25. 1 Acute pancreatitis
| Вид материала | Документы |
- Acute biliary pancreatitis. Treatment tactics, 134.96kb.
- The problem of acute pain and its substantial relief is common for every medical field., 344.88kb.
PERITONEUM
Normal Structure and Function
The normal peritoneum, a glistening transparent membrane is divided into two parts — (a) the visceral peritoneum that surrounds the abdominal viscera completely or partially and the parietal peritoneum that lines the rest of the abdominal cavity and is in close contact with the anterior abdominal wall. The parietal peritoneum is richly supplied with nerves and when irritated, causes severe pain accurately localised to the affected area. The visceral peritoneum, however, is poorly supplied with nerves and pain arising therefrom is vague and poorly localised.
Histologlcally, the peritoneum is a single layer of flattened polyhedral cells resting on a thin layer of flbroelastic tissue. Serous fluid secreted by these cells allows gliding movement between the viscera. The peritoneal cavity normally contains only about 10 ml of fluid to serve as a lubricant. The surface area of the peritoneum is nearly equal to that of the skin and is significantly greater than the filtration area of the renal glomeruli. Because of the large .surface area, bidirectional transfer of various substances is rapid as well as massive. This property of the peritoneal membrane is utilised in peritoneal dialysis for acute renal failure.
Following Injury, the peritoneum heals rapidly. It responds to insult with hyperaemla followed by transudation. Oedema and vascular congestion occur in the subperltoneal tissues. Immediately exterior to the peritoneal membrane. The peritoneal cavity is normally sterile. A small number of bacteria can be efficiently disposed of but peritonitis ensues if the defence mechanisms are overwhelmed by a massive or continued contamination.
The dorsal mesentery of the gastrointestinal tract undergoes a great change during development as the intestine elongates outside the embryo and subsequently rotates before returning to the peritoneal cavity. There is an anticlockwise rotation of the small bowel around the superior mesenteric artery. The mesentery anchors the intestine to the posterior wall of the abdominal cavity. In the mesentery, the blood supply to the Intestine is contained together with the lymph nodes, visceral nerve fibres and fat. The root of the mesentery is only about 15 cm in length but it fans out to be attached to the entire length of the small Intestine. The transverse colon has a long mesocolon, the ascending has no mesentery, and the descending and pelvic colon have mesenteries of variable length.
The mesentery has a similar cell structure and function as the peritoneum.
The omentum is a well-vascularised, pliable, mobile double fold of peritoneum that participates actively in the control of peritoneal inflammation and infection. It seals off leaking viscera or areas of infection (e.g. inflamed appendix) and its scavenger functions include absorption of small particles and destruction of bacteria.
PERITONITIS
Peritonitis is inflammatory response of the peritoneal lining. Although microorganisms are the commonest cause, irritation by extravasated secretions (bile, urine, blood or meconium). chemicals or foreign bodies (talc and starch), may also occur.
Classification of the various forms of the disease is based on the pathogenesis. The important types are the following.
1. Acute secondary bacterial peritonitis
2. Primary (acute) bacterial peritonitis
3. Acute nonbacterial peritonitis
4. Chronic bacterial peritonitis (tuberculous)
5. Chronic nonbacterial peritonitis.
Acute Peritonitis
Sources of Infection
The sources of infection are the following.
1. Directly
a. From perforated hollow viscus
b. Penetrating abdominal wounds
c. Following surgery, e.g. drainage tubes.
2. Extension from the following.
- Inflamed abdominal organs, e.g. appendicitis. Cholecystitis
- Gut wall as In strangulated hernia
- Fallopian tubes following salpingitis.
3. From the bloodstream a. In septicaemia
Nonbacterial (chemical) peritonitis, from leakage of urine from rupture of the bladder or haemoperitoneum, soon becomes infected by transmigration of organisms from the bowel, and bacterial peritonitis sets in.
