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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1093_Библиотеки_им_академика_М_И_Перельмана.pdf
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Surgery

13

General surgery

13.1. Obstructive jaundice
13.2. Gallbladder disease
13.3. Splenic injury
13.4. Pancreatic disease
13.5. The acute abdomen
13.6. Acute appendicitis
13.7. Disorders of the small bowel
13.8. Intestinal obstruction
13.9. Ischaemic bowel
13.10. Diverticular disease
13.11. Tumours of the large bowel
13.12. Abdominal wall hernia
13.13. Lower gastrointestinal bleeding
13.14. Disorders of the rectum and anus
13.15. Investigations
13.1. Obstructive jaundice
Also known as cholestatic jaundice; occurs as a result of obstruction within the extrahepatic or occasionally intrahepatic biliary trees. Observed clinically when serum bilirubin is >30 µmol/l.
Causes of obstructive jaundice
Extrahepatic: gallstones, malignancy (head of the pancreas, cholangiocarcinoma), primary sclerosing cholangitis, strictures, pancreatitis
Intrahepatic: cirrhosis, primary biliary cirrhosis, drugs (e.g. phenothiazines, oestrogens), malignancy (e.g. liver metastases)
CLINICAL FEATURES (DEPEND ON CAUSE)
Jaundice, i.e. yellow pigmentation of skin, mucous membranes or cornea.
May be painless, or present with colicky RUQ pain, depending on cause.
Pruritis.
Weight loss (cachexia) and anorexia.
Ascites.
Dark urine and steatorrhoea (due to fat malabsorption).
Palpable gallbladder.
Courvoisier’s Law: ‘a palpable gallbladder (GB) and jaundice is unlikely to be due to gallstones (where the GB is shrunken and fibrotic)’; this usually indicates malignancy.
137
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
INVESTIGATIONS
Blood tests: FBC (WCC increased in infection), U&Es, Clotting, Glucose.
Liver function tests: increased ALP and GGT; raised (conjugated) bilirubin;
normal/decreased albumin. Urinalysis (for conjugated bilirubin).
Ultrasound: for calculi within gallbladder/duct, pancreatic mass, liver
metastases, and common bile duct (CBD) diameter (if >8 mm suggests obstruction). AXR: unlikely to be helpful (shows <10% of gallstones).
ERCP/MRCP +/– CT scan; liver biopsy may be necessary.
MANAGEMENT
Fluid resuscitation.
Analgesia: NSAIDs +/– pethidine (which relaxes the sphincter of Oddi); use
opiates cautiously in liver failure. Antibiotics if infection: (Gram –ve cover; Klebsiella, E. Coli, Enterococcus sp.
most commonly implicated pathogens). Correct coagulopathy (i.e. vitamin K or FFP).
Antihistamines for pruritis.
ERCP +/– stenting or sphincterotomy to relieve obstruction.
Importantly, treat the underlying cause, e.g. laparoscopic or open
cholecystectomy.
13.2. Gallbladder disease
PRESENTATION
Asymptomatic: i.e. incidental fi nding ( 85%).
Biliary colic: (80% gallstones are mixed; 15% are pure cholesterol; 5% are
pigmented stones).
Clinical features: recurrent, episodic colicky pain in RUQ, epigastrium or
right shoulder tip (referred T5–7 pain) due to impaction of the stone at the GB neck; precipitated by eating fatty foods, and worse on inspiration; often associated with nausea, vomiting and anorexia.
Acute cholecystitis:
as above, with fever. Murphy’s sign – pain on palpation of
the RUQ, which is worse on inspiration, usually positive.
Obstructive jaundice
Clinical features: jaundice, dark urine and steatorrhoea.
Ascending cholangitis: Charcot’s triad – fever/rigors, jaundice and RUQ pain.
