Differential Diagnosis and Medical Therapeutics: A Treatise on Clinical Medicine P Siva Rama Krishna Rao
INDEX
×
Chapter Notes

Save Clear


Acute Abdominal PainChapter 1

Abdominal pain of sudden onset is a challenging task in clinical practice, as early diagnosis and prompt relief, without clouding the picture and loss of precious time, are the principal responsibilities of any clinician. Acute abdomen connotes acute illness of short duration with clinical features confining to the abdomen predominantly. This may be of abdominal or extra-abdominal origin. The acute abdomen need not always find its way to the surgical wards since certain medical conditions may simulate the same very much. Usually, it is associated with vomiting with or without shock.
Three different types of pain are involved in the spectrum of abdominal pain, i.e.
  1. Visceral
  2. Somatic
  3. Referred.
The pain arising from hollow or solid viscera is termed visceral or splanchnic. It tends to be deep, diffuse and full (solid organ) or colicky (hollow organ) with poor localisation. Pain originating in the abdominal wall and parietal peritoneum is called somatic pain, which is well localised and sharp. Referred pain is one in which visceral disease gives rise to localised pain, apparently superficial, usually away from the site of the diseased viscus and often dermatomic.
The mechanism of abdominal pain is:
  1. Parietal due to inflammation
  2. Visceral due to obstruction and/or with inflammation
  3. Muscular (smooth muscle spasm)
  4. Vascular (ischaemia, haemorrhage)
  5. Referred pain and
  6. Psychogenic pain (functional).
The inflammation or ischaemia lowers the pain threshold by releasing some chemicals like bradykinin, histamine, prostaglandins, serotonin and lactic acid. The other stimulus includes increased tension in the wall of the viscus due to distension or contraction.
The painful impulses are mediated over somatic nerves supplying the parietal peritoneum or visceral afferent nerves accompanying the abdominal sympathetic nerve fibres.
Pain may be referred to the abdomen due to disease of thorax or genitalia or spine, since the visceral sympathetic nerve fibres share the neural pathway, with the somatic nerve fibres arising from the same spinal segment. A careful analysis of abdominal pain and the sequential events of the episode form the diagnostic pathway, to arrive at a correct diagnosis in the majority of cases.
 
CAUSES OF ACUTE ABDOMINAL PAIN
In order to obtain a clear insight, the causes can be grouped as: (i) intra-abdominal, (ii) abdominal, (iii) extra-abdominal, (iv) psychogenic (Table 1.1).
 
Intra-abdominal
 
Inflammations
 
Peritoneal
  • Acute peritonitis: It is characterised by severe abdominal pain with the conspicuous presence of a quiet picture and absence of any restlessness. Vomiting with or without fever and diminished respiratory excursions of the abdominal wall are the other presenting features. Palpation reveals board like muscular rigidity, tenderness and rebound tenderness (peritonism). Auscultation may reveal absent bowel sounds. Progressive abdominal distension, ileus and shock may follow. Plain X-ray of the abdomen in an erect position reveals air under the diaphragm. In addition, distension of both bowels, with fluid levels or fluid between the loops of the bowel giving a thickened appearance, may be present. Secondary peritonitis due to a ruptured viscus from peptic ulcer is acute in onset, localised peritonitis may develop gradually to generalised peritonitis if it is due to infection like appendicitis or diverticulitis, or salpingitis.
    Trauma or systemic lupus erythematosus or acute mesenteric vascular occlusion are the other causes of peritonitis.
2
TABLE 1.1   Aetiological classification of acute abdominal pain
I. Intra-abdominal
Pain may arise from peritoneum, viscera or mesentery due to:
  1. Inflammations
  2. Mechanical (obstructive colics) or
  3. Vascular disturbances
  1. Inflammations
    1. Peritoneal: Acute peritonitis: Infective or perforative
    2. Visceral
      1. Hollow organs
        1. Gastroduodenal (peptic ulcer)
        2. Biliary tract (biliary colic, acute cholecystitis, cholangitis)
        3. Intestinal (acute appendicitis, acute gastroenteritis, diverticulitis, colitis, intestinal colic).
      2. Solid organs
        1. Pancreatic (acute pancreatitis)
        2. Renal (acute pyelonephritis)
      3. Pelvic organs: Pelvic inflammatory disease (PID)
    3. Mesentery: Acute mesenteric lymphadenitis
  2. Mechanical
    1. Visceral
      1. Hollow organs
        1. Intestinal (intestinal obstruction)
        2. Biliary tract (biliary obstruction)
        3. Ureteral (ureteric colic)
      2. Solid organs: Renal (pelvi-ureteric junction, Dietl’s crisis)
      3. Pelvic organs
        1. Torsion of the ovarian cyst
        2. Ectopic pregnancy
    2. Mesentery: Omental torsion
  3. Vascular
    1. Ischaemic
      1. Mesenteric (angina, infarction)
      2. Splenic (infarction)
      3. Hepatic (Budd-Chiari)
      4. Sickle cell crisis
    2. Bleeding
      1. Ruptured ectopic pregnancy
      2. Ruptured graafian follicle (Mittelschmerz)
      3. Ruptured spleen
      4. Ruptured mesentery
      5. Ruptured aortic aneurysm
II. Abdominal
  1. Bornholm’s disease
  2. Nerve entrapment
  3. Haematoma of rectus sheath
  4. Abdominal hernias
  5. Referred pain
III. Extra-abdominal
  1. Cardiopulmonary (acute myocardial infarction, pneumonia, diaphragmatic pleurisy, pneumothorax, mediastinal emphysema)
  2. Neurological (herpes zoster, radiculitis, spinal lesions, e.g. tabes)
  3. Genital (torsion of the testicle)
  4. Metabolic (diabetic ketoacidosis, acute porphyria, C’L Esterase inhibitor deficiency)
  5. Alcohol, drugs and metals (lead poisoning)
  6. Hip joint disease
IV. Psychogenic
 
