25. 1 Acute pancreatitis
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Intestinal Obstruction
Intestinal obstruction implies that there is interference with the normal forward progression of intestinal contents. It may be either mechanical (dynamic) or due to paralytic ileus (adynamic).
MECHANICAL OBSTRUCTION
In mechanical obstruction there Is physical occlusion of the lumen preventing the intestinal contents from passing along the Intestine.
There is a vigorous attempt (as manifested by hyperperistalsis) on the part of the intestine, proximal to the obstruction, to overcome it. The causes of mechanical obstruction are as follows.
1. In the lumen
a. Bolus of incompletely digested food
b. FaecoUth
c. Plug of roundworms
d. Gallstone.
2. In the wall
a. Inflammatory stricture, e.g. tubercular
stricture b. Thickening of the gut wall, e.g. Crohn's
disease, hyperplastic Ueocaecal tuberculosis c. Tumours, benign or more commonly
malignant.
3. Outside the wall a. Hernia b. Adhesions c. Volvulus d. Intussusception.
Classification of intestinal obstruction on clinical and pathologic grounds Is also necessary. In simple mechanical obstruction, the lumen is obstructed but the blood supply is intact. If mesenteric vessels are occluded, then strangulation obstruction occurs. Obstruction is further classified vs partial or complete, acute or chronic, high or low, small intestinal or colonic.
The more Important causes of small. bowel obstruction are briefly considered below.
Adhesions
Adhesions are by far the most common cause of mechanical obstruction. They form after most laparotomles. Peritonitis from any cause, whether localised or generalised, can also result in troublesome adhesion formation. Congenital bands or adhesions, however, are an uncommon cause of obstruction.
Hemto
Incarceration of an external hernia may have been present for many years and the patient at times may be unaware of it. An incarcerated hernia may be overlooked by the examining surgeon, particularly if the patient is obese or If the hernia Is of the femoral type.
Internal hernias through anatomical defects, such as the foramen of Winslow or the paraduodenal fossae are rare but must always be considered.
Neoplasms
Intrinsic small bowel tumour may gradually obstruct the lumen or serve as a leadpoint In intussusception.
Intussusception
This is an invaglnation of one loop of Intestine Into another. It is more often seen in children.
Volvulus
Volvulus results from rotation of bowel loops about a fixed point, at times, the consequence of congenital anomalies or acquired adhesions. Volvulus of the sigmoid Is perhaps due to a large loaded colon.
Foreign Bodies and Bezoars
Luminal obstruction may result from Ingestlon of foreign bodies, usually by children or the mentally disturbed. Bezoars usually form in the stomach and may migrate into the small intestine before impacting in the terminal ileum. Human hair (trichobezoar) or undigested vegetable matter (phytobezoar) obstruction is likely to occur when the bowel is narrowed as a result of previous surgery. Passage of a large gallstone, into the intestine through a cholecystoenteric fistula may produce obstruction of the small bowel.
Pathophyilology
The intestine proximal to the obstruction tries to overcome the obstruction by vigorous peristalsis. The increased peristalsis continues for a couple of days. If the obstruction is not relieved, a time is reached when Increasing distension dampens the peristalsis and the obstructed intestine becomes flaccid and paralysed.
The Intestine below the level of obstruction looks normal for the first few hours and shows normal peristalsis. The patient may even pass one or two normal stools with flatus. This is also the reason why there may be a positive result with an enema given for the first time. However, if a second enema is given, the result is negative (two enema test).
The distension of the proximal loop is due to gas and fluid.
Gas There are three sources of gas: (i) the swaUowed air (68%), (ii) diffusion from blood into the bowel (22%), and (ill) as a product of digestion and bacterial activity (10%).
Fluid The major part of the fluid is made up by the digestive juices. About 8000 ml of fluid is secreted dally into the bowel lumen.
Above pylorus:
Saliva 1500 ml
Gastric juice 2500 ml
Below pylorus:
Bile and pancreatic juice 1000 ml
Intestinal juices and secretions 3000 ml
Normally, major part of this fluid is reabsorbed from the bowel lumen. In intestinal obstruction this reabsorption fails to occur but excretion of water and electrolytes into the lumen persists and may even be increased. Prostaglandin release in response to bowel distension is thought to be the mechanism by which secretion into obstructed loops is increased. Enormous quantities of fluid from the extracellular space are thus lost into the gut. Fluid fills the lumen proximal to the obstruction. As the bowel distends with gas and secretions, intralumlnal pressure may rise high enough to impair venous drainage; this contributes to oedema of the bowel wall and loss of fluid from the serosal surface into the peritoneal cavity. The extent of fluid and electrolyte loss into the bowel wall and peritoneal cavity depends on the extent of bowel involved in venous congestion and oedema, and the length of time before the obstruction is relieved.
The most obvious route of fluid and electrolyte loss is by vomiting, or Ryles tube suction after treatment is Initiated. The aggregate of these losses (1) into the bowel lumen, (11) into the oedematous bowel wall. (ill) as free peritoneal fluid, plus (Iv) by vomiting or suction, rapidly depletes the extracellular fluid space leading to profound hypo-volaemia, renal insufficiency, shock and death unless prompt treatment is instituted.
Audible peristalsis Is an attempt by the small bowel to propel its contents past the obstruction. Eventually, the smooth muscle becomes fatigued and bowel sounds diminish. Bacteria proliferate as a result of stasis of the luminal contents, and the vomitus becomes faecal, particularly with distal obstruction. Abdominal distension elevates the diaphragm and impairs respiration so that pulmonary complications are frequent.
Strangulation Obstruction
The occlusion of vascular supply as well as the intestinal lumen most frequently occurs secondary to adhesive band obstruction, hernia and volvulus. In the early hours of strangulation, the veins are occluded by the obstructing band while the arteries are still open. Blood reaches the gut but cannot return and, therefore, accumulates in the wall as well as In Its lumen. For a short loop of gut, this may be insignificant. On the other hand, when a long loop is' involved in strangulation, there may be considerable sequestration of blood in this way.
Ultimately, swelling of the strangulated loop causes obstruction of the arteries as well and the gut turns gangrenous. The luminal contents of the strangulated intestine are a toxic mixture of bacteria, bacterial products, necrotic tissue, and blood. Some of this fluid may enter the circulation by way of intestinal lymphatics or by absorption from the peritoneal cavity; septic shock is the result. Absorption from the peritoneal cavity is maximum in internal hernia; on the other hand, this factor is of less importance in external hernias. (This is the reason why the fluid from the sac of a strangulated external hernia should be removed by opening the sac. before cutting the constriction band, so that entry of this toxic fluid into the peritoneal cavity is avoided).