Bacteriology
The microbial picture reflects the bacterial flora of the involved organ. Perforations of the stomach or duodenum are generally sterile. Perforations or ischaemic injuries of the distal small bowel (e.g. strangulated hernia) lead to infection with aerobic bacteria in about 30 per cent of cases and anaerobic organisms in about 10 per cent of the cases. Faecal spillage with a heavy bacterial load originates from the appendix, colon and rectum. The main aerobic pathogens include the gram-negative bacteria E. coli, Proteus, Enterobacter and Klebslella groups and streptococci. Besides Bacteroides frag His, anaerobic cocci and Clostridia are the prevalent anaerobic organisms.
Clinical Types
Localised The peritoneum adjacent to the inflamed organ usually becomes involved, e.g. right iliac fossa in the early stage of appendicitis, right upper abdomen in the initial stages of cholecystitis, etc. The rigidity or "muscle guard' is localised and so is the area of rebound tenderness. There is no cessation of peristalsis. The general condition of the patient remains stable with not much rise in pulse rate or temperature.
Diffuse (generalised peritonitis) If the process does • not get controlled, the Infection spreads to the whole of the peritoneal cavity. The entire abdominal wall is rigid like a board. There is tachycardia and high fever. No intestinal sounds are heard and there may be abdominal distension. Later, toxiclty gives rise to hypotension and marked deterioration of the patient's general condition.
Natural Factors Determining the Course of Peritonitis
1. Factors favouring localisation
a. Anatomical peritoneal spaces—Pus collects and tends to localise.
b. Adhesions form around the affected organ. The greater omentum by enveloping the Inflamed structure often forms a substantial barrier to the spread of infection.
2. Factors favouring spread of peritonitis
- Rapid spread, e.g. perforation of a hollow viscus discharging a gush of intestinal contents into the peritoneal cavity which spread all over the peritoneal cavity before localisation can take place.
- Violent peristalsis by laxatives or enema may disseminate infection.
- High virulence of the infecting organisms.
- In children, local defence is poor due to a small omentum and natural immunity is underdeveloped.
- Deficient host resistance as In immune deficiency states when drugs like steroids or cytotoxics are being used; and or in old age.
Pathology
The peritoneum responds to infection locally by hyperaemia and increased capillary permeability and serous fluid accumulates. The fluid later becomes turbid and purulent. The glossy appearance of the peritoneum Is lost. It becomes dull in appearance due to deposition of flakes of fibrin. When the virulence of organisms is minimal and the defence mechanism of the body is adequate, localisation is accomplished by matting of the adjacent bowel and mesentery, all wrapped around by the omentum. Administration of antibiotics also helps towards the localisation. The progress and outcome of peritonitis depends on:
(I)persistence of' the source of infection,
(II) virulence of the infection;
(III) extent and duration of contamination; and
(IV) inadequate and inappropriate therapy.
If the cause is not removed or treated, (perforated appendix, perforated peptic ulcer, etc.) the peritoneal and systemic defence mechanisms are unable to localise the inflammation. The continued peritoneal soiling Is almost always fatal.
A mixed bacterial flora is usually responsible and It acts synergistically. Moreover, there is evidence to indicate that apparently nonpathogenic microorganisms may increase the virulence of pathogenic bacteria with which they are associated. Experimental evidence is available that aerobic organisms enhance virulence of anaerobes and these in turn, enhance the virulence of aerobes by elaborating enzymes which destroy antibiotics. The presence of disintegrated products of blood, especially haemoglobin is known to accentuate the virulence of the organisms.
Massive sudden contamination often disseminates bacteria rapidly throughout the peritoneal cavity.
Effects of Spreading Peritonitis
Fluid and electrolyte disturbances In generalised peritonitis, there is outpouring of copious serous fluid into the peritoneal cavity and into the lumen of the atonic and dilated gastrointestinal tract. This translocation of water, electrolytes, and protein into a sequestrated "third space" functionally removes this volume temporarily from the intra-vascular fluid. Vomiting and nasogastric suction if not balanced, further disturb the fluid and electrolyte balance.
Toxic absorption The inflamed peritoneum acts as a bidirectionally permeable membrane, not only secreting fluid into the peritoneal cavity but also permitting ready absorption of both bacteria and bacterial toxins. Many of the strains of E. coll. Bacteroides and CL welchli produce toxins which when absorbed through a k:'"y absorptive area produce septic shock.
