the herniated
viscera, and closing the fascia and skin. Membrane overlying the liver can be left in place. Large omphalocele - treat
omphalocele sac with drying agent topical silver sulfadiazine (topical ATB) and allow it to epithelialize over the ensuing weeks to
months. Then compression is done with elastic bandages until abdominal contents are reduced.

most common 86%

71. Esophageal atresia

Serious birth defect in which the esophagus is segmented and closed off at any point. One or more fistulae may be present
between the malformed esophagus and the trachea with aspiration of pharyngeal secretions.
Types: A (without fistula), B (with fistula in proximal esoph segment), C (most common, with fistula in distal segment), D (fistula
in distal – proximal segments), E (fistula without atresia).
Clinical Presentation: Excessive secretions/ foaming at mouth, chocking, drooling, inability to feed; aspiration pneumonia:
coughing spells, rales, cyanotic attacks even respiratory distress. Distended abdomen.
Associated congenital anomalies (cardiovascular, anus atresia, urinary, skeletal, CNS).
Diagnosis: Inability to pass a catheter (feeding tube) into stomach in case of atresia. X-ray shows coil catheter, presence of air in
abdomen (pneumoperit), esophageal pouch, large gastric bubble. X- Ray w/ water contrast.
Treatment: Incubator. I.V fluid administration. Constant suction of esophageal pouch. Prophylactic I.V ATB (in case of aspiration
pneumonia). Surgical emergency. Surgery should be performed within 24 hours, reconnect the upper esophageal pouch and
lower esophagus.
Complications: Stenosis at the site of anastomosis → dilatations. Abnormal motility of distal esophagus predisposing to GERD.
72. Atresia and stenosis of the intestine stenosis blocked Atresia

Intestinal atresia: complete blockage or obstruction anywhere in intestine.

Stenosis: partial obstruction that results in narrowing of lumen in intestines.
Types: Duodenal, Jejunal, ileal, Anal – Atresia + Duodenal Stenosis.

Duodenal atresia and stenosis

Duodenal atresia is a complete occlusion or absence of the duodenal lumen, whereas duodenal stenosis refers to an incomplete
obstruction caused by narrowing. Both conditions present with signs of obstruction, including a distended upper abdomen,
delayed meconium passage (more severe in atresia), and vomiting.
If the defect is located proximal to the major duodenal papilla, non-bilious vomiting occurs, whereas a defect occurring distal to
the papilla causes bilious vomiting.
Evidence of polyhydramnios on prenatal USG may lead to an early diagnosis of duodenal obstruction.
Dg: Double bubble sign - air and fluid build-up proximal to the obstruction and are separated by the pyloric sphincter, which
resembles two bubbles on imaging (one in the stomach and one in the duodenum).
Tx: preoperative – parenteral nutrition via central catheter after birth, fluid – electrolyte replacement.
Surgery: bypass the atresia or stenosis through anastomosing techniques – duodeno-duodenostomy or duodeno-jejunostomy
with a proximal transverse-to-distal longitudinal anastomosis.

Jejunal atresia and ileal atresia: absence of jejunal / ileal lumen. Associated with abnormalities of intestinal rotation/fixation.
Signs: similar to duodenal, polyhydramnios (intrauterine), bilious vomiting and upper abdominal distension (postpartum). Dg:
Abdominal x-ray shows triple bubble sign (dilated small bowel loops and air-fluid levels) and gasless colon. Tx: Surgical
correction with bypass of occluded part.

Pyloric atresia: obstruction of pylorus. Usually familiar & rare. Signs: child vomiting, swollen distended abdomen (accumulation
of contents/gas) Dx: X-ray: air filled stomach.
Colonic atresia: associated with small bowel atresia, Hirschsprung's disease or gastroschisis Dx: X-ray & X-ray contrast enema.

73. Anorectal malformation

:
Anorectal Malformation, or Imperforated Anus, is a spectrum of abnormalities of the rectum and anus.
Mainly due to failure of the urogenital septum to descent properly – leads to many possible abnormalities:
1) The absence of an anal opening.
2) The anal opening in wrong place.
3) A connection, or fistula, joining the intestine and urinary system.
4) A connection joining the intestine and vagina.
5) In females, the intestine can join with the urinary system and vagina in a single opening, known as cloaca.

Diagnosis: by clinical presentation, physical examination, visible abnormal passage of stool, genitals examination (location of
vagina/urethra, anal opening)
- If there is a fistula (opening) to skin, urethra or vagina, a newborn will pass meconium.
- if there is no anal opening and there is no fistula, the baby will not be able to pass stool after birth and this will lead to a
swollen or "enlarged" abdomen and vomiting.
Associated birth defects: Vertebral anomalies. Anorectal malformation. Cardiac or heart defects. Tracheoesophageal
atresia/fistula. Some children have abnormalities of the urinary system which includes kidneys, ureters, bladder and the urethra.
Limb or abnormalities of the radial bones in the arms that lead to displaced hands.
Treatment: Child will need 3 operations to correct the anorectal malformation, as determined by the anatomy: The first is to
create a stoma, the second is to place rectum through center of the anal sphincter and the third to close the stoma. Some
children will only need one operation, to place rectum through center of anal sphincter.

According to anatomical variation:

- If there is an opening for stool to drain, but it is in the wrong location, it will be placed into the correct location, within
the anal sphincter. This is usually done in one operation.
- If there is no skin opening for stool to drain and the rectum is low and near the anal sphincter, an anal opening will be
made in the correct location, within the anal sphincter. This can be done in one operation.
- If the rectum ends high in the pelvis and is too far from the skin, surgical repair will be done in stages: first - colostomy
and mucous fistula (plus home recovery); second - anal creation and dilations; third - closure of colostomy.
74. Intestinal malrotation

Congenital anomaly of rotation of midgut. It can lead to volvulus – dangerous complication, loop of intestine twist around itself
leading to obstruction. Blood supply to twisted part also may be cutted.
Rotational disorders
Non-rotation: neither colon or duodenum undergo rotation.
Incomplete rotation: counterclockwise rotation of only 180º. Caecum in epigastrium overlying duodenum.
Reverse rotation: rotates clockwise. Causes compression of colon by superior mesenteric artery (SMA) -> obstruction. Ileocecal
volvulus – due to inadequate fixation of right colon.
Associated w/: intestinal atresia, imperforable anus, cardiac anomalies, Merkel diverticula, hernia, Down sy.
Signs: Asymptomatic. Acute volvulus: 1st month of life, bilious vomiting, crampy abd pain, and distention, metabolic acidosis,
melena, hematemesis; if ischemia and necrosis of intestine occurs can lead to septicemia, hypovolemic shock, eventually death.
Chronic volvulus: +2y.o, undiagnosed, recurrent abd pain & vomiting.
Others: duodenal obstruction, malabsorption, chronic motility issues, internal herniation.
Dg: X-ray (show intestinal obstruction, pneumoperitoneum). Barium enema x-ray. USG (inversion of SMA/SMV). CT.
Tx: Surgical correction (Ladd’s procedure) - untwist the volvulus counterclockwise, divide occurring abnormal peritoneal bands,
bring duodenum into right lower quadrant and cecum into left lower quadrant.
Prophylactic appendectomy is often considered, since in later life a delayed/missed diagnosis of appendicitis may occur, due to
lack of awareness that the patient has a left sided caecum/appendix causing left sided abdominal pain. It should be noted that
normal anatomical positioning is not achieved; the duodenum and small bowel remain on the right, and the caecum and colon
are on the left side of the abdomen.