Colon Obstruction
The effects with colon obstruction are usually less dramatic than the effects of small bowel obstruction. First, colon obstruction with the exception of volvulus, usually does not strangulate; second, because the colon is principally a storage organ with little absorptive and secretory functions, fluid and electrolyte loss is less. Systemic effects are, therefore, of lesser magnitude.
Closed Loop Obstruction
When both afferent and efferent limbs of a loop of bowel are obstructed, closed loop obstruction exists. In its typical form it is seen in carcinomatous stricture of the colon. Distally the colon is occluded by the neoplasm, while in one-third of the cases where lleocaecal valve is competent, regurgitation of the contents of the large intestine into the ileum is prevented and the part of the colon proximal to the neoplasm is closed at both ends. The pressure In the caecum becomes so high as to compress the blood vessels within its walls, and perforation occurs.
Clinical Foaturs
Acute Obstruction
This Is mostly small intestinal. Pain is colicky in nature and higher the obstruction, the more profuse is the vomiting. Abdominal distension Is centrally placed. There is absolute constipation. A typical ladder pattern peristalsis is visible. Intestinal sounds are highly exaggerated.
Vital signs may be normal in the early stages but dehydration is noted with continued loss of fluid and electrolytes as evidenced by dry tongue, dry skin and sunken eyes. An obstructed hernia must be looked for.
Chronic Obstruction
This is commonly large intestinal and constipation appears first, may last for days or weeks, and finally becomes absolute when the passage of flatus ceases. Abdominal distension then appears, especially marked on the flanks. Vomiting is very late to appear.
No matter where the obstruction lies, whether in the ascending, transverse or descending colon, the brunt of the obstruction is borne by the caecum and if the ileocaecal valve is competent, the caecum becomes ballooned and can perforate causing general peritonitis. Pain accompanies caecal distension and the caecum can sometimes be seen to distend with each attack of colic, and subside as the colic passes off.
Acute on Chronic Obstruction
This occurs when, following a large bowel obstruction, the Ileocaecal valve is forced open and the contents pass up the ileum. To start with. there are features of chronic obstruction and after a few days, pain, vomiting, dehydration and central abdominal distension also set in.
Strangulation
It is important to recognise a strangulating from nonstrangulating intestinal obstruction because if the former is not relieved by an urgent operation, gangrene follows quickly. Its presence should be suspected in the following.
1. If a colicky pain becomes continuous.
2. If there is evidence of localised tenderness, rebound tenderness and guarding.
3. If there is presence of a tender mass.
4. If an external hernia is tense and tender.
5. If pain is severe and comes in frequent spasms.
6. If pain persists for more than two hours after effective gastroduodenal suction has been commenced.
Shock that appears early in the course of obstruction, suggests strangulation.
When strangulation supervenes In simple obstruction, high fever and out of proportion pulse rate rise may occur.
Investigations
There is markedly reduced urine output. Urinary specific gravity of 1.025 to 1.030 is the rule. In the early phase, in which the effects are predominantly those of extracellular fluid loss, the haematocrit rises roughly in proportion to the fluid loss.
In the untreated patient, sodium free water derived from the catabolism of cells and oxidation of fat, tends to restore the acute loss of extracellular fluid volume but at the expense of plasma osmolality.CThus, there is a gradual reduction of plasma sodium and chloride concentration .J Urine volume gradually Increases though not to normal with excretion of potassium Including the potassium freed by cellular catabolism. Metabolic acldosis results due to the combined effects of dehydration, starvation, ketosis and loss of alkaline secretions (from the small intestinal contents).
The white blood cell count Is markedly raised in strangulation.
X-ray Diagnosis
Plain films of the abdomen are taken with the patient standing and lying down. Obstructed small intestine is revealed by relatively straight segments that generally lie more or less transversely. Jejunum is characterised by its valvulae conpj-ventes; obstructed large intestine by its haustration markings. The gas fluid levels are best seen on the upright film of the abdomen.
In obstruction of the large Intestine, a plain X-ray always shows a large amount of gas in the caecum.
Monagomont
The measures to combat and overcome the Ill-effects of acute intestinal obstruction are (i) gastro-Intestinal suction, (11) maintaining fluid and electrolyte balance, and (ill) operation for obstruction.
Priority of treatment is often a dilemma.
1. If the patient has a strangulation, surgery for relief of obstruction must be given the first priority.
2. In case of a high Intestinal obstruction, the patient is likely to have a low circulating volume; replacement of the deficit must have the first priority.
3. If the obstruction is in the distal colon, there Is little chance of a major circulating volume deficit and relief of distension is the major therapeutic aim.
Gastroduodenal Suction
The aim is to remove fluid and gas frotu the stomach and upper intestines. When strangulation can be ruled out, a few hour suction is a good treatment preliminary to surgery. However, when strangulation cannot be excluded, more time should not be spent in gastroduodenal suction as this may affect the gut viability and thus increase mortality.
Fluid and Electrolyte Balance
Depending upon the level and duration of obstruction, fluid and electrolyte deficits are mild to severe. Fluid losses are isotonic, and resuscitatlon should begin with infusion of normal saline solution. Loss of gastrolntestinal fluid also entails acid-base deficits. Serum electrolyte concentration and arterial blood gas determination are guides to electrolyte therapy; potassium is only administered if the urine output is satisfactory. In a patient showing signs of severe dehydration, as much as 3.5 litres of normal saline, Intravenously, may be necessary. Subsequently, the daily requirement (approximately 2 litres) plus the amount drained by gastrointestinal suction has to be maintained. Antibiotics should be given if strangulation is even remotely suspected.
Operation
Operation should be undertaken immediately if strangulation Is evident or suspected. Otherwise the operation may commence when the patient has been well-hydrated and vital organs are functioning satisfactorily.
A standard groin incision is used for patients with obstructed inguinal or femoral hernia, but other types of obstruction require a laparotomy Incision.
Details of the operative procedure vary according to the cause of obstruction. Decompression of massively dilated small bowel loops facilitates closure of the abdomen and shortens the time for recovery of the bowel function postoperatively.
PARALYTIC ILEUS
Paralytic ileus is a disorder in which there is neurogenic failure (I.e. in the myenteric plexus of Auerbach and the submucous plexus of Meissner) of peristalsis to propel the intestinal contents. There is no mechanical obstruction. This results in collection of fluid and gas in the Intestine resulting in distension, vomiting, absent bowel sounds and failure to pass flatus.