GB perforation (can be free or localised, usually occurs at the fundus due to
gangrene of the GB) +/– peritonitis (seen with free perforation) +/– gallstone ileus (due to a localised perforation of the GB into the duodenum). Pancreatitis
Empyema, mucocele: due to gallstones impacting in Hartmann’s pouch leading
.
to obstruction to mucus flow and pain. Clinical features: palpable RUQ mass.
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Predisposing factors to gallstones
Obesity
Terminal ileum disease: e.g. Crohn’s due to malabsorption of bile salts
Cirrhosis
Haemolytic anaemia: e.g. sickle cell, hereditary spherocytosis (classically, pigmented stones)
Infections of the biliary tree: e.g. E. Coli, Klebsiella sp, Streptococcus sp.
Drugs: e.g. OCP, clofibrate, thiazide diuretics, long-term TPN
GENERAL SURGERY
INVESTIGATIONS
Blood tests: FBC (WCC increased in cholecystitis, cholangitis, pancreatitis),
U&Es, clotting, LFTs, amylase (to exclude acute pancreatitis). Blood cultures.
Urinalysis (for conjugated bilirubin).
Erect CXR: to exclude perforated viscus.
AXR: 10% gallstones radio-opaque; aerobilia (air within the biliary tree seen
with gallstone ileus). Ultrasound.
● ◗ Gallstones – sensitive for 95% GB stones and 80% CBD stones.
Thickened GB wall and pericholecystic fluid diagnostic of acute cholecystitis.
◗ ◗ CBD dilation >8 mm suggests obstruction, i.e. stone/stricture.
MANAGEMENT
Fluid resuscitation.
Intravenous antibiotics (if evidence of infection).
Analgesia.
Correct coagulopathy.
Dietary advice and weight loss.
Interventional options. ERCP/PTC (for CBD stones) +/– sphincterotomy +/– stenting (usually of a
malignant stricture). Open stone removal with T-tube insertion.
◗ ◗ Delayed laparoscopic (or open) cholecystectomy – timing usually about six
weeks post-acute episode, performed acutely in some centres.
Other less common options.
● ◗ Bile salts (however 50% recurrence of gallstones). Extracorporeal shock wave lithotripsy (ESWL).
Complications of laparoscopic cholecystectomy
General
Associated with general anaesthesic (GA) or surgery in general, e.g. LRTI, PE, DVT
Specifi c
Damage to viscera (e.g. bowel or blood vessels – leading to bleeding) on port insertion
Complications of pneumoperitoneum: e.g. carbon dioxide embolus
Infection (e.g. wound)
Incisional or port-site hernia
CBD injury, bile leak
Conversion to an open procedure
Other diseases of the biliary system
Common bile duct/hepatic duct stricture
Clinical features: obstructive jaundice. Causes: iatrogenic; sclerosing cholangitis.
Gallbladder carcinoma
Clinical features: RUQ pain; jaundice; ascites; weight loss and anorexia. Poor prognosis (4% survival at fi ve years).
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ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Cholangiocarcinoma
Associated with CBD stones, UC and sclerosing cholangitis. Clinical features are similar to that of gallbladder carcinoma.
Choledochal cysts
Congenital; can lead to pancreatobiliary reflux. Clinical features: jaundice, RUQ pain and mass.
13.3. Splenic injury
Usually due to trauma – blunt or penetrating (Remember the spleen underlies the T9–11 ribs), or iatrogenic; spontaneous rupture can occur in splenomegaly.
CLINICAL FEATURES
Left shoulder tip (referred) pain due to diaphragmatic irritation by blood/
haematoma. Shock (hypotension, tachycardia, cold, clammy peripheries).
Tenderness or peritonism in the LUQ/fl ank.
LUQ/fl ank bruising.
Splenomegaly (NB: the spleen enlarges below the left costal margin towards the
umbilicus; moves downwards with inspiration; has a palpable notch inferiorly and is dull to percussion unlike an enlarged left kidney). Regional lymph nodes and liver should be examined for enlargement.