75. Meconium ileus

Meconium ileus: a neonatal bowel obstruction of the distal ileum due to abnormally thick & sticky meconium. Risk factors:
cystic fibrosis (most common), low birth weight, pancreatic atresia, stenosis of pancreatic duct. Location of obstruction:
terminal ileum.
Signs: neonate fail to pass meconium with 12-24h after birth. Emesis may be bilious. Abdominal distention. Palpable bowel
loops.
Complications: malrotation, perforation, peritonitis, intestinal atresia, cholestasis.
Dg: plain X-ray (dilated intestinal loops, “soap bubble” mixture of gas with meconium, calcified meconium if peritonitis).
Contrast enema (microcolon with obstruction in terminal ileum). Can be dg in prenatal USG.
Treatment: Conservative: Water-soluble contrast enema (Gastrografin) usually clears the impacted meconium, with a success
rate of over 60%.
Operative: Irrigation with dilute mucolytic fluid. Alternatively resection of distended ileum with enterostomy or primary end-to-
end anastomosis (in case enema doesn’t work).
76. Hirschsprung´s disease
(nerve cells missing
Hirschsprung disease = aganglionic megacolon - birth defect.
It results from absence of ganglion cells in the myenteric plexus of the intestine aganglionic colon doesn’t permit normal
peristalsis to occur – no movement of contents – this causes constrictions and the colon before the constriction becomes dilated
by stool -> constipation -> partial/total obstruction -> megacolon.
Patophys: migratory failure of neural crest cells
Location: begins in internal anal sphincter & extends proximally for variable length of gut.
Types: Congenital (mc). Acquired: vascular causes due to ischemia, non-vascular due to vit b12 def, TBC.
Associated with: usually is solitary, but Down syndrome, prematurity, GI, urinary, CVS abnormalities.
Signs: failure to pass meconium within 24h after birth. Obstruction: bilious vomiting, abd distention, refusal to feed. Recurrent
enterocolitis. Toxic megacolon: fever, explosive diarrhea, dehydration, shock, vomiting. Perforation. Chronic constipation.
Growth retardation.
Dg: history. Physical exam: anal sphincter is hypertonic, rectum empty, hard fecal mass.
X-ray abdomen/Contrast Enema (shows dilatations). 24h delayed barium enema (shows poor emptying of barium through
colon). Rectal manometry and biopsy for definitive diagnosis: absence of ganglion cells.
Tx: decompression (introduce rectal tube & irrigation). Surgical resection of aganglionic bowel segments (transanally), then
joining of healthy ends. (Pull-through procedure

unperforated
and all

77. Congenital malformations of the colon and rectum and their surgical management

Hirschsprung disease: results from absence of ganglion cells in the myenteric plexus of the intestine aganglionic colon doesn’t
permit normal peristalsis to occur - no movement of contents - this causes constrictions and the colon before the constriction
becomes dilated by stool -> megacolon. Dg: failure to pass meconium after first 24 hours, severe constipation or ileus, bilious
vomiting, abdominal distension, poor weight gain, in older children possible mass in sigmoid colon, Irigography, rectal
manometry and biopsy. 10% have diarrhea due to bacterial overgrow enterocolitis (can cause perforation). Tx: resection of
aganglionic bowel segments (transanally), sometimes colostomy.
Omphalocele: mass of bowel and solid viscera, protrudes outside the central abdomen, covered by thin, transparent membrane
– repositioning and closure of defect (possible temporary patch).
Gastroschisis: Laparoschisis – defect of anterior abdominal wall – intestine lie free outside the abdominal cavity, not covered.
Return and reposition intestine (not compressing vena cava), silo can be used.
Anorectal malformations: wide spectrum of diseases involving the distal anus and rectum as well as urinary and genital tracts –
range from very minor to complex with poor functional prognosis. Tx: Anal reconstructive surgery (primary anoplasty) or
temporary colostomy in more complex malformations.
Unperforated anus: 1 in 5000 live births, gender affected equally, (either high or low, depending on whether the anus ends
above or partially descends through the levator ani muscle) – detected by contrast X-ray and inspection. Treatment: in low
lesions – only perineal operation required; In high lesions – colostomy in newborn period, anorectoplasty at about 6 months old.
Intestinal malrotation/midgut volvulus: Emergency surgery — Ladd procedure: Surgical procedure to treat intestinal
malrotation, consisting of division of Ladd's intestinal bands, widening of the small intestinal mesentery, appendectomy, and
correcting the location of cecum and colon. Procedure: volvulus is reduced/untwisted, and the Ladd bands removed. Necrotic
bowel, if present, is resected and anastomosed or created into a stoma.
78. Atresia of the biliary tree

Obliteration or discontinuation of extrahepatic biliary system (most commonly the common bile duct).
Etiology: unknown – most possibly embryonal malformation or acquired lesion (rotavirus, CMV).
Pathophys: discontinuation due to obliteration or fibrosis causing obstruction of bile flow (cholestasis); this causes secondary
biliary cirrhosis and portal HTN.
Signs: prolonged neonatal jaundice (>2 eeks), acholic stools, dark urine, hepatomegaly.
Diagnosis: Labs (conjugated hyperbilirubinemia, increased aminotransferases and alkaline phosphatase and GGT); USG (absence
of gallbladder no dilation of biliary tree); Liver biopsy (active inflammation with bile duct degeneration and fibrosis, bile duct
proliferation, portal stromal edema); Hepatobiliary scintiscanning (failure of the tracer to be excreted into the bowel);
Intraoperative cholangiography.
Treatment: Kasai procedure (hepatoporto-enterostomy) – connection is created between liver and the small intestine to allow
bile drainage. In liver cirrhosis: liver transplantation.