The following varieties are recognised, of which the first two are the commonest.
Postoperative
Some degree of ileus occurs after every abdominal operation. In the absence of infection it is not serious and there Is full recovery of the intestinal motillty. The rate of recovery of motor function is different in different segments of the gastrointestinal tract. Small bowel motllity returns within 24 hours, and gastric motillty within 48 hours, but +-colonic inertia persists for 3 to 5 days. Oral intake can be resumed on the third or fourth postoperative day.
Infective
Common causes include intraperitoneal inflammation such as acute appendicitis or acute pancreatitis. Peritonitis gives rise to a prolonged ileus. At the outset, peristalsis ceases as a normal response to prevent spread of Infection but later bacterial toxins disturb the activity of the nerve plexuses of Auerbach and Meissner.
Reflex
It may be associated with retroperitoneal pathological conditions such as ureteric colic, retroperitoneal haematoma, fracture of the spine or fractured ribs.
Systemic Causes
Uraemia, severe toxaemia, hyponatraemia or hypokalaemia may also lead to paralytic ileus.
The incidence of paralytic ileus has gone down because of (i) routine nasogastric suction and withholding fluids by mouth after laparotomy until normal bowel sounds return, and (11) maintenance of fluid and electrolyte balance.
Clinical Features
The primary disease causing the Ileus may, at times, dominate the clinical picture. In postoperative ileus, there may be abnormal prolongation of bowel hypofunctlon. Instead of passing flatus and feeling hungry about the third day, as expected following abdominal operation, the patient is found to be distended. Examination confirms distension with only occasional bowel sounds. The Investigations may reveal the causes of ileus such as anaemia, sepsis, hypokalaemia, etc.
There is no colic and often no abdominal pain. There is fair abdominal distension and prolonged distension may increase the risk of burst abdomen. A plain X-ray shows multiple intestinal fluid levels.
Management
The treatment of Ileus is essentially the treatment of the primary lesion. Postoperative ileus is caused in the vast majority of patients either by infection (leaking anastomosis, abscess following contamination) or by gross fluid and electrolyte derangement. When these problems are promptly eradicated, the ileus will take care of itself.
Liver disease.
HEPATIC ABSCESSES
Mainly two types of hepatic abscesses are seen — 1. By pyogenic organism causmgpyogenic absess and 2. By Entamoeba histolytica causing amoebic liver abscess.
PYOGENIC LIVER ABSCESS
Aetiology.— Pyogenic liver abscess may result from :
- Via portal vein as occurs in appendicitis or diverticulitis.
- Via the biliary tree (ascending biliary infection) as in cholangitis.
- Via hepatic artery as in sepsis or generalised septicaemia.
- Via direct extension from infection in the neighbourhood such as advanced cholecystitis, subhepatic abscess etc.
- Following hepatic trauma. Nowadays the most frequent cause has been cholangitis secondary to biliary calculi or some obstruction of the common bile duct (mostly carcinomatous). The second most common cause is from generalised septicaemia. Liver abscess from portal venous root is becoming rare. In a few cases no apparentcause of hepatic abscess has been found. These cases are not very negligible and has been reported in various series from 2 to 20%. These are called cryptogenic liver abscess.
Clinical features.—
1. Fever is the most important and common symptom of this condition. Fever is usually hectic, showing a 'picket fence' type of pattern. Fever is frequently associated with chill and sweating.
2. Pain is the second symptom and is rather late in appearance. Continuous pain in the right subcostal area or in the epigastrium is noted. Pain may radiate to the right flank. Diaphragmatic irritation may lead to the referral pain to the right shoulder or right side of the neck.
3. Nausea, vomitingand anorexia occurwith varied frequency. It is more common in case of large single abscess. Jaundice may appear though relatively uncommon. On palpation liver enlargement has been noted in half the cases. Liver tenderness is also present in half the cases.
Special Investigations.— 1. Blood'examination. —Leucocytosis is usually present. The white blood count ranges between 12,000 and 18,000. Blood culture may be positive to find out becteria in approximately l/3rd of patients. This is usually positive in case of abscesses secondary to systemic septicaemia. Hypoalbuminemia is also seen. Alkaline phosphatase level is often increased. Transaminases and lactic dehydrogenase (LDH) «re also seen to be elevated in this condition. Bilirubin is normal in 90% of patients.
2. Radiologic Investigation.— Chest X-ray reveals elevation and restriction of movement of the right cupola of the diaphragm. The right cardiophrenic angle is obliterated. Slight effusion or atelectasis is not uncommon.
3. Barium enema X-ray may be performed to exclude occult diverticulitis.
A.Ultrasonography.— Echography should be done as the initial test in confusing cases followed by other imaging technique for accurate localisation of the abscess. Ultrasonography not only diagnoses and indicates the position of the abscess, but it also indicates the stage of resolution of the abscess with medical therapy.
5. Liver scan.— It has limitations as it fails to differentiate between solid and cystic structures. It also cannot detect lesions less than 2 cm in diameter. Yet in certain series it is claimed to be accurate in 80 to 90% of cases. Liver scan is an acceptable screening test in evaluation of a patient with fever of unknown origin. Computed tomography seems to be better than radionuclide studies for this purpose.
6. Other radionuclide Imaging techniques.—;, Gallium scanning, which detects uptake by inflammatory tissue may be used, but whether it is more informative than the usual imaging technique is yet to be proved.
7. Computed tomography (CT scan).— This is recommended to be the first method for detection of suspected hepaticabscess. Its accuracy has been claimed to be more than 95%. The abscess may vary inappearance from smooth margins, fluid filled cavities to poorly defined masses. A dense rim around the abscess may be found after contrast enhancement. At the end it may be said that if the CT scan is normal, liver abscess can be excluded, but a positive CTscan may not be definite to diagnose an abscess.
8. Fine needle aspiration biopsy (FNAB).— Its main advantage may be taken by using it in case of CT diagnosed suspected liver abscess. It is safe. But it should not be used in case of hydatid cyst where there is risk ofanaphylaxisand dissemination. So if the cyst wall is calcified in CTscan or the patient is from the area where hydatid disease is endemic, aspiration should be deferred.
After aspiration the fluid should be cultured for organisms.
9.Angiography.— CTscan has almost replaced this mode of investigation in diagnosing liver abscess. Its ability remains in only doubtful cases where metastatic disease or vascular lesion cannot be excluded with certainty.