Septic shock in normovolaemic patients begins with a hyperdynamic response associated with increased cardiac output, normal or high central venous pressure, low peripheral resistance, warm extremities despite a low blood pressure, hyper-ventilation, and respiratory alkalosis.
When sepsis is superimposed on hypovolaemia, the typical situation in peritonitis is an Initial hypodynamic pattern usually characterised by low cardiac output, low central venous pressure, vasoconstrictlon with high peripheral resistance, cold extremities, and low blood pressure. Hypovolaemic septicaemia is a dangerous situation and if treatment is delayed or unsuccessful, death may ensue.
Paralytic ileus The initial response of the bowel-to peritoneal Irritation is transient hypermotility. After a short interval, motility becomes depressed . and nearly complete adynamic ileus follows. The bowel distends and both air and fluid accumulate in the lumen. The source of the accumulating gas is largely swallowed air. Fluid secretion into the lumen of the bowel increases in ileus while absorption is relatively impaired, promoting sequestration of fluid in the bowel lumen.
Endocrine disturbances due to stress Peritonitis acts as an urgent systemic stress and excites vigorous response from the pituitary-adrenal axis.
ACTH increases the secretion of hydrocor-ticosteroids. Secretion of aldosterone is increased, as a response to hypovolaemia. This aggravates potassium loss and sodium retention. Excessive production of catecholamines is in large part responsible for vasoconstriction, tachycardia and sweating.
Cardioresplratory upsets The volume deficit results in decreased venous return and diminished cardiac output. The heart rate increases in an attempt to maintain cardiac output, but compensation usually is incomplete. Progressing acldosis brings about disturbance in cardiac contraction and a further decrease in cardiac output.
Abdominal distension, primarily due to paralytic ileus results in a decrease in the ventilatory volume and basal atelectasis. This may also be due to restriction of both diaphragmatic and Intercostal respiratory movements due to pain.
Renal response Hypovolaemia, reduced cardiac output, and Increased secretion of antidiuretic hormone and of aldosterone in peritonitis, all act together on the kidneys. Renal blood flow is diminished. Reabsorption of both sodium and water is increased and potassium is wasted. Urine output is diminished and the kidneys may not be able to handle excess solutes. The tendency to develop metabolic acidosis is thus enhanced.
Clinical Features
Clinical features of the causative lesion (e.g. acute appendicitis, acute diverticulltis) usually precede those of localised or spreading peritonitis. Perforation of a duodenal ulcer may, however, occur without any antecedent exacerbation or history of dyspepsia. There is sudden severe epigastric pain which spreads to the entire abdomen and is due to chemical Irritation by the escaping gastric Juice.
The pain of established bacterial peritonitis starts in the quadrant related to the primary lesion and later spreads to other areas or the entire abdomen. Movement and coughing increase the pain. There is guarding and rigidity over the area of the abdomen which is involved. There Is rebound tenderness.
Absence of peristaltic activity characterises all forms of acute generalised bacterial peritonitis. In the absence of adequate nasogastric decompression, progressive intestinal distension may interfere with diaphragmatic movement. The sequestration of fluid and electrolytes in the dilated loops and the peritoneal cavity results in hypovolaemia and electrolyte imbalance. There is rise in temperature and pulse rate. The pain increases and, usually, there is associated vomiting.
In generalised peritonitis, severe generalised abdominal pain is the predominant symptom. There is fever often with chills and rigors. On examination, the tongue is dry, the pulse rate is rapid, and the respiration is hurried. The face may be flushed with sunken eyes, cold clammy skin, hypotension and oliguria or anuria. Fortunately, the later stages of acute peritonitis are not so common due to a better understanding of the problem and its management.
On Inspection, the abdomen is distended. Movements of the abdomen with respiration are restricted or absent. The abdomen is rigid and tender on palpation. Deep palpation is painful. The abdomen is dull on percussion but shifting dullness is usually not present. Bowel sounds are sluggish or may even be absent. On rectal examination, there Is usually fullness and tenderness in the rectovesical pouch.