79. Acute appendicitis in childhood

Appendicitis in children accounts for more than 90% of acute abdominal problems and emergencies.
Clinical features: usually presents with diarrhea, fever, vomiting, pain in right lower quadrant, guarding, McBurney’s sign and
migration of periumbilical pain to the right lower quadrant.
The most reliable symptoms in children are emesis and duration of pain. The most reliable signs are abdominal tenderness and
pain with walking, jumping or coughing.
USG is the diagnostic procedure of choice.
Treatment: appendectomy.
80. Heart transplantation

Cardiac transplant is a surgical transplant procedure performed on patients with end-stage heart failure, severe coronary artery
disease, idiopathic dilated / ischemic cardiomyopathy. Post-operation survival periods averaged 15 years. immunosuppression
✓

History: first human heart allograft was performed in 1967 by Christian Barnard. Introduction of cyclosporine as IS treatment
resulted in improved survivability.
Donors: max 60 y.o. ABO-compatible, within 20% of recipient’s ideal body weight. There should be no history of preexistent or
intercurrent cardiac disease.
Contraindications: increase the chances of complications: systemic disease (infection, DM type 1, severe peripheral vascular
disease, poorly controlled hypertension), Recent thromboembolism; Substance abuse.

Procedures

Pre-operative: typical transplantation begins when a suitable donor heart is identified. Triple IS therapy with calcineurin
inhibitor, antimetabolite and CS is typical. Sometimes perioperative monoclonal Ab are used.
[
Corticosteroid

Operative: once the donor heart passes inspection, the patient is taken into the operating room and given a general anesthetic.
1) Orthotopic procedure: (Lower-Shumwat technique) begins with a median sternotomy, opening the chest and exposing
the mediastinum. Pericardium is opened, the great vessels are dissected; patient is attached to cardiopulmonary bypass
machine; donor's heart is injected with potassium chloride (KCl) which stops heart beating before the heart is removed
from the donor's body, packed in ice (keep usable 4 - 6h). Then failing heart is removed by transecting the great vessels
and a portion of the left atrium; patient's pulmonary veins are not transected; rather a circular portion of the left
atrium containing the pulmonary veins is left in place. Donor heart is trimmed to fit onto the patient's remaining left
7. atrium and the great vessels are sutured in place. New heart is restarted.
2) Heterotopic procedure: patient's own heart is NOT removed. New heart is positioned so that the chambers & blood
vessels of both hearts may be connected to form what is known as 'double heart'.
Advantage: give patient's original heart a chance to recover and if the donor's heart fails (rejection...), it can later be removed,
leaving the patient's original heart.
USED ONLY in cases where the donor heart is not strong enough to function by itself (because either the patient's body is
considerably larger than the donor's, the donor's heart is itself weak / the patient suffers from pulmonary hypertension).

Post-operative: Immunosuppressive (IS) agents are continued in the intensive care unit in both cases. The patient is regularly
monitored to detect rejection. This surveillance may be performed via frequent biopsy / a gene expression blood test known as
AlloMap Molecular Expression Testing. Typically, biopsy is performed immediately post-transplant and then AlloMap replaces it
once the patient is stable.
Complications: Infection, sepsis, organ rejection, side-effects of the immunosuppressive medication. Recipients may get kidney
disease from a heart transplant.

81. Fundamental techniques in plastic surgery – general principles and surgical techniques

Plastic surgery is one of the medical specialties concerned with the «correction»/restoration of form and function. Though
cosmetic/aesthetic surgery is the best-known kind of plastic surgery, most plastic surgery is not cosmetic, plastic surgery
includes many types of reconstructive surgery.
General principles: different suturing techniques, precise approximation of the skin edges without tension is essential to ensure
primary healing with minimal scar. Types of excision:
- Simple excision: plan the excision direction parallel to skin wrinkle or natural skin line, contour junction or relaxed skin
tension lines.
- Wedge excision: when lesion is adjacent to free margin (lip, lid).
- Circular excision: used according to diameter.

Reconstructive plastic surgery is performed to correct functional impairments caused by burns, traumatic injuries, such as facial
bone fractures and breaks, congenital abnormalities, such as cleft palates/cleft lips, developmental abnormalities, infection and
disease, cancer / tumors. Reconstructive plastic surgery is usually performed to improve function, but it may be done to
approximate a normal appearance.
The most common use is in tumor removal, laceration repair, scar repair, hand surgery and breast reduction, breast
reconstruction after a mastectomy for the treatment of cancer, cleft lip and palate surgery, contracture surgery for burn
survivors.
Flap surgery — involves moving healthy, live tissue from one location of the body to another. Often to areas that have lost skin,
fat, or that have lost muscles movement and/or skeletal support.
Other: Skin grafting, cleft surgeries, hand surgery, aesthetic surgery.
82. Skin graft and skin flaps, musculocutaneous flaps

Skin graft: involves the transplantation of skin.

Indications: extensive wounds or trauma, burns, extensive skin loss due to infection (necrotizing fasciitis or purpura fulminans),
after surgeries. Procedure: debridement of wound or excisional surgeries.
Types
1) Removal of thin layer from a healthy part of body (split-thickness graft) – can be done under less favorable conditions
but shrinks and has little abnormal pigmentation and is susceptible to trauma.
2) Full thickness graft – more chance the body won’t accept it – heals quicker and is less painful, resist contraction,
potential for growth nut needs well vascularized bed.
3) Meshed graft: has incisions (little holes) to allow coverage of larger area and allows exudate to drain freely and adapt
better to irregular bed.

Skin flap: Flap surgery is a piece of tissue that is still attached to the body via a major artery and vein – it is then repositioned
and set into a recipient site.
Indications: tissue loss on any part of the body – often used to repair defects after traumatic injuries or surgical interventions,
also for facial reconstructions after skin cancer excision.
Can be Local Flap (tissue is freed and rotated to move to and adjacent area to cover the defect but remains attached at the base)
or Free Flap (tissue from another area of the body is detached and transplanted to recipient site and the blood supply is
surgically reconnected - microsurgical technique).
Flap classification according to composition: Cutaneous (blood supply originates from either musculocutaneous or
septocutaneous artery); Fasciocutaneous (flap contains the fascia and is thus more circulatory enriched and insures preservation
of skin circulation); Muscle and musculocutaneous (consists of muscle and overlying subcutaneous tissue and skin – muscle flaps
mainly used in deep defects or to bring back lost muscle function).

83. Benign and malignant skin tumors, malignant melanoma

Bening skin tumors are non-cancerous skin growths. Include:

- Hemangiomas: most common acquired cutaneous vascular anomaly. Red dome-shaped papules.
- Hypertrophic scars: high fibroblast proliferation and collagen production as excessive skin tissue response to penetrating
trauma. Does not grow beyond the boundaries of the original lesion.
- Keloid scars: skin lesions caused by high fibroblast proliferation and collagen production as excessive tissue response to
typically small skin injuries. Grows beyond the boundaries of original lesion.
- Warts: related to HPV. Verruca vulgaris (common), Verruca plana (flat), verruca plantaris (plantar).
- Seborrheic keratosis: common benign skin lesion of elderly. Benign growth of immature keratinocytes.
- Dermatofibromas — Fitzpatrick’s sign (pinching —> dimple)
- Nevi — Mongolian spot, Becker nevus, spitz nevus, melanocytic nevus, dysplastic nevus (atypical mole)
- Lipoma — common benign tumor of subcutaneous soft-tissue, made up of mature fat cells. Skin tags.