TREATMENT. — Management ofpyogenic liverabscess is based on two principal lines —(a) antibiotic therapy and (b) surgical drainage.
(a) ANTIBIOTIC THERAPY.— This therapy is greatly dependent upon the results of culture obtained by percutaneous needle aspiration or at the time of surgical drainage. But antibiotic should be started before surgical intervention and it should be directed at commonly encountered pathogens —gram negative bacteria and enteric anaerobes. Intravenous administration of aminoglycoside and metronidazole generally cover these organisms. In addition ampicillin or penicillin should be considered in patients with generalised sepsis. Clindamycin is also quite effective, similarly is the 3rd generation cephalosporin, though these are quite expensive. Whatever antibiotics are chosen, they should be modified on the basis of the culture results.
Antibiotic treatment should be continued for 4 to 8 weeks. When multiple abscesses are present and have been drained, antibiotics should be given for 6 to 8 weeks. When multiple abscesses could not be drained antibiotic therapy should be continued for 8 to 12 weeks. '
(b) SURGICAL DRAINAGE.—This is particularly indicated forsolitary abscess and for large multiple abscesses. The abscesses may be drained percutaneously under ultrasonography or CT control. About 80% success has been claimed by this technique. This technique should definitely be adoped in whom there is no evidence of biliary tract orgastrointestinal causative factors. Inother cases, the safest approach is opensurgical drainage.
The route of surgical drainage depends on the position of the abscess. It may be transthoracic(transpleural) or transabdominal (transperitoneal). The transperitoneal approach has two clear advantages — (i) it gives a clear view to the liver to detect any unsuspected abscesses and (ii) it gives access to the biliary tree or gastrointestinal tract to exclude any cause there. The disadvantage of transperitoneal approach is that the abscesses situated in the superior or posterior surface are difficult to drain.
If the abscess is in the anterior or anteroinferior surface of the liver, the incision is made anteriorly just beneath and parallel to the costal margin. The muscles are incised, so is the transversalis fascia. The parietal peritoneum is reflected down from the inferior surface of the diaphragm. The abscess is reached and drained extraperitoneally.
If the abscess is posteriorly placed, skin incision is made over the 12th rib. The rib is resected subperiosteally. A transverse incision is then made through the bed of 12th rib. The parietal peritoneum is reflected from the inferiorsurface of the diaphragm. Thus the abscess is reached and drained extraperitoneally.
AMOEBIC ABSCESS
Amoebic abscess is a complication of amoebic dysentery.
Pathology.—Entamoeba histolytica pass from the colonic lesion via the portal vein into the liver. Usually the upper and posterior portions of the right lobe are affected. Actually the disease can be divided into two stages — (1) Amoebic hepatitis and (2) Amoebic abscess.
Amoebic hepatitis is a type of diffuse involvement of the liver characterised by increased lymphocyte, mononuclear infiltration, fatty changes and lysis of hepatic cells. But the exact pathology of amoebic hepatitis has not yet been clear. It is still questioned that whether diffuse hepatitis at all takes place or not. ' It therefore seems more or less clear that the only proven amoebic lesion of the liver is the abscess. In the beginning when Entamoeba enter the liver, liver infection begins with intrahepatic portal thrombosis and infarction. The cytolytic activity starts and leads to liquefaction of the surrounding stromal and parenchyma! structures. Coalescence of such small necrotic areas results in the formation of a large single abscess. As has been described earlier the usual location of amoebic abscess is in the right lobe. In 30% of cases there may be more than one abscess.
Gross appearance.— The liver is usually enlarged and there may be adhesions to the diaphragm. The liquefied material within the abscess is characteristically viscid and semitransparent. The content is a mixture of red blood cells, leucocytes, broken down liver cells and this looks chocolate or reddish-brown coloured. Such pus of amoebic abscess is variously described as 'chocolate sauce' or 'anchovy sauce'. In early cases the wall of the abscess is thin with little fibrosis. But in older abscess it has a fibrous capsule which demarcates it from the normal liver. The earlier the stage, more likely that the amoebae will be found. But in later stages these amoebae are not so easy to be detected. These amoebae are present not in the central necrotic zone but near the wall adjacent to the fibrous capsule. From aspirated material amoebae are found in only 20% to 40% of cases.
Complications.— Prognosis of amoebic abscess is much better than pyogenic abscess. However if the abscess remains untreated, it may burst.
It may burst into (a) right pleural cavity, (b) right lung, (c) peritoneal cavity. The abscess when bursts into the pleural cavity empyema may result. When it bursts into the lung it may cause bronchohepatic fistula, lung abscess or pneumonia. Single large abscess of the left lobe may rupture into the peritoneal cavity or even to the pericardium. Amoebic peritonitis carries a mortality rate of 20% even with early surgical intervention. Extension of abscess into the pericardium is more dangerous. Amoebic abscess rarely may extend to the kidney.
Clinical features.—Amoebic abscess develops after an attack of amoebic dysentery. This may occur soon after the attack or may take a long time to appear after the attack. It had even occurred after many months of amoebic dysentery and even a few years after an attack of amoebic dysentery. Amoebic abscess may develop even in a carrier, who has not shown definite symptoms and signs of amoebic dysentery. Amoebic abscess has also appeared in persons who had mild diarrhoea not diagnosed as typical amoebic dysentery and consequently no specific treatment of that condition was given.
Though anaemia and loss of weight are first to appear, yet the typical symptoms of amoebic abscess are (i) fever and (ii) liver pain.
(i) Fever may shoot upto 39° С or even more particularly at night. But unless complicated by secondary -infection the temperature is usually less than that of pyogenic abscess. Fever is usually accompanied by chills and sweating.
(ii) Pain is present in nearly 90% of patients.Thesiteofpain is usually related to the location of the hepatic abscess. Pain is usually felt over the right lower intercostal spaces. There may be slight bulging and pitting oedema. Superior surface abscesses may cause pain referred to the right shoulder. Abscesses in the bare area of the liverwhich is not in contact with peritoneum may remainpainless forquite sometime. Left lobe abscesses present as pain in the epigastric region.
Enlargement of liver may be demonstrated. Tender hepatomegaly is often seen in this condition. Tenderness and rigidity may be felt just below the right costal margin. In case of left lobe liver there may be tender swelling in the epigastric region.
Unfortunately only Vorrd of patients offer a history of previous diarrhoea. Clinical jaundice is relatively rare but may be seen in a few cases. Abnormal pulmonary signs may also be looked for.