Visceral
  • Peptic ulcer, biliary colic, acute cholecystitis and cholangitis (Refer to Chapter titled ‘Chest Pain Dyspepsia, Haematemesis and Jaundice’).
Acute appendicitis: This is one of the most common causes of acute abdomen. There is a typical history of central abdominal pain of short duration with nausea or vomiting and mild rise of temperature. The pain may be colicky in character and may be followed by a shift to right iliac fossa. It gets sharply localised and causes discomfort on coughing or moving. Well localised tenderness to one finger and slight muscular rigidity are elicitable over McBurney’s point. Cough, tenderness, rebound tenderness, tachycardia, obturator test (pain is elicited when right hip is flexed and internally rotated) and neutrophil leucocytosis are valuable for arriving at a diagnosis. The pain is poorly localised and may not shift if the appendix is retrocaecal (loin) or pelvic or retroileal. Abdominal X-rays are helpful in these atypical cases. Localised air-fluid levels or increased soft tissue density in the right iliac region is seen in 50% of the cases of early appendicitis. Ultrasound examination of the abdomen is also of immense value in diagnosing appendi­citis. Any delay in the diagnosis leads to complications like gangrene, perforation, peritonitis/abscess.
Acute gastroenteritis: Acute gastroenteritis generally presents as profuse watery diarrhoea and vomiting with fever. There may be acute abdominal pain localised especially in Salmonella gastroenteritis due to intestinal inflammation and colic. The other common pathogens are enteric viruses, and Shigella and staphylococcal food poisoning. In severe cases, there may be dehydration, prostration and collapse.
Diverticulitis (Refer to Chapter titled ‘Chronic Diarrhoea’).
Colitis: It may be general or localised to one segment involving the mucous membrane and submucous tissue. In acute colitis, there may be diarrhoea with blood and mucus, and paroxysms of colicky pain. This may be a result of specific infections of the bowels from food, water or septic foci or due to toxaemias like uraemia or acute exacerbations of amoebic colitis.
Intestinal colic: Intestinal colic may produce severe intermittent abdominal pain due to tension or spasm of the smooth muscle. This is colicky in nature with freedom from pain between the attacks. It can be due to inflammation as seen in acute enteritis, or due to intestinal obstruction or lead poisoning or as a functional disturbance in spastic colon.
Acute pancreatitis (Refer to Chapter titled ‘Chest Pain’).
Acute pyelonephritis: It is characterised by a sudden onset of pain in the loin radiating down to the iliac fossa and hypogastric region. Fever with rigor, urinary symptoms 3(like dysuria, strangury and frequency) and tenderness in the renal angle are the striking features. It is due to acute inflammation of the parenchyma and pelvis in the kidney as well, due to infections like E. coli with or without obstruction of the urinary tract. The diagnosis can be confirmed by urinalysis particularly the microscopic examination, which reveals numerous pus cells, few red cells and epithelial cells with or without motile bacteria.
Pelvic inflammatory disease (PID): Acute PID may present as lower abdominal pain sometimes severe cramp like, particularly, in either or both the iliac fossa as in salpingitis, fever, vaginal discharge, dyspareunia and urinary symptoms. On examination there is adnexal tenderness, tenderness on cervical motion or rebound tenderness of the lower abdomen. Inflammatory mass may be found on pelvic examination. There may be a past history of menstrual irregularities or abortion. PID is due to the ascending spread of organisms from the genitalia or endogenous species in the genital tract. The diagnosis is confirmed by obtaining cultures from the fallopian tubes, cul-de-sac and endocervix at laparoscopy or a sonogram.
 
Mesentery
  • Acute mesenteric lymphadenitis: It is characterised by diffuse abdominal pain with tenderness in the lower right quadrant and fever due to enlarged lymphadenitis at the root of the mesentery. The exact site of pain cannot be indicated and the point of maximum tenderness varies from time to time. Leucocytosis with relative lymphocytosis may be present. It is usually nonspecific and filariasis may be the causative factor. Children and young adults are usually affected and it has to be differentiated carefully from acute appendicitis.
 