Malignant skin tumors

1) Squamous cell carcinoma: 2nd mc skin cancer. It occurs because of malignant transformation of keratinocytes in the
stratum spinosum (prickle cell layer) of the epidermis. Rf: exposure to sunlight, chemical carcinogens, precancerous
lesions of skin (e.g. actinic keratosis), and sites of skin damage (e.g. scars, burns, ulcers). Classical presentation is a
painless, non-healing bleeding ulcer with everted edges, but may present as plaques, nodules. Most commonly on face;
typical location lower lip.
2) Basal cell carcinoma: most common malignant skin tumor, primarily affects people with light skin. Rf: excessive sun
exposure, chemical - genetic factors. BCC is characterized by slowly growing nodules with a classic «pearly»
appearance, which tend to ulcerate during the course. Tx: excision, no MTS.
3) Malignant melanoma: responsible for most cancer-deaths due to skin tumors, highly malignant arise from
melanocytes. Rf: UV radiation, age, family history. Symptoms: pruritus, persistent bleeding skin lesion. Examine skin
with ABCDE criteria - Asymmetry, Border (irregular), Color (changes in pigmentation), Diameter >6mm, Evolving (new
lesion or changes in size, shape).
Dg for all: Dermoscopy, full thickness excisional biopsy. Staging USG or MRI.
Tx for all: surgical excision and resection with safety margin (depending on stage 1-2 cm) – secondary excision may be
necessary after diagnosis, Mohs micrographic surgery (layer by layer is removed until no more cancer cells are found). Medical
Tx for malignant melanoma: BRAF kinase inhibitor (vemurafenib) in metastatic or unresectable melanomas.
84. Cleft lip and palate, aesthetic surgery

Most common congenital orofacial deformities.

Etiology: Genetic predisposition: family history, multifactorial inheritance pattern; part of chromosomal abnormalities (Edwards,
Patau). Environmental factors: nicotine, alcohol, antiepileptics, MTX, excess vit. A.
Pathophysiology
- Lip: partial or total failure of primary palate formation (6-7 th week), failed fusion of maxillary prominence and
medial nasal prominences in the midline.
- Palate: failed formation of secondary palate (8-12 th week) failed fusion of either lateral palatine processes or of
the palatine shelves with the nasal septum and/or primary palate.
Symptoms:
- Lip: incomplete (cleft on upper lip, doesn’t extend to nostril) complete (Extends into nostril, more common with
cleft palate), microform (mild, incomplete cleft).
- Palate: incomplete (only of the secondary palate), complete (entire hard palate, soft palate and uvula, often
associated with cleft lip), submucosal (muscular and/or bony palatal defect masked by intact palatine mucosa).
Feeding difficulties, speech difficulties, dentition defects, hearing loss (recurrent or persistent otitis media with
effusion).
Diagnosis: Prenatal (prenatal USG after 12 th week), amniocentesis (karyotyping) Postnatal: clinical.
Treatment: Conservative before surgery (proper feeding, nasoalveolar molding (prosthesis), nasal stent, lip taping, lip adhesions.
Surgical: Cleft lip repair (cheiloplasty): at 3 months – first cleft lip surgery, then cleft palate. Tympanostomy tubes placed at same
sitting. Cleft palate repair (palatoplasty): 6-9 months (further surgery often required).

85. Traumatic injuries of the liver and spleen

In the awake, alert, responsive patient with isolated abdominal injury, physical examination and history are very helpful in
predicting the presence of significant visceral injury. For this reason, additional laboratory, radiographic, and invasive procedure
have a limited role as adjuncts to physical examination in the patients with isolated abdominal injuries. The accuracy of CT scans
in abdominal trauma has improved with experience and an understanding of what constitutes abnormal finding.
The spleen is the most commonly injured intraabdominal organ. Splenic injury must therefore be suspected in any patient with
blunt abdominal trauma, particularly if associated with left lower rib fracture. The diagnosis is often suspected on physical
examination, but generally confirmed by USG or abdominal CT scan, and rarely by diagnostic peritoneal lavage. Although
splenectomy has long been considered the only option for splenic injuries, trauma surgeons must now also consider splenic
repair or nonoperative management as viable options in selected patients. These new options have been fostered by the
recognition of the rare but highly lethal syndrome of overwhelming post-splenectomy sepsis.

The liver is the second most injured organ following blunt trauma and is the most injured parenchymal organ following
penetrating trauma. 50 % of all liver injuries are nonbleeding at the time of initial exploration, and an additional 20% can by
managed either by direct suture or by hemostatic agents such as microfibrillar collagen. Nonetheless, severe liver injuries are
difficult to manage and are responsible for the high overall liver injury mortality. There are seven basic techniques that are
useful in operative management: suture, drainage, inflow occlusion, resection, hepatic artery ligation, packing, and atriocaval
shunting. The anatomy of the liver and the distribution of injuries permit the separation of the roles of these approaches.
86. Traumatic duodenum and pancreas injury

Duodenal injuries are relatively rare. Approximately one-quarter of duodenal injuries are the result of penetrating trauma, and
three-quarters are the results of blunt injuries in Middle Europe. The most common mechanism producing blunt injury is a
steering wheel blow to the abdomen in an unrestrained automobile driver in adults or after compression on a bike directional
frame in children. A duodenal hematoma usually does not require operative intervention. Initial diagnosis after blunt trauma is
difficult because clinical signs on the abdomen is pure. Mortality was about 50 per cent among the patients in whom the
diagnosis rupture was delayed more than 24 hours. Early suspicion of retroperitoneal duodenal rupture is best confirmed or
(Contrast
media
excluded by Gastrografin upper gastrointestinal series or abdominal CT with oral and intravenous contrast enhancement. About
80 percent of duodenal wounds can be primarily repaired safely.

Pancreatic trauma is relatively uncommon, representing less than 15 percent of all abdominal injuries. Although the pancreas is
relatively protected in the retroperitoneum, the increasing frequency of high-speed motor vehicle accidents and gunshot
wounds contribute to an increased incidence of pancreatic injury. CT can be helpful in diagnosing pancreatic injury The mortality
rates from several large series of pancreatic trauma patients are 10 to 25 percent. Major complications such as pseudocysts,
abscesses, hemorrhage, or pancreatic fistulas develop in 30 to 40 percent of patients surviving their initial injury.

87. Injury of tissues around joints, joint dislocation (luxatio)

Joint sprain: ligaments surrounding joint are over-extended or pushed beyond their range of movement; this often happens as a
result of stretching. Common sites: ankle, shoulder and wrist sprains.
Symptoms: pain, swelling in the affected area as well as bruising and decreased movement around the joint.
Diagnosis: X-ray, MRI. Treatment: ice, NSAIDs, rest, compression and elevation to decrease swelling.
Grading
- Grade 1 Sprain: few torn ligamentous fibers, mild joint pain reproduced on local palpation, firm endpoint with minimal
laxity, no joint instability.
- Grade 2 Sprain: increased joint instability, joint swelling and pain, firm endpoint with some joint laxity, decreased
function.
- Grade 3 Sprain: complete ligamentous tear, minimal/no endpoint, gross joint laxity, unstable joint.