Special Investigations.—
1. Blood examination will reveal leucocytosis in early cases. In chronic cases anaemia may be revealed.
2. Serological tests to detect antibodies to E.histolytica are essential to evaluate a case of suspected liver abscess. Indirect haemagglutination and complement fixation tests are useful in this regard. Antibody litres are higher in patients with amoebic abscess than in those with amoebic dysentery. About 95% accuracy has been claimed in these tests. One great advantage of such test is that negative serologic tests exclude amoebic abscess as a diagnostic possibility.
3. Examination of stool for amoebae is not very diagnostic. Though in certain series they found amoebae in the stool in about 45% of cases, yet these are only found in less than 20% of cases.
4. Liver function tests are also not helpful in establishing the diagnosis.
5-Sigmoidoscopy may reveal characteristic amoebic ulcers which will give a clue to the causative lesion.
6. Radiography often reveals elevation and fixation of the right cupola of the diaphragm.
7. Diagnosis is 100% confirmed by aspiration of the liver abscess. The 'anchovy sauce' pus is quite diagnostic. Occasionally the abscess content may be creamy white even though there is no secondary bacterial infection. Only in these cases definite diagnosis remains in doubt. Amoebae may be demonstrated in the aspirate in'/rd of the patients.
Treatment.— Management of amoebic abscess is mainly drug therapy with amoebicidal drugs. A few abscesses, particularly the large ones, may require needle aspiration.
AMOEBICIDAL DRUG should be tried first. Metronidazole which acts on both the intestinal and hepatic amoebiasis is the drug of choice. The recommended dose of Metronidazole in amoebic liver abscess is 500 mg or 750 mg orally 3 times daily for 5 to 10 days. Alternatives to metronidazole include Emetine, Dehydroemetine and Chloroquine. Emetine and dehydroemetine are cardiotoxic. Metronidazole has fewer side effects. In many cases even after a course of metronidazole patients continue to pass cysts in their stools. In these cases diidohydroxyquinolone 600 mg orally daily for 10 days or diloxanide furcate 500 mg orally 3 times daily for 10 days should be given to clear intestinal amoebiasis.
NEEDLE ASPIRATION is only employed inselected cases. Though inareas where amoebiasis is endemic aspiration of abscess is done as a routine procedure without radiologic imaging. Since most patients respond to medical management, indications foraspriation are — (i) persistence of clinical features of amoebic abscess following a course of amoebicidal drugs; (ii) Clinical or radiographic evidence of presence of hepatic abscess. Drug therapy should be instituted several days before aspiration. No drug should be injected directly into the abscess cavity.
Technique of aspiration.— Aspiration should be conducted in the operation theatre. A long needle with wide bore is selected. The preferred route is through the 9th or 10th interspace between the anterior and posterior axillary lines. The needle may better be introduced through the guidance of CT or ultrasound.
Surgical drainage of amoebic abscess carries great morbidity and mortality. It should be avoided. It is only indicated (i) when the abscess is secondarily infected as evident by needle aspiration; (ii) Amoebic peritonitis requires surgical drainage.
CYSTS OF THE LIVER
Cysts of the liver arc generally benign. They may be solitary or multiple. They may be unilocular or multilocular. The various types of cysts seen in the liver are: (i) Hydatid cyst; (ii) Retention cysts —(a) Solitary cysts and (b) Multiple cysts (polycystic disease); (iii) Lymphatic cysts; (iv) Endothclial cysts ; (v) Blood and degenerative cyst; (vi) Dermoid cyst; (vii) Cystoadenomas. Cysts of the liver can be classified into two major groups — A. Parasitic cyst e.g. hydatid cyst and B. Non-parasitic cysts which include the other varieties described above.
HYDATID CYSTS
Pathology.— This condition is caused by a parasite called Echinococcus Granulosus. Unilocular cyst is almost always caused by E.granulosus, while the alveolar type may be caused by Echinococcus multilocularis.
Dogs are the chief mediators of hydatid disease. Animals, particularly sheep, are infected by eating contaminated grass (as eggs of the Echinococcus are discharged through the faeces of the dog and this contaminates the grass). Human being is also almost similarly affected as the dog either (i) by taking uncooked vegetables contaminated with infected canine faeces or (ii) by direct handling of the infected dogs or (iii) by allowing the dog to feed from the same dish. Human infection does not occur through contaminated water. This is the mode a/infection in case of human being. Animal like sheep, pig, horse or goat are considered to be intermediate hosts. The eggs of echinococcus after being swallowed by the intermediate hosts behave in the same pattern as after being swallowed by human beings. The only difference is that once the hydatid cyst is formed in the liver or in the lung the intermediate hosts are eaten by the definitive host like the dog. The cycle continues. The life cycle of the eggs of echinococcus in the human beings is exactly the same as that occurs in the intermediate hosts. But human being is not designated as the intermediate host, the reason being that the definitive host like dog does not get an opportunity to eat human being to continue the cycle. So intermediate host like sheep, pig or cattle is essential to continue the cycle and hence hydatid disease is mainly seen in the sheep rearing areas.
Hydatid cyst.— This cyst is formed by the embryo. The cyst consists of three layers — (i) Adventitia consisting of fibrous tissue and is grey in colour, it is blended immediately with the liver;
(ii) The laminated membrane (ectocyst) is formed by the parasitic cells. To the naked eye the ectocyst has the appearance of the white of a hard boiled egg. It is elastic and when incised or ruptured it curies on itself exposing the inner layer;
(iii) Inner germinal layer (endocyst) is cellular and consists of a number of nuclei embedded in a protoplasmic mass. It is very thin. It is the vital layerofthe cyst and gives rise to (a) brood capsule with scolices, (b) secrete hydatid fluid and (c) forms the outer layer.
Brood capsules sprout from the germinal layer. It is at first spherical, but soon becomes vacuolated and transformed into a vesicle. The scolices, numbering 5 to 20 or more develop within these brood capsules. A fully developed scolex presents the future head of the adult worm. The hydatid cyst when ingested by the definitive host the scolices fix atthe small intestine with success and gradually form into the adult worms inside the intestine of the definitive host.
