History Taking & Examination
UPPER GASTROINTESTINAL BLEED (HEMATEMESIS)
DEFINITION : Any bleed, occurring into the G.I. tract from a source above the ligament of Treitz is described as ‘upper gastrointestinal bleed’.
Blood loss of G.I. tract can manifest in five ways.
Hematemesis – is bloody vomitus, either fresh and bright red or older and “coffee-ground” in character.
Malena – is black, tarry, and foul smelling stools. It results from degradation of blood, minimum of 60 ml of blood which stays in G.I. tract for > 14 hrs cause malena.
Hematochezia – is passage of bright red or maroon blood from rectum. This is usually caused by lower G.I. sources but massive upper G.I. bleed (>1000 ml) may also lead to hematochezia.
Occult blood loss – detected by stool examination.
Symptom of blood depletion without G.I. symptoms.
INITIAL ASSESSMENT OF THE PATIENT
Rapid assessment is carried out to gauge the urgency of the situation.
Whether the bleed is acute or chronic?
Is the patient haemodynamically stable or unstable?
It is helpful to confirm the presence of bleeding by inspecting the vomit or the nasogastric aspirate or stool. But first goal is always stabilization of the patient. Blood is sent for CBC, biochemistry, clotting studies typing and cross matching is done. If blood loss is chronic, then depletion of bone marrow iron stores causes microcytic hypochromic anemia with low MCV. In acute blood loss hematocrit is a poor indicator of magnitude of loss in the initial hours, because with hemorrhage there is proportional loss of plasma and RBC (i.e. people bleed whole blood). Hence during this time the MCV will be normal. It takes 24-72 hours for the extra-vascular fluid to enter the vascular compartment and subsequently replace the plasma volume causing decrease in hematocrit. This sequence is modified by preexisting abnormalities in vascular volume or by the administration of exogenous fluids and blood.
DIAGNOSTIC EVALUATION
[A] HISTORY:
Any prior h/o bleed?
Illness such as ulcers, necrosis, cancer, bleeding disorder.
Prior surgery for ulcer disease.
Use of alcohol / NSAIDS / Anti-coagulants.
[B] EXAMINATION:
Skin – cutaneous stigmata of cirrhosis.
Evidence of underlying cancer (acathosis nigricans, Kaposi sarcoma)
Pigmented lip lesion (Peutz-Jeghars Syn.)
Tumor (blue rubber bleb nevus, neurofibromatosis, Henoch schonlein purpura ).
Vascular abnormalities.
Lymphadenopathy (malignancy).
Abdominal masses (malignancy).
Abdominal tenderness (pancreatitis, ulcer).
Splenomegaly (cirrhosis, splenic vein thrombosis)
MANAGEMENT GUIDELINE FOR A BLUNT INJURY PATIENT WITH SIGNS OF HEMORRHAGE
OBSTRUCTIVE JAUNDICE
CAUSES OF OBSTRUCTION TO THE BILE DUCTS
Causes within the lumen of the bile ducts
Gallstones
Parasites
Causes affecting the wall of the ducts
Accidental division
Acute pancreatitis
Chronic pancreatitis
Carcinoma of the bile duct
Congenital obliteration of the bile duct
Causes Compressing the bile duct or invading it from the outside
Tumours of the pancreas
Peritoneal adhesions
Enlarged portal lymph nodes
Aneurysm of the hepatic artery
Hydatid cysts
Retroperitoneal cysts
Duodenal diverticulum
HISTORY
The age, sex, parity of the patient and possible addictions or habits should be noted. Most cases of hepatitis occur under age 30. A history of drug addiction may suggest serum hepatitis transmitted by shared hypodermic needles. Chronic alcoholism can usually be documented in patients with cirrhosis, and acute jaundice in alcoholics usually follows a recent binge. Bile duct stones or tumours are more common in older people.
Patients with jaundice due to CBD stones may have associated biliary colic, fever & chills and may report previous similar attacks.
History of Jaundice
Physical signs associated with jaundice
Jaundice with generalised hepatomegaly
Infective hepatitis
Biliary tract obstruction
Cholangitis
Portal pyaemia
Jaundice with irregular hepatomegaly
Extensive secondaries
Cirrhosis
Causes of jaundice with palpable gallbladder
· Carcinoma of head of pancreas
· Enlarged liver masking the palpable gallbladder
· Prior cholecystectomy
· Calculi in the gallbladder
Curvoisiers Law : When the gallbladder is palpable and patient is jaundiced the obstruction of bile duct causing the jaundice is unlikely to be a stone because previous inflammation will have made the gallbladder thick and non-distensible.
Liver function tests and urinalysis in jaundice
Surgical Treatment of Ascites
Decrease production
· Lymphovenous anastomosis
· Omentopexy
· Side to side portosystemic shunting
· TIPS
· Liver transplantation
Increase removal or resorption
· Large volume paracentesis
· Peritoneovenous anastomoses
· Peritoneovenous shunting
BENIGN BILIARY STRICTURES
CAUSES:
I. Congenital stictures, biliary atresia
II. Bile duct injuries:
A. Postoperative bile duct strictures
· Cholecystectomy and exploration of common bile duct/ Laparoscopic cholecystectomy
· Other operative procedures
o Biliary enteric anastomoses of previously normal bile duct
o Operations on liver or portal vein,
o Pancreatic operations,
o Gastrectomy.
o Variety of operations if any
B. Stricture after blunt or penetrating trauma
III. Postinflammatory strictures associated with:
A. Cholelithiasis/ choledocholithiasis
B. Chronic pancreatitis
C. Chronic duodenal ulcer
D. Abscess or inflammation in subhepatic region or in the liver
E. Parasitic infection
F. Recurrent pyogenic cholangitis
IV. Primary sclerosing cholangitis
V. Radiation induced stricture
VI. Papillary stenosis.
Bismuth has developed a classification of benign bile duct strictures based on anatomic pattern of involvement.
TYPE DESCRIPTION INCIDENCE(%)
Type 1 Low common hepatic or bile duct (CHD > 2 cm) 18-26
Type 2 Mid common hepatic duct (CHD < 2 cm) 27-38
Type 3 Hilar stricture 20-33
Type 4 Destruction of hilar confluence (right and left hepatic 14-16
Type 5 Involvement of sectoral right branch alone or with 0-7
common duct
CHOLEDOCHOLITHIASIS
CLASSIFICATION
Stones may be classified on the basis of
1) Composition
· Cholesterol
· Pigment
· Calcium carbonate stones
2) Site of origin
· Primary
· Secondary
· Retained stones.
3) Location
· Intrahepatic (Hepaticolithiasis)
· Extrahepatic (Hepatodocholithiasis or Choledocholithiasis)
· Both intrahepatic and extrahepatic.