Luxation / dislocation: abnormal separation in the joint, where 2 or more bones meet (Subluxation = partial separation). Can
damage ligaments-tendons-muscles-nerves.
- Shoulder = Most common dislocated joint. 95% = anterior dislocation. 3% = post. Rare = super/infer.
- Elbow = Posterior dislocation 90%.
- Wrist = Lunate and perilunate dislocation most common.
- Finger = Interphalangeal (IP) / metacarpophalangeal (MCP) joint dislocations.
- Hip = Posterior and anterior dislocations.
- Knee = Patellar dislocation.
- Foot = Lisfranc injury / 5th metatarsal.
Etiology: Sudden trauma such as fall / blow. Hyper Mobile joints also dislocate frequently.
Clinical presentation: Intense Pain. Joint instability. Deformity of joint area. Reduced muscle strength. Bruising / redness of joint
area. Difficulty moving joint.
Diagnosis: History. Physical – passive & active movement range, may feel out of place. X Ray: confirms bones are out of place &
shows fractures. CT / MRI.
Treatment: Reduction of dislocation. May be possible directly / need local anesthetics / general surgery. Support in position to
allow healing (sling). Splint straight joints. Bandage complex joints. Physiotherapy to strengthen ligaments and muscles nearby.
Repeated dislocations: May need surgery to correct joint support (shoulder capsule).
88. Muscle and tendon injuries

Muscle injury
- Common problem is bruising, may cause pain but doesn’t require treatment if no other injuries.
- Crush injury can cause acute tubular necrosis, hyperkalemia (arrythmias, HF),
- Swelling and edema pose risks of compartment syndrome.
- Minor injuries require RICE (Rest+Ice+compression+Elevation) for discomfort and healing.

Tendon injury = tendinopathy: usually caused by long term of overuse that result in deterioration of tendon without
inflammation (tendonitis = inflammation: responds well to anti-inflamm tx).
Risk factors: aging. Certain jobs, sports. DM, arthritis, gout.
Symptoms: pain, stiffness, and loss of strength. Area may be tender, red, warm, swollen (inflamm). Diagnosis: History and
physical examination. X-ray, USG, or MRI.
Tx: long, focused on improving strength & rebuilding tissue.
Tendonitis: rest, ice, compression, and elevation. NSAID
Tendinopathy: characterized by swelling, tenderness and gradual loss of tendon functions, collagen becomes disorganized. It
takes 2-6m to heal or become chronic.
Methods of rehab: ultrasound, medications, massage, bracing or splinting (take off pressure from tendon). Last stage:
strengthening and flexibility exercises.
Specific types: Tennis Elbow (Lateral Epicondylitis). Golfer's Elbow (Medial Epicondylitis). Achilles Tendinitis. Wrist Tendinitis.
Carpal Tunnel Syndrome.

89. Pneumothorax – types and therapy

The presence of air in the pleural space with secondary lung collapse. Can be divided into:
*Spontaneous or acquired (by trauma/invasive procedures). Spontaneous pneumothorax further divided to primary/secondary.

Primary spontaneous pneumothorax: In young, tall, male smokers. MC in right side (unilateral). Rupture of small subpleural
blebs (collections of air < 2cm), at apex of the upper lobe / apical segment of the lower lobe. Rest of lung parenchyma is normal.
Clinical: dyspnea, angina, cough & tachyp, ↓ chest wall movement, percussion (hyper resonant), auscultation (absent breath.
Diagnosis: chest x-Ray. CT: size of pneumothorax & asses remaining lung parenchyma & contralateral lung.
Treatment: Conservative: Observation (small; less than 20% pneumothorax). Needle aspiration. Tube thoracostomy (5th
intercostal space in midaxillary line). ± chemical pleurodesis. Surgery:
First episode: Prolonged air leak, tension pneumothorax, hemothorax, bilateral pneumothorax, residual collapse of lung after
conservative treatment, 100% pneumothorax, pneumothorax secondary to giant bulla, previous contralateral pneumonectomy
(surgical removal of part / all lung).
Recurrent pneumothorax: The aim is to resect the blebs / bullae & obliterate the pleural space with adhesions using chemical /
abrasion pleurodesis / parietal pleurectomy (apical / full). Performed through a minithoracotomy, axillary incision /
thoracoscopically.
Complications: Tension pneumothorax. Pneumomediastinum. Hemopneumothorax. Recurrent pneumoth.

Secondary spontaneous pneumothorax:

Etiology: Cystic fibrosis, COPD, asthma. Interstitial lung disease. Infections: AIDS, mycobacterial, Pneumocystis carinii, bacterial,
parasitic, mycotic. Malignancy: bronchogenic carcinoma, metastatic lung cancer (sarcoma & lymphoma). Collagen diseases,
Ehlers-Danlos syndrome, histiocytosis X, scleroderma, lymphangioleiomyomatosis, Marfan's syndrome. Rupture of the
esophagus.
Cystic fibrosis (CF): Remember these patients may be candidates for future lung transplantation when considering management
options. Full parietal pleurectomy is a contraindication for lung transplantation.
Chronic obstructive airway disease: Patients often have very little pulmonary reserve. They may not tolerate surgical
management & single lung ventilation. Treatment: tube thoracoscopy & chemical pleurodesis / long- term tube thoracoscopy.
Infection: Cavitating pulmonary lesions rupture into pleural space.
AIDS: Usually secondary to Pneumocystis carinii & pneumonia. May be the presenting feature of AIDS. Most effective treatment
is surgical.
Primary spontaneous pneumomediastinum: Uncommon. More frequent in men. Occurs following exertion / increased intra-
abdominal pressure. Commonly associated with cocaine, marijuana usage. It is caused by rupture of alveolar sacs with air
tracking along the peribronchial & perivascular spaces into the neck.
Clinical Presentation: Sudden onset of chest pain, dyspnea, dysphagia, cough. Subcutaneous emphysema over neck & chest wall
(Hamman's sign). Chest x Ray confirms diagnosis.
Treatment: Conservative. Emergency surgical decompression very rare.
90. Tracheostomy – indications, tracheal stenosis

Tracheostomy is a surgical procedure to create an opening through the neck into the trachea. A tube is usually placed through
this opening to provide an airway & remove secretion from the lungs. This tube is called a tracheostomy tube / trach tube.
Description: General anesthesia is used unless the situation is critical. If that happens, a numbing agent is placed into the area to
reduce pain during the procedure. The surgeon creates an opening into the trachea (vertical midline or transverse incision 1cm
below cricoid cartilage), 2nd – 3rd tracheal cartilages are exposed and incised, then inserts the tracheostomy tube and tracheal
balloon is inflated to prevent air leaking.
Indication: large object blocking the airway, inability to breathe on your own, inherited abnormality of the larynx / trachea,
inhaled harmful material (smoke, steam / other toxic gases) that swell & block the airway, cancer of the neck (can affect
breathing), paralysis of the muscles that affect swallowing, severe neck / mouth injuries, surgery around the voicebox (larynx)
that prevents normal breathing & swallowing. (Acute respiratory distress-covid).
Complications: from anesthesia (problems breathing, reactions to medications). Bleeding, infection, nerve injury (paralysis),
scarring, damage to the thyroid gland, erosion of the trachea, puncture of the lung, lung collapse, scar tissue in the trachea that
causes pain / trouble breathing.