Mechanical
 
Visceral
  • Intestinal obstruction: The failure to facilitate the onward passage of the intestinal contents is called intestinal obstruction. A distinction must be made between the obstruction of mechanical origin (dynamic) and paralysis of the intestinal muscle (i.e. paralytic ileus). Peristalsis is absent or it may be present in non-propulsive form, e.g. mesenteric vascular occlusion or Pseudo-obstruction (adynamic). Intestinal obstruction can occur either in the small intestine or large intestine. The obstruction may be at one point (simple) or at two points (closed loop).
    Mechanical, nonstrangulating obstruction of the small intestine results in central abdominal pain, which is colicky at the outset and tends to become constant few hours later, particularly in the low small bowel obstruction. This is followed by vomiting, the frequency and faeculent nature of which depends on the level of obstruction. In higher obstruction of the small bowel, vomiting is an early feature which may be profuse and not faeculent. Constipation and obstipation with failure to pass gas per rectum is present if there is complete obstruction and sometimes it may be preceded by diarrhoea. Visible peristalsis may be seen in thin individuals especially during colicky episodes. Abdominal distension is minimal in higher obstruction and more in lower obstruction. Mild tenderness may be elicited. A palpable mass due to tense fluid in the loop is suggestive of closed loop strangulated obstruction. Auscultation may reveal rush of bowel sounds (peristaltic activity). Signs of dehydration and hypovolaemia may set in due to absorbed toxins and sequestration of large volume of fluid in obstructed bowel.
    Strangulation is suspected when shock appears during the course of obstruction. Previous cramping pain assumes continuous character. High fever and peritonism may develop. Most of the strangulations occur in the closed loop variety.
    X-rays of the abdomen in supine as well as upright positions show ladder like pattern of distended small bowel loops with air fluid levels (Fig. 1.1). There will be no gas in the colon in nonstrangulating obstruction. A widened space between the dilated bowel loops due to intraperitoneal fluid is seen in simple obstruction and strangulation as well. Loops due to intraperitoneal fluid and thumb printing, absence of mucosal pattern and gas within the bowel wall may be seen in strangulation.
    Large bowel obstruction also presents as above but for its slow onset, pain of less intensity in the lower abdomen, delayed vomiting with faeculent odour and significant marked distension. Obstipation and continuous abdominal pain of severe intensity suggest strangulation and a tender mass may be palpable in closed loop strangulation.
    Abdominal X-rays, in colonic obstruction, may show distension with gas proximal to the block, and without gas in the rectum. If the ileocaecal valve is incom­petent, it may appear like a small bowel obstruction.
The common causes of small intestinal obstruction are:
  1. Adhesions due to previous operations
  2. Internal and external hernias
  3. Intussusception
  4. Occlusion of superior mesenteric artery
  5. Mesenteric panniculitis.
The common causes of large intestinal obstruction are:
  1. Carcinoma of the bowel
  2. Diverticulitis
  3. Volvulus
  4. Occlusion of inferior mesenteric artery.
4
zoom view
Fig. 1.1: Plain X-ray of the abdomen in erect position showing distended small intestine loops with fluid levels—small bowel obstruction
  • Paralytic ileus: It is characterised by absence of colicky abdominal pain and bowel sounds. Abdomen is distended and vomiting is frequent. Peritonism may be present. It accompanies inflammatory abdominal condition (intraperitoneal sepsis), postoperative periods, intestinal ischaemia or associated with low cardiac output states.
     Plain X-ray shows dilated colon and the gas is present throughout the bowel including rectum.
  • Biliary obstruction (Refer to Chapter titled ‘Chest Pain’).
  • Ureteric colic (Renal pain): In renal colic, the pain radiates from the loin to the groin and testicle or labia. There will be restlessness, groaning in agony, sweating and vomiting. The intensity reaches the peak in 30 minutes and usually subsides within two hours. This is usually due to stone in the pelvi-ureteric junctions or ureter or vesicoureteric junction. Sometimes, this may be an inaugural symptom of acute pyelonephritis. Urine may show plenty of red blood cells and crystals (oxalate) or pus cells and protein.
  • Dietl’s crisis: They are characterised by severe pain down the ureter radiating to the back and are uncommon. Fever with rigors, nausea or vomiting, haematuria and shock may be the associated features. There may be a history of constant dragging pain due to a movable kidney with a traction on the renal plexus. The crises are due to kinking of the ureter. A floating kidney usually feels larger and its shape with the easy mobility are highly suggestive.
  • Torsion of the ovarian cyst: Any severe abdominal pain in a known patient of ovarian cyst should suggest torsion of the ovarian cyst. Pelvic examination may not be helpful because of marked tenderness. Nevertheless, it may be palpable during pelvic examination under anaesthesia.
  • Ectopic pregnancy (Vide infra).
 