Diagnostic Aids
1. Polymorphonuclear leucocytosis is invariably present. Dehydration manifests as a rising haematocrit and blood urea. Elecrolyte disturbances, usually hyponatraemia, may be there.
2. Peritoneal diagnostic aspiration may at times help but is usually unnecessary. Bile-stained fluid indicates perforated peptic ulcer, the presence of pus indicates bacterial peritonitis, and blood is aspirated with intraperitoneal bleeding.
3. Serum amylase estimation excludes acute pancreatitis as the cause of acute peritonitis.
4. The demonstration of gas under the diaphragm on an erect and lateral decubltus abdominal film confirms the diagnosis of a perforated viscus. There may be multiple fluid levels.
5. Ultrasound and CT may demonstrate free peritoneal fluid but are rarely helpful in diagnosis.
Differential Diagnosis
Basal pneumonia is sometimes accompanied by peritonism and can be misdiagnosed, especially in children, as peritonitis. In peritonism, the bowel activity is present and rebound tenderness is minimal or absent.
Other conditions which should be considered in the differential diagnosis include ureteric colic cholecystitis, hepatitis, acute pancreatitis and urinary tract infection.
Diabetic ketosis may present with abdominal pain and vomiting. Urine testing for sugar and ketones should be performed on all patients with acute abdominal pain.
Treatment
This is considered under two headings — supportive and definitive.
Supportive measures These include gastroduodenal aspiration, intravenous fluids to correct the hypovolaemla and electrolyte deficiencies and adequate pain relief.
The intravenous fluid therapy is monitored by the CVP and hourly urine output (which should be kept between 30 and 50 ml/hr). Several litres of balanced salt or lactated Ringer's solution may be , required to correct hypovolaemla and to bring the blood pressure and urinary output to satisfactory levels. Potassium supplements are withheld until renal perfusion (urine output) is adequate.
Oxygen, vasoactive drugs and steroids may be required to support the respiration and circulation In several cases.
Analgesics should be given as soon as a working diagnosis has been established.
Definitive Measures
A loading dose of parenteral antibiotics directed against the anticipated bacterial pathogens are given. Combination antibiotic therapy is essential against a mixed flora. Current regimes include aminoglycosldes or third generation cephalosporins for gram-negative coliforms, ampicUlin for entero-cocci and metronldazole for anaerobic organisms. The regime may need to be modified after results of culture and sensitivity become available.
Laparotomy is most commonly performed through a midline or paramedlan approach. Material for culture and sensitivity Is obtained immediately after the abdomen is opened. The first objective is to establish the cause of the peritonitis and then to remove the inflamed organ or to close the perforated viscus. Removal of Infected material by peritoneal lavage is thought to reduce mortality. Occult pockets of infection are located by thorough exploration, and contaminated and necrotic material removed. The use of a large volume of antibiotic saturated saline (1-2 litres) has been shown to be very effective for cleaning the peritoneum. If there is a chance of continued collection, a drain should be left in. Draining the peritoneal cavity as a routine is not advised as it is Ineffective.
The abdominal wall is sutured with mono-filament material but the skin wound is left open and packed with gauze soaked In acriflavine glycerine. In the absence of infection, secondary suture of the skin is performed 5-7 days later.
In patients with heavily contaminated peritoneal cavity a Marlex (or polypropylene) mesh with a zip-fastener is sutured to the wound edges. This approach allows repeated inspection of the peritoneal cavity under intravenous sedation and may reduce the recurrent sepsis rate. This method is, however, under extensive trial before it can be recommended as a routine measure.
Assessment of Severity of Peritonitis
The estimation of severity of peritonitis from clinical and laboratory findings determines specific care, need for surgery, and also predicts the outcome.
Clinical findings The age, general health of the patient and duration of infection must be noted.
Physical findings can be divided into abdominal signs arising from the initial cause and manifestations of systemic infection. Local findings Include abdominal pain, tenderness, guarding or rigidity, distention, free peritoneal air, and diminished bowel sounds. Systemic findings include fever, chills or rigors, tachycardia, sweating, tachypnoea. restlessness, dehydration, oliguria, disorientation, and ultimately refractory shock. Shock is due to the combined effects of hypovolaemia and septicaemia with multiple organ failure.