Tracheal stenosis: Abnormal narrowing of the central air passageways. This may occur at the level of the larynx, trachea, carina /
main bronchi.
Etiology: trauma (most common cause – after external or internal one, after endotracheal intubation), chronic inflammatory
diseases (amyloidosis, sarcoidosis, relapsing polychondritis), benign neoplasm (eg, respiratory papillomatosis), malignant
neoplasm (eg, primary tracheal, secondary invasion, metastatic), and collagen vascular diseases (eg, tracheopathia osteoplastica,
Wegener granulomatosis).
Clinical features: Worsening breathlessness (dyspnea). Added respiratory sounds (stridor, wheezing).
Treatment: Tracheal dilation using rigid bronchoscope – temporarily enlarges airway, few days to 6 months. Laser surgery.
Tracheal resection and reconstruction- best alternative.

91. Pleural exudates from surgical point of view

Pleural effusion: excessive accumulation of fluid in the pleural space.

Types
- Transudate: extravascular fluid with protein-poor ultrafiltrate of plasma due to alterations ins systemic hydrostatic
colloid pressure – caused by liver cirrhosis, CHF, nephrotic syndrome, hypoproteinemia, peritoneal dialysis). Low specific
gravity (<1.012).
- Exudate: extravascular fluid with protein content caused by changes in capillary permeability due to inflammation or
infiltration of the pleura. High specific gravity (>1.020).

Etiology: malignancy (mesothelioma, lung cancer), infection (viral, bacterial, parasitic), infarction, trauma, SLE, RA, sarcoidosis,
Uremia.
Clinical presentation: Small effusions often asymptomatic. Larger effusions cause cough, pleuritic pain, dyspnea. Decreased
ipsilateral chest expansion, dullness to percussion, decreased breath sounds over the effusion on auscultation, crepitations may
be heard.
Diagnosis: thoracocentesis (pleural aspiration cytology) either diagnostic and therapeutic. Chest radiograph, US, CT to show
pleural effusions and lesions.

Treatment: drainage is ineffective in transudative effusion due to reaccumulating, underlying condition needs to be resolved.
Exudative often need more aggressive approach: surgical drainage – malignant are often massive and symptomatic, bloody.
Tube thoracostomy. Surgical pleurectomy (open or thoracoscopic). Pleuroperitoneal shunt.
Complications: Infection and empyema (pus in pleural space). Treatment failure with recurrence of pleural effusion. Damage to
underlying lung parenchyma, leading to prolonged air leak and bronchoalveolar air leak.
92. Thoracic empyema

Empyema: accumulation of pus in the pleural space, commonly after pneumonia.

Stage I. Acute exudative phase: occurs 2–5 days after a pneumonia. Accumulation of fluid with low cellular content and
viscosity. Characterized by low WCC, LDH, and glucose, and a normal pH. Can be successfully treated with antibiotics only.

Stage II. Fibrinopurulent phase: occurs 5–14 days after a pneumonia. Turbid or purulent fluid with heavy fibrin deposits.
Appearance of simple loculations and septations. May have bacterial invasions and high numbers of PMNs and lymphocytes.
Characterized by low pH and glucose and increased LDH. Antibiotics and chest tube drainage is required, may need video
assisted thoracoscopic surgery (VATS) decortication.

Stage III. Chronic organizing phase: Lung trapping, unable to expand, by collagen visceral and parietal pleural peel with ingrowth
of fibroblast and capillaries. Antibiotics and aggressive decortications, generally by thoracotomy. Bacteriology.
Etiology: Pneumonia (Streptococcus, pneumococcus, gram- bacteria, TB), Hematological spread, trauma, surgery.
Clinical presentation: Cough, fever, sputum production, chest pain, dyspnea, sweats. In chronic phase – weakness, low-grade
fever and weight loss.
Diagnosis: Chest X – Ray shows pleural effusion. Thoracocentesis. CT – complicated effusion, abscesses.
Treatment: Treat underlying disease, broad spectrum ATB, VATS – Drainage, thoracotomy, thoracostomy (chest tube
placement), if lung doesn’t expand decortication (removing the pleura).

93. Lung abscess

Lung abscess is most commonly a complication of necrotizing pneumonia secondary to aspiration and is, therefore, located in
segments that are dependent in the supine position (i.e., posterior segments of the upper lobes and superior segments of the
lower lobes). Other causes are bronchial obstruction, seeding from systemic sepsis, pulmonary trauma, and direct extension
from extra parenchymal infection.
Patients present with fever, appear chronically ill, and describe recent onset of foul-smelling sputum production. Massive
hemoptysis can occur.
Diagnosis is based on chest radiograph and CT. Bronchoscopy,
Treatment: conservative – ATB (clindamycin IV), for MRSA use Linezolid.
Surgery - chest tube drainage or surgical resection of lung abscess with surrounding tissue (Lobectomy).
94. Tumors of the lungs

Most common cancer related to cancer deaths in both genders – most common in right upper lobe.
Tumors arising from respiratory epithelium (bronchi, bronchioles and alveoli). 95% are bronchial carcinomas.
Risk factors: Tobacco smoking. Occupational: asbestos, arsenic, nickel & polycyclic aromatic hydrocarbons (PAH). Ionizing
radiation. COPD, genetics.

Small cell carcinoma (20%)

Poorly differentiated, highly malignant, neuroendocrine tumor, high metastasis rate, mainly to brain, liver & bones. Shows a
wide variety of paraneoplastic syndromes (Neuroendocrine), due to its production of peptide hormones (ACTH, arginin
vasopressin, atrial natriuretic factor, & gastrin- releasing peptide).
Treatment: chemotherapy (cysplastin + etoposin) & palliative radiotherapy. Median survival 9 - 18m.