INVESTIGATIONS
Blood tests: urgent clotting, FBC, blood film, U&Es, LFTs, cross match six units
of blood. CXR: for rib fractures.
AXR: look for a displaced gastric bubble, soft tissue shadowing.
CT scan with contrast (diagnostic).
MANAGEMENT
Fluid resuscitation.
Admit and observe in cases of trauma.
Splenectomy is indicated in cases of:
rupture malignancy haematological disorders.
Lifelong antibiotic cover post-splenectomy is controversial; vaccination against
pnemococcus is however required.
COMPLICATIONS OF SPLENECTOMY
Bleeding +/– shock.
Thrombocytosis (risk DVT, PE; consider Aspirin).
Sepsis, LRTI (atelectasis) + subphrenic abscess.
13.4. Pancreatic disease
Acute pancreatitis
Acute inflammation of the pancreas. Peak incidence: 40–50 years. Men and women equally affected.
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GENERAL SURGERY
Causes of acute pancreatitis
The classic mnemonic is ‘GET SMASHED’ but note that 15% are idiopathic
Gallstones (45%)
Ethanol (25%)
Other causes are rare:
Trauma, post renal or cardiac transplant; Steroids; Mumps; Autoimmune; Scorpion venom (rare!); Hyperlipidaemia, hypercalcaemia; ERCP (4%); Drugs, e.g. thiazide diuretics, fibrates
CLINICAL FEATURES
Epigastric pain radiating to the back with associated nausea, vomiting, anorexia
+/– obstructive jaundice. Dehydration.
Tenderness +/– guarding in the epigastrium + decreased/absent bowel sounds.
Grey-Turner’s sign: blood tracking into the left paracolic gutter (fl ank).
Cullen’s sign: periumbilical echymoses.
INVESTIGATIONS
Blood tests: FBC (WCC increased in inflammation), CRP (prognostic indicator
in first 48 hours and useful for monitoring disease), U&Es, LFTs, serum glucose (hyperglycaemia due to destruction of β-islet cells), clotting, serum calcium, arterial blood gas. Amylase >1000 U/l or 4× normal is diagnostic; falls after 24 hours; serum
lipase. Blood cultures.
Erect CXR: to exclude perforation, ARDS, effusion.
AXR: for loss of psoas shadow, ileus, calcified head of pancreas (suggests
chronic pathology). Ultrasound gallbladder: for gallstones (cause).
CT abdomen: for necrosis and haemorrhage.
Disease is scored as mild, moderate or severe using predictive criteria, e.g.
Ranson’s or the modified Glasgow criteria.
Glasgow scoring system (mnemonic = ‘PANCREAS’)
P – PaO2 <8 kPa A – Age >55 years N – Neutrophilia, i.e. WCC >15×10
9
/l
C – Calcium <2 mmol/l R – Renal function: Urea >16 mmol/l E – Enzymes: LDH>600 U/l A – AST/ALT >200 U/l S – Sugar, i.e. Glucose >10 mmol/ml
The presence of three or more factors within the first 48 hours suggests severe pancreatitis.
MANAGEMENT
Transfer to ITU/HDU as appropriate.
Oxygen therapy and respiratory support as necessary.
Keep NBM, i.e. rest pancreas, NG tube for drainage of stomach contents.
Insert urinary catheter and fluid resuscitate; consider CVP line insertion to
guide fl uid regimen.
141
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Analgesia.
Medical treatment includes:
antibiotics – if infection (Gram and anaerobic cover); prophylactic use is
controversial correct electrolytes: e.g. hypocalcaemia, hypomagnesaemia
◗ ◗ sliding scale insulin consider TPN/NJ feeding after five days of NBM.
Treat underlying cause, e.g. gallstones with cholecystectomy, alcoholism with
rehabilitation. Surgery: indicated for complications, e.g. pancreatic necrosis or abscess,
pseudocyst.