Mesentery
Omental torsion: Torsion of the omentum occurs when it gets caught up in the opening of a hernia or fixed by adhesions with consequential twist and impaired blood supply. It is characterised by severe abdominal pain and tenderness over the affected area with nausea and vomiting. The twisted omentum may be felt as a mass on palpation.
 
Vascular
 
Ischaemic
  • Mesenteric angina (Chronic intestinal ischaemia):
    This is an uncommon cause of abdominal pain. If superior mesenteric artery is stenosed, it is termed as intestinal angina and if two or more major arteries are affected, it is known as abdominal angina. However, this has to be considered in aged patients who have evidence of atherosclerosis with angina pectoris or intermittent claudication. The pain starts at the mid-umbilical region 30 minutes after food and persists for two hours. There may be diarrhoea and loss of weight. Only angiographic demonstration of more than 50% of narrowing of the major arteries will be diagnostic.
  • Mesenteric infarction: Severe abrupt onset of colicky and progressively constant pain located in periumbilical area with minimal abdominal signs is the inaugural symptom in the early stage. Fever, bloody diarrhoea, bleeding per rectum, tenderness and blood in the nasogastric tube aspirates or vomitus may develop due to infarction. In addition, signs of intestinal obstruction may follow and eventually generalised peritonitis with hypovolaemic shock occurs. Previous history of abdominal angina may be forthcoming. The mesenteric infarction occurs in the superior mesenteric artery with small bowel obstruction or inferior mesenteric artery with large bowel obstruction and may be due to myocardial infarction or atrial fibrillation. Raised phosphate concentration in the serum of peritoneal fluid is suggestive. X-rays show thumb printing in the lumen of the colon due to mucosal oedema. Intramural gas or gas in the portal venous system may occur late.
  • Splenic infarction: Infarction of the spleen may be aseptic or septic. The pain is attributed to perisplenitis. The septic infarction may lead to splenic abscess which may burst giving rise to generalised peritonitis.
  • Budd-Chiari syndrome: It is suspected when there is sudden pain over the liver with vomiting, tender hepatomegaly and ascites (with rapid filling after paracentesis). Absence of hepatojugular reflux is highly suggestive. Insidious onset be associated with Jaundice cirrhosis/portal hypertension.
  • Sickle cell crisis: The painful crisis like abdominal crisis (biliary colic) or chest (pulmonary infarction), localised 5(bones and joints) may occur in sickle cell anaemia due to microinfarcts as a result of vaso-occlusive process. (Biliary colic may also be due to possible cholelithiasis). The crisis consists or severe, sudden abdominal pain of chest or joints, sometimes associated with fever. The tender rigid abdomen may be mistaken for a surgical illness. The presence of normal bowel sounds, absence of rebound tenderness and demonstration of sickling are diagnostic. Crisis can also be from marrow aplasia due to parvoviruses or sequestration wherein rapid enlarge­ment of liver and spleen occur due to trapped RBCs.
 
Bleeding
  • Ruptured ectopic pregnancy: Ectopic implantation is tubal in majority of the cases. Acute severe lower quadrant pain of sudden onset is the usual presentation in a woman with history of amenorrhoea or recent menstrual irregularity. Vaginal bleeding with or without passage of decidual tissue and a tender palpable pelvic mass outside the uterus are the cardinal features. The important complications are haemorrhage and shock. Plain X-ray of the abdomen may reveal a pelvic mass and culdocentesis demonstrates haemoperitoneum.
  • Ruptured graafian follicle: Sudden onset of severe pain in the middle of the menstrual cycle in a young female, apparently not looking ill with no gastrointestinal symptoms, is suggestive of rupture of the Graafian follicle. The pain sequence is characteristic in being severe initially and fading gradually (Mittelschmerz).
  • Ruptured spleen: The acute abdominal pain in the left upper quadrant or referred pain to the left shoulder or cervical region (Kehr’s sign) due to diaphragmatic irritation usually elicited by palpating left quadrant or by adopting Trendelenburg decubitus. Tenderness over the 9th and 10th ribs or increased splenic dullness or abdominal distension may be present. Hypovolaemic shock may be associated. There is usually, a history of abdominal trauma. Plain X-ray of the abdomen may show medial displacement of the gastric air bubble or inferior displacement of the transverse colon.
  • Ruptured mesentery: Haemorrhage may be due to spontaneous rupture of the mesenteric arteries leading to haemorrhage in the peritoneal cavity (mesenteric apoplexy). The characteristic picture will be the sudden onset of diffuse abdominal pain followed by hypoten­sion. There is diffuse tenderness and distension due to peritoneal irritation and free fluid in the peritoneal cavity.
  • Ruptured aortic aneurysm: Aorta may increase in length or diameter or both and the resulting aneurysm may be painful or even rupture. Severe abdominal pain radiating to the legs together with features of shock may appear. Femoral pulses may be absent and an expansile pulsating swelling may be seen in the abdomen. A loud continuous murmur is heard if it has ruptured into inferior vena cava. If the rupture occurs into retroperitoneal tissues, manifestations due to loss of blood may be mild initially.
 