Clinical features.— Approximately 80% of hydatid cysts are initially single and in the right lobe. In only l/4th of the cases there are multiple cysts. Hydatid cyst remains symptomless for quite a long time. When symptoms occur, they are usually caused by pressure to the adjacent organs. A visible and palpable swelling in the upper abdomen can be discovered on careful examination. Pain is sometimes caused by pressure on the adjacent organs. Once a palpable mass is detected, it is found to be connected with liver and is cystic. So called 'hydatid thrill' and fremitus may be elicited. Jaundice and ascites are uncommon. When complicated with secondary infection fever with chill may occur. When it ruptures in the biliary tree, biliary colic, jaundice and urticaria may be noted. Intraperitoneal rupture will cause abdominal and anaphylactic shock. Intrathoracic rupture may be associated with shoulder pain and cough which contains blood and bile. Expectoration may contain membranes. Presence of hydatid membrane in the vomitus(hydatidemesis)or in the stool (hydatidenteria) may occur very rarely.
Alveolar hydatid cyst occurs from ingestion of echinococcus multilocularis. The chief character of the lesion is the absence of the capsule of the hydatid cyst and that is why it shows tendency to metastasise. Most of the alveolar hydatid cysts (multilocular hydatid cyst) are sterile.
Complications.— 1. Intrabiliary rupture is the commonest complication and occurs in 5 to 10% of cases.
2. Suppuration is the second commonest complication caused by the bacteria from the biliary tract. This turns the hydatid cyst into a pyogenic abscess with death of the parasites.
3. Intraperitoneal rupture will cause contamination of peritoneum with hydatid fluid, brood capsule and scolices. The scolices may survive and produce new cyst (secondary echinococcosis) of the peritoneum.
4. Cyst in the superior portion ofthe liver may push into the pleural cavity, with the formation of empyema and bronchopleural fistula. It may rupture into the lung. It must be remembered that lung is also a primary site ofthe hydatid cyst. Such secondary invasion canbe determined by presence of bile pigment inside the cyst.
Special Investigations.— 1. BLOOD EXAMINATION will reveal eosinophilia of 20 to 25%. Mildly elevated liver function tests may be noted.
2. Ofthe SEROLOGIC TESTS the indirect haemagglutination test, Casoni's test and complement fixation will be positive.
Casoni's test.— Intradermal injection of 0.2 ml of fresh sterile hydatid fluid produces a wheal of 5 cm in diameter within half an hour. This is a quite sensitive test and becomes positive in majority of cases. Problems with the Casoni skin test are that it may cause false positive result and may produce anaphylaxis.
3. RADIOGRAPHYCALLY calcification of the cyst wall may be visualised in 50% of cases.
4. CT SCAN furnishes useful information.
5. ULTRASONOGRAPHY and ARTERIOGRAPHY are also diagnostic of hydatid cyst. The finding of daughter cyst or hydatid sand on ultrasonography and CT scan help to differentiate this cyst from pyogenic or amoebic liver abscess. This differentiation is extremely essential as percutaneous needle aspiration, which is the treatment of pyogenic and amoebic liver abscess, will cause spillage and spread of the cyst to cause disaster.
Treatment.— Treatment is primarily SURGICAL (excision). After exploring the abdomen it is carefully packed with mops around the cyst to reduce the risk of peritoneal contamination. Chlorhexidine, 80% alcohol and 0.5% cetrimide may by instilled into the cyst cavity. This will destroy 80% to 90% of scolices. Excision of the hydatid cyst using the natural cleavage plane which exists between the germinative layer and the adventitia is carried out. Adventitial layer may also be excised. In case of-large and multiple cysts partial hepatectomy may be performed. When a hepatic cavity remains after excision ofthe hydatid cyst, it should be treated by either (i) suturing and closure of the cavity, (ii) omentoplasty or (iii) marsupialization and drainage. Omentoplasty is the choice of majority surgeons.
Alveolar hydatid cyst by echinococcus multilocularis is fatal though extensive hepatic resection should be tried and has been successful in a few cases.
PORTAL HYPERTENSION
Portal hypertension is defined as an increase in portal vein pressure above the normal level of 5 to 10 mm Hg. Inestablished cases of portal hypertension, direct portal pressure measurement may be elevated to 15 mm Hg or even more.
Portal hypertension is due to obstruction somewhere in the portal vein or its tributaries (pre-hepatic), in the portal venules and sinusoides in the liver (hepatic) or in the hepatic veins draining into the inferior vena cava (post-hepatic).
Aetiology.— The various causes of portal hypertension can be classified into : (a) Pre-hepatic causes, which constitutes about 20% of cases of portal hypertension; (b) Hepatic causes, which constitutes 80% of cases of portal hypertension and (c) Post-hepatic causes, which are rare and occasionally seen.
A. PRE-HEPATIC CAUSES.— (i) Congenital atrcsia or hypoplasia, as an extension of the obliterative process of the umbilical vein and ductus venosus.
(ii) Cavernomatous transformation of the portal vein, which represents thrombosis and recanalisation within the vessel.
(iii) The most common in this group is portal vein thrombosis associated with sepsis or thrombosis in neonatal period. Bacteria may be transmitted through a patent umbilical vein, there may be history of neonatal omphalitis.
(iv) Trauma and extrinsic compression caused by adhesions.
(v) Tumours pressing on the portal vein.
(vi) Isolated splenic vein thrombosis may be caused by alcoholic pancreatitis (in this case splenectomy only cures portal hypertension).
B. HEPATIC CAUSES—
(i) Nutritional cirrhosis.
(ii) Postnecrotic cirrhosis.
(iii) Biliary cinhosis.
(iv) Haemochromatosis.
(v) Wilson's disease.
(vi) Congenital hepatic fibrosis.
(vii) Infiltrative lesions.
(viii) Schistosomiasis, in which there is fibrosis of the terminal portal venous radicles.
Nutritional cirrhosis is the most common cause and in the Western World it is frequently associated with chronic alcoholism. Postnecrotic cirrhosis represents progression of viral hepatitis or toxic hepatic injury. Biliary cirrhosis may be due to extrahepatic obstruction. Portal cirrhosis is almost an invariable feature of haemochromatosis. Wilson's disease (hepatolenticular degeneration) is characterised by alteration of hepatic function and structure and mental deterioration. Congenital hepatic fibrosis, an autosomal recessive disease, is usually characterised by firm consistency of the liver, cholangrtis and manifestation of portal hypertension.
C. POST-HEPATIC CAUSES.— (i) Budd Chiari syndrome.
(ii) Failure of the rightside of the heart, may be caused by tricuspid valvular incompetence and constrictive pericarditis.
Budd chiari syndrome is obstruction of the hepatic veins, most frequently associated with endophlebitis of the hepatic veins, which may be isolated or part of the generalised thrombophlebitic process. A web in the suprahepatic part of the inferior vena cava may cause such syndrome and has been reported from Japan. Neoplastic encroachment of other organs also accounts for this syndrome. This syndrome is often associated with polycythemia, clotting diseases and the use of hormones for contraception. The clinical picture may be acute or more commonly chronic. In acute cases there is sudden and complete obstruction of the outflow and it is characterised by nausea, vomiting and severe abdominal pain due to rapid enlargement of the liver as a result of congestion. Death may occur from hypotensive shock.