Complications of acute pancreatitis
Sepsis, SIRS (Systemic Inflammatory Response Syndrome), ARDS (Adult Respiratory Distress Syndrome), MODS (Multi-Organ Dysfunction Syndrome)
Hypocalcaemia, Hypomagnesaemia
Hyperglycaemia (diabetes)
Pancreatic necrosis
Pancreatic pseudocysts or abscess or haemorrhage
Chronic pancreatitis
Splenic vein thrombosis
Death (5–10%)
Chronic pancreatitis
Irreversible pancreatic inflammation characterised by chronic pain requiring opiate analgesia, and pancreatic atrophy with loss of exocrine and endocrine function. Associated with an increased risk of pancreatic carcinoma. Peak incidence 35–45 years.
Causes of chronic pancreatitis
Alcohol (70%)
Obstruction, i.e. ductal strictures, gallstones, tumours, pancreatic divisum
Metabolic: hypercalcaemia, hyperlipidaemia
Cystic Fibrosis
Radiation
Idiopathic (30%)
Clinical features: classically, chronic epigastric pain radiating into the back with acute severe episodes; associated nausea, weight loss, polydipsia and polyuria (diabetes) and steatorrhoea (due to fat malabsorption); cachexia, epigastric tenderness +/– abdominal mass +/– jaundice (if pseudocysts develop).
INVESTIGATIONS
Serum amylase, lipase and CRP usually normal.
Blood glucose (for diabetes); GGT (for alcohol excess).
Abdominal x-ray (may show a calcifi ed pancreas).
Ultrasound (for dilated CBD or gallstones).
Abdominal CT scan (for complications, i.e. cysts, abscess, necrosis) +/– ERCP.
Pancreatic function tests, i.e. Lundh, pancreolauryl test, rarely used.
142
GENERAL SURGERY
MANAGEMENT
Keep NBM – rest pancreas, IV fluids, NG tube, analgesia +/– TPN or NJ feeding
in the acute phase. Treat underlying cause: e.g. help with stopping alcohol.
Chronic pain management – refer to pain team.
Treat metabolic complications: diabetes control; pancreatic enzyme and
vitamin supplements; proton pump inhibitor. Surgery: to relieve obstruction, for intractable pain or failed conservative
treatment.
Cancer of the pancreas
More common in men.
Risk factors: smoking; chronic pancreatitis, carcinogens.
Pathology: 90% ductal adenocarcinoma.
Spread: direct extension to CBD, duodenum, blood vessels, stomach and spleen;
lymphatic and haematogenous to liver and lungs. Prognosis is poor: five year survival <2%.
CLINICAL FEATURES
Weight loss, anorexia.
Epigastric pain – radiating to the back.
Painless obstructive jaundice.
Diabetes.
On examination: cachexia, jaundice, epigastric tenderness +/– epigastric mass,
ascites.
INVESTIGATIONS
Blood tests: FBC (for anaemia), U&Es, LFTs (for obstructive jaundice), clotting,
glucose, CA19-9 (90% sensitive). Staging: CXR, CT scan +/– laparoscopy +/– endoluminal ultrasound.
MANAGEMENT
Treat jaundice: prurutis with anti-histamines; ERCP +/– stenting to relieve
obstruction. Surgery: e.g. Whipples’s procedure, distal pancreatectomy.
Palliation: control pain (opiate analgesia, coeliac plexus block, radiotherapy);
involve palliative care team.
13.5. The acute abdomen
Pain in the abdomen of acute (<1 week) duration, with associated symptoms, e.g. anorexia, nausea, vomiting, change in bowel habits, jaundice, fever and urinary or gynaecological symptoms.
Diagnosis relies on a comprehensive history, examination and focussed investi­ga tions. On examination, there is tenderness of the abdomen (+/– rebound or percussion tenderness) with or without abdominal distension, guarding and decreased or absent bowel sounds. In addition, there may be signs of dehydration and sepsis.
Differential diagnosis depends on the site of pain
The abdomen can be divided into nine regions (see diagram) or four quadrants:
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