Abdominal
  • Bornholm disease (Refer to Chapter titled ‘Chest Pain’).
  • Nerve entrapment: A nerve can be entrapped by a nonabsorbable suture and may cause pain in the abdominal wall like causalgia. Hyperaesthesia of the skin over the dermatome is highly suggestive.
  • Haematoma of rectus sheath: Haematoma in the rectus sheath may usually appear as a swelling in the lower quadrant due to trauma or anticoagulants or bleeding diathesis. Sudden abdominal pain with nausea and vomiting are the presenting features. A tender mass can be palpated which becomes more distinct on raising the head. Ultrasound examination helps in localisation.
  • Abdominal hernias: A protrusion of the intra-abdominal tissue through a defect in the abdominal wall includes inguinal hernia, femoral hernia, umbilical hernia or epigastric hernia (Fatty hernia of the linea alba) or incisional hernia (ventral) and Spigelian hernia. This hernial mass is made up of outer coverings of skin, etc. a peritoneal sac and any viscus. The neck of the sac is narrow which may endanger strangulation of the protruding bowel. In all cases of abdominal pain, careful inspection and palpation of the hernial orifices, umbilical area, linea alba above the umbilicus, incisional areas and lateral border of the rectus muscle may become imperative.
  • Referred pain: Any visceral pain may be referred to superficial areas of the abdomen away from the affected viscus or area. The classical examples are myocardial infarction, diaphragmatic pleurisy or spinal lesions or diseases of hip joint and genitalia. Pain is referred to cutaneous root areas which are innervated by the same segments supplying the painful viscus. It may or may not be associated with cutaneous hyperalgesia.
 
Extra-abdominal
 
Cardiopulmonary
Acute myocardial infarction, pneumonia, diaphragmatic pleurisy, pneumothorax, and mediastinal emphysema. (Refer to Chapter titled ‘Chest Pain’).
 
Neurological
Pain arising from posterior roots is of lancinating or burning character and precipitated by body movements or coughing. It is caused by inflammation in herpes zoster (preceding the eruption or postherpetic neuralgia) or compression in 6spinal tumours or disc prolapse or degeneration in tabes dorsalis. The gastric crisis in tabes is uncommon now and characte­rised by attacks of epigastric pain of short duration associated with vomiting which is due to increased motility and muscle spasm of the viscus.
 
Genital
Torsion of the testicle: Testicular pain is so sudden that the patient is unable to walk. On examination, the scrotum is enlarged with rubor. Testis is elevated, transversely placed and exquisitely tender. The duration influences the speed of infarction and so, it has to be recognised early enough to save the testis. Four hours is the said limit after which the testis is damaged irreversibly.
 
Metabolic
In any obscure abdominal pain, the metabolic causes may have to be entertained.
Diabetic ketoacidosis: Abdominal pain may be present with vomiting and abdominal rigidity especially in children. The pain may be shifting with variable intensity and is attributed to dryness of the endothelial surfaces. Examina­tion of urine for sugar and acetone will clinch the diagnosis.
Acute intermittent porphyria: Acute colicky abdominal pain with vomiting and constipation may accompany porphyria, which is rather uncommon. Examination of the urine will help in the diagnosis by the presence of elevated porphobilinogen (PBG). The urine turns deep red on standing and PBG is detected by Ehrlich’s Reagent, which forms a red complex that cannot be extracted with butanol. Rare genetic disease due to (autosomal dominant conditions) error in haem biosynthesis.
C1 esterase inhibitor deficiency: This deficiency may be associated with attacks of severe abdominal pain with angioneurotic oedema. This hereditary angio-oedema is an autosomal dominant condition and is suggested by the family history, attacks of laryngeal oedema besides colicky episodes. Urticarial lesions may or may not be present. Sometimes, this deficiency may be seen with lymphoproliferative disorders. Diagnosis is confirmed by low serum levels of C1 inhibitor and C4 levels.
 
Alcohol, Drugs and Metals
Alcohol and drugs have been incriminated in the development of pancreatitis. Heavy alcoholic bouts may precipitate acute pancreatitis. Chronic alcoholism may result in atrophy of the acini due to obstruction by the proteinaceous plugs in the small duct. Antimetabolite drugs like L-asparginase are associated with pancreatitis.
Lead poisoning: It can result in crampy diffuse abdominal pain accompanied by vomiting and constipation probably due to effect of lead on smooth muscle. Diagnosis of lead poisoning is confirmed by:
  1. Occupation history
  2. Punctate basophilic stippling of the red cells
  3. Associated features of anaemia and wrist drop (lead palsy)
  4. Increased levels of coproporphyrin or, delta-amino levulinic acid or lead concentrations.
 