In chronic cases obstruction to the hepatic venous system appears to be gradual and is characterised by mild abdominal discomfort and ascites. There may be simultaneous development of oedema of the legs which signifies involvement of the inferior vena cava in the occlusive process.
Collateral circulation.— When there is obstruction to the portal veins, nature tries to reduce portal pressure by diverting blood from portal system to systemic system through a few known collaterals.
When the obstruction is pre-hepatic, collaterals between the portal vein distal to the obstruction and the portal vein proximal to the obstruction enlarge. Thus the accessory veins of Sappey, the hepatocolic and hepatorenal veins and veins of the suspensory ligament become enlarged.
When the obstruction is intrahepatic, a few known collaterals between the portal and the systemic systems become dilated and transfer the blood from the high pressure portal system to low pressure systemic systems. These collaterals are :
(i) Collaterals around the lower end of the oesophagus between the oesophageal branches of the left
(ii)Collaterals around the lower third of the anal canal between the superior haemorrhoidal veins (portal venous system) a nd the middle and inferior haemorrhoidal veins (systemic venous system). This of course very rarely dilates and causes haemorrhoids in this disease.
(iii) Collaterals around the umbilicus between the paraumbilical veins, which accompany the ligamentum teres hepatis (portal venous system) and the superficial veins of the abdominal wall which drain into the superior and inferior epigastric veins. Dilatation of such collaterals occur in about 20% of patients with portal cirrhosis and is known as the Caput Medusae.
Special Investigations.—
1. BLOOD EXAMINATION.— (i) Anaemia, usually microcytic hypochromic, is almost inevitable in portal hypertension. It is usually due to various causes e.g. bleeding, haemolysis and nutritional deficiency.
(ii) Leukopenia and thrombocytopaenia may also occur due to splenomegaly and hypersplenism of portal hypertension. Anaemia, leukopenia and thrombocytopenia may also be due to bone marrow depression occurred in alcoholic cirrhotics.
(iii) Coagulation defects are common and mostly due to thrombocytopaenia and impaired synthesis of coagulation factors by the damaged liver.The liver is responsible for synthesis ofprothrombin and factors V, VII and X.
2. LIVER FUNCTION TESTS.— Functional disturbance of the liver indicated by the various tests e.g. serumalbuminestimation, estimation ofserumtransami nases (SGOTandSGPT),serumalkaIinephosphatase estimation, serum bilirubin estimation, bromosulphthalein test and turbidity and flocculation test are not very good indices as to the severity of liver damage. The tests may be entirely normal in the presence of established cirrhosis. Serum bilirubin is a measure of combined functions of production, hepatocyte uptake and secretion." SGOT (serum glutamic oxaloacetic transaminase) and SGPT (serum glulamicpyruvic acrd tra lisa mi nase) are markers of hepatocyte injury or necrosis. Elevations of these markers are seen in hepatitis of all aetiologies.. Alkaline phosphatase is raised when there is biliary obstruction. Serum albumin level falls in liver diseases.
3. ENDOSCOPY.—Upper gastrointestinal endoscopy represents the most reliable single technique, as it shows the oesophageal varix and bleeding point. It should be carried out with fibreoptic instrument to visualise the inside of the oesophagus and stomach. Oesophageal varices are seen as dilated longitudinal veins running a zig-zag course. Such endoscopy is equally important to exclude peptic ulcer as a source of bleeding in a patient with documented varices.
4. RADIOLOGY.— (i) UPPER GASTROINTESTINAb, BARIUM series may demonstrate oesophageal varices as filling defectsatthe lowerend of the oesophagus. But this demonstration is present in only half the patients. This investigation iseven less accurate inthe diagnosis of gastric varices. This examination may. detect other gastroduodenal pathology e.g. peptic ulcer disease. But it must be confessed that its role is limited and has largely been superseded by endoscopy.
(ii) LIVER ANG10GRAPHY has two main advantages — (a) measurement of portal pressure and (b) visualisation of abnormal venous anatomy incase of portal hypertension.
(a) Measurement of portal venous pressure.— This can be performed by direct measurement through transhepatic portography, umbilical vein catheterisation or splenoportography. These methods also provide good visualisation of the venous anatomy.
Measurement of portal venous pressure may also be performed by indirect method by means of wedged hepatic vein pressure. This is performed by wedging a catheter in a peripheral hepatic vein. In case of intrahepatic portal obstruction measurement of portal blood pressure may be performed by catheterising hepatic vein. Under local anaesthesia an antecubital vein is opened and a cardiac catheter is passed through it. The catheter is advanced through the right atrium and inferior vena cava under radiographic control. The tip is then passed through a hepatic vein until a peripheral radical is occluded. The tip of the catheter should be in a peripheral position. Pressure recordings are then taken. In established cirrhosis case with oesophageal varices the portal pressure may rise to 30 mm Hg or more. It must be remembered that the degree of portal hypertension does not correlate with the risks of variceal haemorrhage or ascites formation, hence its significance is questioned.
(b) Portal venography or portography.— This is often performed by splenoportography. Under local infiltration anaesthesia a fine lumbar puncture needle is passed upwards and backwards through the 9th intercostal space in the left midaxillary line. The needle is pushed into the spleen, which is evident by respiratory movements seen on the needle. The stylet of the needle is removed and blood will be seen coming
out through the spleen. The intra-splenicpressure is recorded which is often closely related to the portal venous pressure. 40 ml of 70% Diodone is injected quickly and a series of X-rays are taken at short intervals. The dye reaches the portal circulation and thus the portal tree and the splenic vein can be seen in X-ray. Wilh this splcnoportography one can assess (a) if there is any block in the portal vein (pre-hepatic obstruction); (b)Distortion ofintrahepatic radicles of the portal vein, which indicates intrahepatic obstruction and (c) a large number of portosystemic collateral vessels, particularly the oesophageal varices. It must be remembered that
before doing splenoportography one should assess the prothrombin time and platelet count to avoid risk of haemorrhage.
MANAGEMENT.— When a patient comes with acute variceal bleeding the management is performed in three stages : 1. Resuscitation, 2. Diagnosis and 3. Specific treatment.