The findings in abdominal sepsis are modified by the patient's age and general health. They are difficult to interpret in very young or very old or in those who are debilitated, immunosuppressed, receiving cortlcosterolds, or in the recent postoperative period. Diagnostic peritoneal lavage may be employed in these difficult cases.
Laboratory findings Blood studies should include blood cell count, arterial blood gases, a blood coagulation profile, and liver and kidney function tests. Samples of blood, urine and peritoneal fluid are taken for culture studies.
Assessment of Severity Sepsis Scoring
It has been found that the outcome of the management of diffuse peritonitis depends upon the severity of the septic state. Various indices have been evaluated.
The Mannheim Peritonitis Index (JvlPI) This incorporates information regarding age, gender, organ failure, cancer, duration of peritonitis, involvement of the colon, extent of spread within the peritoneal cavity, and the character of the peritoneal fluid to define risk. The possible scores range from 0 to 46, and patients with scores above 26 are defined as having severe peritonitis. For a score of up to 15, the mortality is virtually 0; for a score more than 29, the mortality rate exceeds 50 per cent.
The Peritonitis Index Altona (PIA) The peritonitis index uses age, extent of infection, malignancy, cardiovascular risks, and leucopenia to classify patients. In this study, the mean peritonitis index for those who died was 1.59 whereas that for patients who lived was 0.38.
Acute Physiology and Chronic Health Evaluation Score (APACHE II) While the first two scoring systems base the prediction on anatomical and physiological findings this accounts mainly for physiological changes.
The scoring consists of various parts. The first part indicates as to how far from normal homeostasis a patient has strayed as a result of acute illness (using 12 initial values of routine laboratory tests and physical findings; APS 12, 0 to 60 points). The other part of the score is a chronic health evaluation. This examines the patient's preadmission health by reviewing his medical history as to his functional status and the type of medical attention received during 6 months before admission.
This scoring system can also be used to assess * therapeutic progress or deterioration and has a definite value in predicting mortality rates.
Postoperative care Abdominal distension Is managed by gastroduodenal suction and fluid, nutritional and other supportive measures are continued postoperatively. Antibiotics are given for 10-14 days depending on the severity of peritonitis. Clinical improvement is evidenced by good urine output, reduction in fever and return of bowel sounds.
Primary (Spontaneous) Bacterial Peritonitis
Primary peritonitis occurs without any obvious source of the infection being demonstrated. This is much more common in children who have undergone a splenectomy or who have nephrotic syndrome and in adults with cirrhosis. It usually follows an acute febrile illness. Only one organism may be found in the cultures of the peritoneal cavity. Pneumococci used to be a common Isolate but E. coli and Klebslella are now more frequently cultured.
The disease has an Insidious course and localising signs of peritonitis may be minimal. The common manifestations include abdominal pain, fever, rebound tenderness and diminished or absent bowel sounds. The full-blown picture is accompanied by septic shock. A peritoneal tap should be performed and fluid immediately gram-stained.
It may be difficult to differentiate between primary and secondary peritonitis. Exploratory laparotomy is advisable in doubtful cases. Moreover, caution must be exercised in accepting the diagnosis of primary peritonitis as an unusual pathology may be missed.
Treatment is conservative by an appropriate antibiotic (amoxycillln, ampiclllln or augmentin).
Acute Nonbacterlal Peritonitis
The most common form is after perforation of a duodenal ulcer when the gastric contents and bile enter the peritoneal cavity. Secondary overgrowth with intestinal flora occurs if the peritoneal contamination persists. Bile escaping from a ruptured gall bladder and pancreatic enzymes collecting in patients with acute pancreatitis can also cause this type of peritonitis. Blunt abdominal trauma may release blood, pancreatic enzymes, bowel contents and urine into the peritoneal cavity following rupture of the relevant organs.
Meconlum peritonitis can occur in neonates from Intestinal rupture of the gut during the intrauterine life. It may lead to intense flbrosis and calcification. It may become secondarily infected. It presents as intestinal obstruction in the newborn. Treatment entails relief of obstruction.