Hip Joint Disease
Certain diseases (acute bursitis) of the hip joint may produce pain radiating into the lower quadrant but the examination of the hip joint helps to clarify the diagnosis.
 
Psychogenic
Sometimes abdominal pain may be perceived without any obvious cause especially in emotionally disturbed young females or hysterics. Psychogenic pain varies erratically in intensity and location without any specific character. There are no associated features of vomiting and constipation or tenderness or spasm of the abdominal musculature. On the other hand, features of conversion reaction or dissociation reaction may be perceptible. Nevertheless, psychogenic pain is not entertained in acute abdomen unless organic causes are eliminated with absolute concrete evidences.
Some malingerers travel from place to place seeking hospital admissions by picturesque acts of illness in whom multiple laparotomy scars may provide the clue. This is a classical example of Munchausen syndrome of malingering.
 
CLINICAL APPROACH
Acute abdomen is a temple of surprise and the clinician’s primary responsibility is to assess the extent of critical illness and decide whether possibility of any immediate surgery, without undue delay, is necessary. For this, careful history, which by itself reflects underlying pathology and critical physical examination to determine the direction of investigations, so as to arrive at a correct diagnosis, should be endeavoured.
 
Analysis of Pain
Is pain associated with shock or not is an important observation before analysing the pain?
 
Location
Enquiry must be made regarding the site of the pain initially and any shift of the pain thereafter. This depends on the organs involved in general:
  1. 7Epigastric: Perforated peptic ulcer, acute pancreatitis, acute myocardial infarction.
  2. Rightupperquadrant: Acute Cholecystitis, biliary colic, initial stage of acute appendicitis (retrocaecal), pancreatitis, pneumothorax.
  3. Rightlowerquadrant: Acute appendicitis, intestinal obstruction, renal colic, salpingitis, ruptured ectopic pregnancy.
  4. Umbilical or periumbilical: In affections of small intestine.
  5. Leftupperquadrant: Pancreatitis, renal pain, splenic infarction or rupture, acute myocardial infarction.
  6. Leftlowerquadrant: Obstructive lesions of the colon, diverticulitis, renal colic, ectopic pregnancy.
Well localised pain implies inflammation of the peritoneum in relation to the area affected (vide supra). Poorly localised or diffuse pain is suggestive of acute peritonitis, mesenteric vascular occlusion, sickle cell crisis and intestinal obstruction.
 
Character
  1. Colicky intermittent pain suggestive of spasm or obstruction and arises usually from a hollow viscus. The pain is not aggravated by movement. The classical examples are intestinal colic (acute enteritis, intestinal obstruction, lead poisoning), biliary (Fig. 1.2) and ureteric, colics.
  2. Gnawing pain suggestive of ulcer.
  3. Excruciating pain suggestive of infarction or rupture.
 
Intensity
  1. Is it severe and constant? For example, mesenteric vascular occlusion.
  2. Is it agonising with intervals of remission (colicky)?
  3. Does the intense pain suddenly disappear sponta­neously? For example, rupture of a hollow viscus.
  4. Is the pain slight to begin with and steadily increasing in severity? For example, peritonitis.
 
Duration
  1. If duration is brief—suggestive of colics.
  2. If present for more than six hours—invariably suggestive of surgical problems like inflammations or neoplasms.
 
Radiation
Pain from gallbladder disease may be radiated to right tip of the shoulder or inferior angle of scapula. Renal colic may arise from back and travels through lumbar region and is radiated to the testicle or labia (Fig. 1.3).
In pancreatitis, pain radiates to the back (Fig. 1.4).
zoom view
Fig. 1.2: Ultrasound scan of the abdomen showing cholelithiasis
 
Aggravating Factors
  1. Fatty food may initiate biliary colic.
  2. Heavy meal may herald acute pancreatitis.
  3. Movement aggravates pain in peritonitis.
  4. Pain is aggravated during menstruation in PID.
 
Relieving Factors
  1. Epigastric pain present in the lying position and relieved by sitting, is suggestive of pancreatitis.
  2. Hypogastric pain associated with diseases of sigmoid colon may be relieved by passing motion or flatus.
 