Non-small cell carcinomas (80%)

- Squamous cell carcinoma: morphologically identical to other small cell carcinomas (head & neck). Found mostly in men
& highly correlated with smoking. Typically occurs centrally.
- Large cell carcinoma: tends to occur peripherally & defined as poorly differentiated carcinoma of the lung composed of
larger malignant cells without evidence of squamous, glandular differentiation / features of small cell carcinoma.
- Adenocarcinoma: occurs mainly in the periphery of the lung & is the lung cancer occurring in the "never smokers". Seen
more in women. Tumor cells metastasize widely & earlier than in squamous cell carcinoma, to bone, liver & brain.
Clinical presentation: cough, chest pain, dyspnea, hemoptysis, weight loss.
Complications: airway obstruction, pleural effusion (infiltration), hoarseness, dysphagia, rib destruction, pericarditis, cardiac
tamponade.
Diagnosis: chest X-ray, CT, bronchoscopy, fine needle aspiration, biopsy, cytology (of sputum).
Treatment: surgery (solitary nodule, lobulectomy, lobectomy), radiotherapy, chemotherapy (cisplastin + another agent) &
palliative (maintenance of airways).

95. Mediastinal tumors

Mediastinum structures that are bound by the thoracic inlet, diaphragm, sternum, vertebral bodies & pleura. May be divided
into 3 compartments: anterior upper, middle & posterior.
Etiology
- Anterior compartment (sternum to anterior border of pericardium): more likely malignant.
Lymphoma, lipoma, Thymoma, pericardial cyst.
- Middle compartment (anterior to posterior pericardium): Pericardial cyst, bronchogenic cyst / tumor, lymphoma, lymph
node enlargement, aortic aneurysm.
- Posterior compartment (posterior pericardium to vertebral column): Neurogenic tumors, meningocele, enteric cysts,
lymphomas, diaphragmatic hernias, esophageal tumor, aortic aneurysm.
Clinical presentation: 50% asymptomatic (usually benign). When symptomatic ~ 50% are malignant.
Chest pain, cough, dyspnea, recurrent respiratory infections. Hoarseness, dysphagia, Horner
CPtosis,
miosis,
syndrome, facial
anhidrosis
/ upper extremity edema (SVC compression). Paraneoplastic syndromes (myasthenia gravis - thymomas). Diagnosis: CXR. CT
Sup. Vena. Cava

with contrast. MRI (for neurogenic tumors). USG (best for assessment of structures near the heart & pericardium). Radionuclide
scanning 131 Iodine (for thyroid), Gallium (for lymphoma). Biochemical studies: thyroid function, serum calcium, phosphate,
parathyroid hormones, AFP, beta-hCG. Biopsy (mediastinoscopy, percutaneous needle aspiration).
Treatment: Decide if the lesion should be excised (most isolated benign masses should be removed). Needle aspiration of
suspected benign, cystic lesion. Resection via minimally invasive video assisted procedures (bronchogenic cysts, localized
neurogenic tumors). Exploration via sternotomy/thoracotomy.
Diagnostic biopsy rather than major operation if mass is likely to be a lymphoma, germ cell tumor / unresectable, invasive
malignancy. Post-op radiotherapy / chemotherapy if malignant.
96. Principles of the lung transplantation

Transplantation is often combined heart and lungs. Lungs alone is difficult, heart often to another donor (domino procedure).
Possible single lungs operations exist but infection level in other lung matters.
Candidates for lung transplantation have irreversible end-stage disease for which there is no other therapy, are oxygen
dependent and are likely to die of their disease within 12-18 months.
Immunosuppressive management of lung transplant recipients is based on calcineurin inhibitors.
The addition of an omental wrap to bronchial anastomosis and the avoidance of steroids during first 3 weeks has allowed
bronchial healing and clinical success.
Postoperative management focuses on prevention of sepsis and detection of treatment of rejection - bronchoscopy and
transbronchial biopsy are used to diagnose lung transplant rejection.
Indications
- Cystic Fibrosis (3rd most common). Genetic defect in chloride transport over cell membranes. Thick mucus & secretions
in ducts (lungs, pancreas). Bacteria multiply & cause chronic infect. High risk of mortality.
- Advanced stage pulmonary disease - COPD (most common). Forced expiratory volume in 1 second (FEV1) < 30%
associated 60-80% 2y survival.
- Restrictive lung disease – Pulmonary fibrosis. UIP-type median survival of approximately 2.5 - 3.5y from the time of
diagnosis. Forced vital capacity < 60% is predictive of increased mortality. Diffusing capacity of lung for carbon monoxide.
- Primary pulmonary Hypertension: survival is 2.8y. Poor survival is NYHA class III/IV, elevated mean right atrial pressure,
elevated mean pulmonary arterial pressure and decreased cardiac index and reduced diffusion. Mean pulmonary arterial
pressure > 85 mm Hg is associated to survival < 12m. Transplant is indicated only if the patient cannot tolerate / fails
prostacyclin therapy.
- Alpha1-Anti Trypsin Deficiency: relatively common genetic condition, often undiagnosed. Predisposition to obstructive
lung disease and liver disease. Primary manifestation is paracinar emphysema, later leads to COPD. Slowly progressive
dyspnea is primary symptom. + cough, wheezing.

Referral guidelines for transplantation:

- Life expectancy is not predicted to exceed 24-36m despite optimal-maximal medical management
- Class III and IV New York Heart Association (NYHA) symptoms
- Have a stable nutritional status. Be motivated for rehabilitation
- Have an intact psychological support system.
- When they have < 50% chance of surviving 24-36m & transplantation is expected to confer a survival advantage. Poor
quality of life is an additional consideration.
NYHA Classification:
- Class I: Symptoms with more than ordinary activity. Class II: Symptoms with ordinary activity.
- Class III: Symptoms with minimal activity. Class IIIa: No Dyspnea at rest. Class IIIb: Dyspnea at rest.
- Class IV: Symptoms at rest.
Contraindications:
- Malignancy in the last 2 years (5-y disease-free interval is prudent).
- Non-curable chronic extrapulmonary infection (chronic active hepatitis B/C /HIV)
- Untreatable advanced dysfunction of another major organ system, including Cr-clear < 50mL/min.
- Poor rehabilitation potential.
- Significant psychosocial problems (smoking, drinking, drugs). Steroids over 20ml/kg/d.

97. Esophageal tumors

Squamous cell carcinoma most common type worldwide, adenocarcinoma frequent in patients with GERD (squamous
epithelium is replaced with metaplastic columnar cell).
Risk factors: smoking, chronic alcohol exposure, poor oral hygiene, chronic consumption of hot liquids/foods, nutritional
deficiencies, GERD, achalasia, Barrett’s esophagus.
Symptoms: Dysphagia is most common, initially for solids but eventually progress to liquids; weight loss in more than 50% of
patients, pain when swallowing, hoarseness (left recurrent laryngeal nerve), pain (due to metastases), retrosternal pain,
heartburn, regurgitation.
Diagnosis: Barium swallow x-ray show location and extend, irregular intraluminal mass or stricture – endoscopy with biopsy; CT
for staging; bronchoscopy to rule out invasion of tracheobronchial tree, endo USG.
Treatment: resection – esophagectomy: if no spread is evident to structures next to the esophagus, no distant metastases,
patient is fit from respiratory and cardiovascular standpoint. Continuity made by either stomach or colon. Most patients already
have lymph node metastases, poor 5-year survival – neoadjuvant chemo and radiation with following surgery. Non operative –
palliative chemo, insertion of stent to keep lumen open, palliative radiation (dysphagia). Laser/Photodynamic therapy for
adenocarcinoma.
98. Injuries of retroperitoneum

Duodenal injury: relatively rare. Etiology: May occur by blunt / penetrating trauma. Isolated injury is unusual.
Duodenal hematoma usually does not require operative treatment. Duodenal rupture has high mortality if not treated within 24
hours, best diagnosed by Gastrografin upper gastrointestinal series or abdominal CT.
Diagnosis: not always obvious, CT (localized air / extravasation). Laparotomy.
Tx: Surgical management depends on injury degree. Suture and drainage following local tissue debridement.