Chronic Bacterial Peritonitis
In the majority the infection is tuberculous In origin. It is described elsewhere.
Chronic Nonbacterlal Peritonitis
It Is also known as granulomatous peritonitis.
Talc (magnesium silicate) and starch may irritate the peritoneal surface to produce granulomatous change. The associated inflammation encourages adhesion formation. It represents a foreign body reaction.
Modem operating gloves are starch and talc free and this should help solve the problem for the future.
The patient presents with abdominal pain, distension and pyrexla. The diagnosis needs to be confirmed by peritoneal biopsy. Malignant and tuberculous peritonitis have to be considered in the differential diagnosis. Treatment is conservative but systemic steroids may help in some.
INTRA-ABDOMINAL ABSCESSES
An intra-abdominal abscess may be an intra-peritoneal or a retroperitoneal one.
ABSCESSES SUBDIAPHRAGMATIC SPACE
ccur less commonly In the retroperltoneum than in the peritoneal cavity. The abscess results when peritonitis remains localised or when generalised peritonitis fails to resolve completely. Localisation can occur either in anatomical spaces, when omentum prevents spread, or due to adhesions.
Intraperltoneal Abscesso*
An intraperitoneal abscess may develop adjacent to a diseased viscus (e.g. with perforated appendix or divertlculitis), or as a result of external contamination (e.g. postoperative subphrenic abscess). In a fair number of cases, the abscess occurs as a sequel to generalised peritonitis. Interloop and pelvic 'abscesses form if extravasated fluid gravitating into a dependent or localised area becomes secondarily Infected. Resolution of peritonitis with formation of a pelvic or subphrenic abscess is dictated by the anatomy of the peritoneal cavity. The upper part of the abdomen is divided nearly in half by the vertebral column. Both the pelvis and subphrenic spaces on either side form deep and dependent cavities in which Infected material collects by gravity. In addition, the suction effect of respiration tends to draw infected peritoneal fluid up under the diaphragm.
Anatomy of the subphrenic space Subphrenic space is bounded above by the vault of the diaphragm and below by the shelf of the transverse colon with the attached mesocolon'. The liver divides this space into a subdiaphragmatic compartment and a subhepatic compartment. The attachments of the triangular and the falciform ligaments of the liver further subdivide these spaces into four intraperitoneal and three extraperitoneal spaces. The extraperitoneal spaces lie one on each side of the body and the third is the bare area of the liver.
The intraperitoneal subphrenic spaces (Fig. 43,1) are the following.
1. The right subdiaphragmatic space
2. The right posterior subhepatic space (Morison's pouch)
3. The left subdiaphragmatic space
4. The lesser sac (left posterior subhepatic space).
The extraperitoneal spaces are three in number.
1. Right and left extraperitoneal arc the names given to perinephric spaces.
2. Bare area of the liver.
Infection of the subdiaphragmatic space is much more common than infection of the subhepatic space. The right subdiaphragmatic space is the most frequently Infected (Fig. 43.2). The left subdiaphragmatic space is the next most commonly involved.
Clinical Features
Intraperitoneal abscess is generally polymlcroblal and anaerobic organisms are the predominant flora. A common history is that when some infective focus in the abdominal cavity has been dealt with, the condition of the patient improves temporarily but after an interval of a few days or weeks, recurring or persisting fever is seen. Fever is typically intermittent or spiking in character at first, then becomes progressively more persistent as the abscess matures.
In patients with subphrenic abscess, irritation of adjacent structures may produce local chest pain, referred shoulder pain, hiccup or basal pleurisy. In patients with pelvic abscess, it may produce diarrhoea or urinary urgency. Pelvic abscess can often be detected on pelvic or rectal examination as a fluctuant mass.
Investigations
There is leucocytosls. Chest X-ray In subphrenic abscess may show a small pleural effusion and a raised diaphragm. Ultrasonography is most useful for lesions in the right upper quadrant, paracolic and pelvic areas. CT-scan study Is highly sensitive. A CT or ultrasonography guided needle aspiration can be helpful. Radlonuclide scanning with Indium111 labelled autologous leucocytes may sometimes disclose an abscess.