Associated Symptoms
  1. Pain with shock occurs in perforative peritonitis, acute pancreatitis, acute intestinal obstruction, acute enteritis, internal haemorrhage (ruptured ectopic pregnancy or solid viscera due to trauma or aneurysm), mesenteric vascular occlusion, torsion of the ovarian cyst, and acute myocardial infarction.
  2. Restlessness is present in colics whereas the patient is very quiet, because of possible pain during any movement in peritonitis.
  3. Nausea and vomiting accompany most cases of acute abdomen. The frequency of vomiting; the amount of vomits and its colour; faeculent character; time of onset of vomiting in relation to pain (occurring early in high obstructions and late in the low obstructions, preceding onset of pain as in enteritis; or pain preceding vomiting by few hours as in appendicitis).
  4. Bowel function: If the bowels have not moved for two days and no gas has been expelled (obstipation), it is suggestive of obstruction. If a feeling of constipation and the need for enema is felt, it is suggestive of classic or retrocaecal appendicitis (gas stoppage sign).
    8
    zoom view
    Fig. 1.3: Ultrasound scan of the abdomen showing calculus in the left kidney
    zoom view
    Fig. 1.4: Ultrasound scan of the abdomen showing swollen pancreas and ill-defined peripancreatic fat planes in the region of the body and tail, suggestive of acute pancreatitis
    If diarrhoea is associated, it is a manifestation of acute enteritis or in the early stages of mechanical obstruc­tion. If it is bloody diarrhoea, it is ischaemic colitis.
  5. Dysuria or haematuria in renal colic.
  6. Pyrexia: Fever is not usually high in appendicitis. Chills and high fever may be due to infections of renal or biliary tract.
 
Clues from History
  1. Any past history of indigestion, peptic ulcer disease, dysentery, jaundice, gallstones, haematemesis and melaena, haematochezia or diabetes mellitus.
  2. Drug history
  3. Alcohol ingestion
  4. Trauma
  5. Menstrual history.
 
Physical Examination
 
Age and sex
If the acute abdomen is seen in a child then it is intussuscep­tion; adolescent, (appendicitis) middle age, (cholecystitis or diverticulitis) and old age (neoplasms).
Acute abdomen in women usually may be of gynaecolo­gical origin.
 
General Examination
  1. Decubitus: Gnawing or rolling in the bed (colic); hip flexed (PID).
  2. Facies: Anxious looks or agonising appearance or Hippocratic facies.
  3. Skin: Pallor, sweat or signs of dehydration.
  4. Any jaundice or anaemia.
  5. Vital data
    1. Pulse: Rate and volume of all peripheral pulses.
    2. Respiration: Whether it is abdomino-thoracic with normal excursions or purely thoracic (peritonitis) or any decrease in any phase of respiration.
    3. BP: Hypotension suggestive of shock.
    4. Temperature: Fevers are associated with inflammatory causes.
 
Examination of the Abdomen
  1. Inspection of any operation scars.
  2. Movement of the abdomen (immobile in peritonitis).
  3. Contour: Retracted or distended abdomen. If retracted, then suggestive of peritonitis and scaphoid perforated duodenal ulcer; if distended, epigastric (pyloric obstruction); central, (small intestine obstruction) and flanks, (colon obstruction).
  4. Visible peristalsis
    1. Gastric peristalsis: In pyloric stenosis, peristaltic waves travel left to right and the dilated stomach is at a lower position than normal.
    2. Small intestine peristalsis: Waves are central in position and there are to and fro movements.
    3. Large bowel instruction: The visible peristalsis is less and the colonic distensions is seen in transverse colon with right to left movement.
Palpation: Ask the patient to point out the area of maximum pain. Examine the hernial orifices both inguinal and femoral canals. By gentle palpation, note for tenderness or rigidity or 9any mass in the abdomen. Guarding may be encountered, which is voluntary or involuntary, and the latter is due to peritoneal inflammation or perforation of viscus. If rebound tenderness is elicited (by exerting pressure with the hand over the painful region and suddenly releasing the pressure when sharp pain is felt), it is suggestive of inflamma­tion of viscus or parietal peritoneum. Coughing may also elicit rebound tenderness without the need for palpating hand. Well localised tenderness may be felt by one finger palpation.
Hyperaesthesia and hyperalgesia of the skin in the original area or segmental area of referred pain may be elicited by superficial palpation. Masses can be detected by deep palpation.
If both rigidity and tenderness are present, it is suggestive of peritonitis. If only tenderness is present without rigidity, it is suggestive of inflammation of the intestines, e.g. gastroenteritis without peritonitis.
Percussion: Gentle indirect percussion with the first over the anterior chest wall on either side elicits sharp pain if there is inflammation between diaphragm and liver or diaphragm and stomach or diaphragm and spleen. Obliteration of liver dullness is suggestive of perforation. Presence of free fluid is detected by shifting dullness. If the percussion note is resonant, it is suggestive of obstruction.
Auscultation: If the peristaltic sounds are absent even after auscultating for three minutes (silent abdomen), it indicates diffuse peritonitis. Intermittent peristaltic tinkling sounds with free intervals, synchronising with episodes of pain (noisy abdomen), are suggestive of mechanical intestinal obstruction.
Abnormal peristaltic sounds not synchronising with pain is seen in gastroenteritis. A succussion splash is heard over the abdomen in pyloric obstruction which may have to be differentiated from the splashing sound observed in normal individuals after a meal.
 