Pancreatic injury: pancreas lies deep within the abdominal cavity and is well protected by surrounding structures, such that
direct injury is uncommon. Etiology: penetrating trauma, epigastric crush-type injuries.
Diagnosis: Not always obvious. Laparotomy, visible hematoma around the pancreas, CT. Treatment:
- Simple injuries without duct involvement may be managed by local tissue debridement and drainage.
- Distal pancreatectomy is used for other injuries in the tail and body, with ligation of pancreatic duct.
- More complex injuries may require resection.
Complications: Fistula formation. Acute pancreatitis. Pseudo cyst formation. Intra-abdominal abscess.

99. Anuria and acute urinary retention – classification, causes, diagnosis

Anuria: condition characterized by urine output < 50 ml/day (no passage).

Etiology: shock, kidney (function) failure, urinary tract outlet obstruction (stones, tumors), end stage renal disease, acute renal
failure
Clinical presentation: Often associated with lack of appetite, weakness, nausea & vomiting.
Dg: USG (kidney, bladder); Labs (Crea, eGFR, BUN, Potassium); CT; retrograde pyelography, cystoscopy (malignancy?).
Treatment: according to cause - stone removal, resection of malignancy, stents.

Acute urinary retention: obstructive etiologies more common (BPH) – more common in men.
Symptoms: sudden onset, painful inability to void, suprapubic discomfort/pain, palpable bladder, patient is restless and
distressed. Chronic urinary retention: functional or gradual progressive mechanical obstruction (BPH, cancer). Symptoms:
painless incomplete voiding, bladder may be palpable, may present with overflow incontinence and nocturnal enuresis.
Diagnosis for both: abdominal and pelvic exams (discharge, stenosis – vaginal exam for pelvic mass, DRE). Neurological exams
(spinal cord compression, stroke, MS, diabetic neuropathy).
I Benign prostatic hyperplasia (BPH)
Not in the question but you need to know -> BPH: benign glandular and stromal hyperplasia of the transitional zone of the
prostate. Etiology: hormonal factors (testosterone, estrogen) genetics. Symptoms: frequency, urgency, weak stream, hesitancy,
intermittent stream, straining, dribbling – DRE: smooth enlarged tender prostate, elastic texture.
Tx: medical: alpha blockers – tamsulosin, doxazosin; relaxation of smm of bladder neck (5-aplha reductase inhibitors –
finasteride); decrease prostate size (inhibits testosterone conversion); antimuscarinics decrease muscle tone/symptoms control
(oxybutynin).
Surgical: transurethral resection of the prostate – with monopolar or bipolar resectoscope. Prostatectomy if prostate >60g
(open, laparoscopic, robotic); laser enucleation.
100. Hematuria, hemoglobinuria, pyuria, chyluria – classification, diagnosis and treatment

Hematuria: RBC in the urine.

Etiology: BPH, UTI, urolithiasis, glomerulonephritis, polycystic kidney disease, malignancy
Diagnosis: gross hematuria can be seen by eye; microscopic hematuria can be diagnosed using dipstick.
Treatment: treat underlying cause – UTI with ATBs; BPH with alpha-blocker, resection of malignancy.
Stop active bleeding (cystoscopy – coagulation, irrigation).

Hemoglobinuria is a condition in which oxygen transport protein Hb is found in abnormally high concentrations in the urine.
Mainly caused by excessive intravascular hemolysis, in which large numbers of RBC are destroyed, thereby releasing free Hb into
the plasma. Excess Hb is filtered by the kidneys, which excrete it into the urine, giving urine a purple color. Hemoglobinuria can
lead to acute tubular necrosis which is an uncommon cause of a death of uni-traumatic patients recovering in the ICU.
Etiology: Acute glomerulonephritis, Burns, Renal cancer, Malaria, Paroxysmal nocturnal hemoglobinuria, Microangiopathies (e.g.
HUS, TTP), Transfusion reactions, IgM autoimmune hemolytic anemia, G6PD deficiency, Pyelonephritis, Sickle cell anemia.
Diagnosis: medical history, blood - urine samples. Absence of urine RBC casts microscopically despite a positive dipstick test
suggests hemoglobinuria or myoglobinuria.

Pyuria is the condition of urine containing WBC or pus. Defined as the presence of 6-10 or more neutrophils per high power field
of unspun, voided mid-stream urine, it can be a sign of a bacterial UTI. Pyuria may be present in people with sepsis, or in older
people with pneumonia. Others additionally require discoloration, clouding or change in the smell of urine for pyuria to be
present. Without these additional features, there is said to be leukocyturia. Sterile pyuria is urine that contains WBC while
appearing sterile by standard culturing techniques. It is often caused by STI (gonorrhea), or viruses that will not grow in bacterial
cultures.
Etiology: side effect from some drugs (paracetamol), Kawasaki disease, genitourinary TBC, systemic or infectious disease, kidney
pathology. Diagnosis: Urinalysis culture. Treatment for pyuria depends on its cause.
Chyluria is the presence of chyle in urine stream, which results in urine appearing milky white. The condition is classified as
being either parasitic or nonparasitic. Chyluria's appearance is irregular and intermittent.
Etiology: Filariasis (parasite Wuchereria bancrofti) lead to obstruction of peripheral lymphatic vessels and increased pressure
within the vessels causing collateral flow of the lymph, redirecting the lymph flow from the intestinal lymphatic vessels into the
lymphatic vessels of the kidney and ureter. Because of obstruction, subsequent local inflammation leads to the dilation and
rupture of lymph vessels and development of urinary fistulae, which allows for the passage of WBC, fat, and fat-soluble vitamins
into the urine.
Treatment: low fat, high fluid diet; Medicines that inhibit cholesterol absorption in the small intestine, such as Ezetimibe, may be
effective. An anti-filarial drug (diethylcarbamazine) may be prescribed.
Severe damage to lymph channels may require surgery. Sclerotherapy with instillation of 1% of silver nitrate or povidone iodine
(2ml of 5% + 8ml distilled water).

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Chyle= a milky fluid containing fat droplets which drains from the lacteals of the small intestine into the lymphatic system during digestion.

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