1. Resuscitation.—This is almost similar to all the patients who present with acute upper gastrointestinal G.I. tract bleeding. Only a few special points which need stress are discussed here :
(i) Blood volume should be maintained by transfusing blood. But over-transfusion should be avoided. Coagulation abnormalities require fresh frozen plasma and platelets as indicated.
(ii) Saline should be avoided because of ascites.
(iii) Pulse rate, blood pressure, central venous pressure and urine output should be monitored frequently.
(iv) Sedation should be used with caution as these drugs are usually metabolised in the liver, but the liver is damaged. But an agitated patient runs greater risk of precipitating recurrent haemorrhage and this should be considered against the abuses of extra sedatives. Valiuin can be given intravenously. Librium is a good drug in the alcoholics facing withdrawal.
(v) Rapid clearing of the blood from the bowel should be effected by mild purgatives and enemas. This will reduce ammonia load and hence encephalopathy.
(vi) Gastric acid secretion should be decreased by cimetidine administration. (vii) In patients with ascitcs sodium intake should be minimised. Spironolactone (aldactone) should be used. Paracentesis is required to reduce intra-abdominal pressure.
In this phase the patient is quickly stabilised so that one can go for proper diagnosis of the case.
2. Diagnosis.—Endoscopy is the main diagnostic stool. If too much bleeding is obscuring the view through cndoscopy, lavage through an Ewaled tube is necessary. Assessment of the size and extent of the varices is made. One must exclude bleeding from other causes particularly peptic-ulcer. It must be remembered that bleeding due to gastritis in patients with portal hypertension should be managed as variceal bleeding.
3. Specific Treatment.—
(i) VASOPRESSIN (PITRESSIN).—This is potent vasoconstrictor and is used to control variceal ( bleeding by splanchnic vasoconstriction. Pitressin has a short half life (10 to 15 minutes) and should be given by continuous infusion after a primary bolus dose. In acute bleeding 20 units in 100 ml of 5% dextrose should be given intravenously over 20 minutes. This should be followed by a continuoninfusion of 0.4 unit per minute.
The side effects of pitressin are (a) due to generalised smooth muscle contraction. Cramping abdominal pain, which may be associated with bowel evacuation is distressing to the patient, (b) Coronary artery vasoconstriction may lead to myocardial ischaemia. (c) Peripheral vasoconstriction may cause Raynaud's syndrome.
Recently propranolol is being used to prevent recurrent bleeding by reducing cardiac output./sopro/ereno/ may be given to reduce the haemodynamic hazards of vasopressin. I.V. soinatostatin is often used nowadays
(ii) ENDOSCOPIC VARICEAL SCLEROSIS.— This has revolutionised the treatment to variceal haemorrhage. This has definitely decreased the mortality rate in such haemorrhage. A sclerosant solution is injected through an endoscope into the varices. Injection may be para-variceal or intra variceal. In acute bleeding intravariceal injection is preferred, but to stop recurrence of bleeding para-variceal injection is preferred. Flexible endoscopy is used. There is wide choice of sclerosant solutions, but 2.5% sodium morrhuate is probably the best, followed by ethanolamine oleate
Complications of this method are primarily (a) retrosternal chest pain due to phlebitis, (b) Local microperforation, though major perforation is rare. (c) Pulmonary complications such as effusion which may be accompanied by fever.
(iii) Balloon tamponade.—This is a temporary method to control acute bleeding, if the above methods have failed to control it. The aim should be to use tamponade for as short time as possible. This step may be even omitted in case of good risk patients where one can think of urgenLshunt operation after preliminary trial of pitressin and sclerotherapy.
Sengstaken-Blakemore tube is usually used for balloon tamponade. Balloons must be checked. The tube is advanced well into the stomach. The gastric balloon is then fully inflated with 300 ml air and appropriate traction must be applied. The oesophgeal balloon should be inflated to 45 nun Hg only if the gastric balloon does not control the bleeding. Oesophageal suction is continued above the balloons.
Treatment of complications.—
- Shock: Sedation with barbiturates. Fresh blood transfusion should be given.
- Clotting Problems: It may either be due to prothrombin deficiency from liver damage or thrombo-cytopenia from splenic enlargement. Vitamin К may be administered. Fresh blood transfusionalso works here.
(3) Encephalopathy : This is prevented by continuous gastric lavage which will prevent absorption of blood protein. Magnesium sulphate and neomycin should be given through Sangstaken tube. Neomycin is given 500 ing. in the first hour and then every two hours. High bowel wash also helps in these cases.
(4) Liver failure: Plenty of Carbohydrate should be given by month. Fat should very much be reduced indict.
(5) Ascites : This means severe liver failure and mortality is much higher in these cases. Low salt diet and diuretics should be given in these cases.
EMERGENCY OPERATIONS
These operations are only temporary measures designed to arrestbleedine. But these do not decrease theportal vein pressure or prevent subsequent haemorrhages.
Tanner's Operation.— In this operation the stomach is transected two inches (5 cm.) below the cardia and all its vessels having been divided and ligatured is immediately reanastomosed. This operation may be performed when the bleeding varices are mostly in the stomach, otherwise this operation does not prove to be very useful.
Oesophageal transaction with paraoesophageal devascularisation.—The main components of this treatmentare (i)oesophageal transection, (ii)splenectomy, (iii)paraoesophagcal and gastricdevascularisation (this means all the vessels supplying the distal part of the oesophagus and upper half cf the stomach arc ligated individually and divided) and (iv) selective vagotomy and pyloroplasty. This procedure was advocated by Sugiura and Futagawa. In this technique portal hypertension is maintained which ensures portal venous.
Endoscopic sclerotberapy.— The method has already been discussed in the conservative management. A few surgeons advocate this treatment as a definitive procedure. Predominantly poor risk cirrhotics who are not even fit for emergency operations, may be given the advantage of this method. It has been reported that about 65% of cases were alive from 1 to 10 years. The rebleeding rate was 24%. 80% of patients require multiple sclerotherapy sessions. The benefits ofsclerotherapy lie in the preservation of portal perfusion (portal blood flow is maintained) and maintenance of hepatic function. The complications have also been mentioned in the conservative treatment.
The present role ofendoscopic sclerosis in definitive management is undefined. The poor risk patients who will not tolerate major surgery will mostly be benefited.
SHUNT OPERATIONS
There are principally three types of shunt operations :
(i) Portacaval, (ii) Lieno-renal and (iii) Mesenterico-caval. Other shunt operations between portal and cava vien.
INTESTINAL OBSTRUCTION
R. Scott Jones, M.D.