Special Signs
  1. Cullen’s sign: Faint blue discolouration around the umbilicus due to haemoperitoneum.
  2. Grey-Turner’s sign: Brownish green discolouration in the loins in certain cases of pancreatitis.
  3. Murphy’s sign: Palpation of right upper quadrant during deep inspiration may hold up the breathing if there is inflammation of the gallbladder.
  4. Boas sign: Area of hyperaesthesia in infrascapular area in gallbladder disease.
  5. Courvoisier’s sign: Distended palpable gallbladder due to compression of common bile duct.
  6. Iliopsoas sign: If the pain is elicited when the patient’s thigh is flexed against the resistance of the examiner’s hand, it is suggestive of inflammation of Iliopsoas muscle.
  7. Obturator sign: When the thigh is flexed to right angle and rotated internally or externally, it may produce pain if there is strangulated small bowl in the obturator canal or sometimes in pelvic inflammation or appendicitis.
Rectal and pelvic examination: Rectal examination must invariably be done to elicit any tenderness of pelvic perito­neum due to peritonitis, or a ballooning feeling obstruction or pelvic abscess. Vaginal examination is helpful to assess the state of pelvic peritoneum or ectopic pregnancy. So is the importance of examination of scrotum.
Examination of chest: This must be carefully examined for diagnosing intrathoracic causes, producing upper abdominal pain like pleurisy or cardiovascular degenerative disorders.
Examination of CNS: Careful inspection for tenderness over the spinal column is beneficial to diagnose abdominal pain due to vertebral disease and nerve roots. Sometimes hypersensitivity can be elicited in the back and front of the trunk in certain situations of irritation of peritoneum.
Reviewing the changes or progress of the clinical features often, during the course of the abdominal episode may be rewarding.
 
Investigations
 
Urine
  1. Albuminuria and cellular deposits like pus cells and RBCs suggest urinary tract infection or RBCs alone nephrolithiasis.
  2. Urine is allowed to stand for six hours and if it darkens, it indicates porphyria.
  3. If sugar and acetone are present, suspect diabetic ketosis as a cause of abdominal pain.
  4. Bile pigments and urobilinogen in urine indicate hepatobiliary disease.
 
Motion
  1. Intestinal parasites like roundworm ova and EH cysts may be present.
  2. Presence of blood and white blood corpuscles may be due to Salmonella enterocolitis.
  3. Faecal lipase is high in acute inflammations of pancreas.
  4. Occult blood may be seen in cases of haemorrhage with perforation.
 
Blood
  1. High haematocrit values suggest dehydration and low values indicate existing anaemia or bleeding.
  2. Leucocyte count may be helpful especially in the progressively rising count which indicates progress of 10the infective process. Polymorphonuclear leuko­cytes suggests appendicitis whereas low count with a relative lymphocytosis may be seen in viral gastroenteritis.
  3. Low RBC and haemoglobin percentage suggest bleeding.
  4. ESR is raised in infections.
  5. Sickle cell preparations: Sickling suggests haemolytic crisis.
  6. Electrolytes: Serum sodium and potassium may indicate the amount of the fluid loss.
  7. Serum bilirubin (both direct and indirect): if indicated.
  8. Blood sugar.
  9. Blood urea and serum creatinine.
  10. Enzymes.
    1. In acute pancreatitis, serum amylase is elevated due to sudden release into the bloodstream which is normally earmarked for the duodenum. This is also seen in bowel perforation or obstruction or perforation of peptic ulcer. Serum lipase is more sensitive than amylase in acute pancreatitis.
    2. SGOT raised in obstruction of common bile duct with cholangitis and early cardiac infarction.
    3. LDH and CPK raised in cardiac infarction.
    4. CL esterase.
  11. Arterial PaO­­2 (may be reduced).
  12. Night blood for microfilaria (MF) or quantitative buffy coat (QBC) for MF may be useful to diagnose mesenteric lymphadenitis.
 
Peritoneal Fluid
  1. Test for blood and pus.
  2. Elevated amylase levels are highly diagnostic of acute pancreatitis.
 
Radiology
  1. Plain films of the abdomen
    1. Erect position: Presence of abnormal gas shadows or gas-fluid levels are highly diagnostic.
      (Normally gas is present in the fundus of the stomach and throughout the large bowel, although it may be visible in the small bowel occasionally).
      1. Gas beneath the diaphragm is seen in perforation of peptic ulcer. If present underneath both the diaphragm, it is suggestive of colonic perforation.
      2. Dilated loops of small bowel with horizontal fluid levels, without gas or much less than normal, in the large intestine are suggestive of small bowel obstruction.
      3. Presence of gas proximal to the block and no gas seen in the rectum is suggestive of colonic obstruction.
      4. Marked dilatation and rotation of sigmoid or caecum are suggestive of volvulus.
      5. Distension of both small and large bowels (including the rectum) with copious gas or retention of large amounts of gas and fluid in the dilated loops of the small and large bowels, and absence of ‘J’ loops (as compared to presence of the same in obstruction) are characteristic of a dynamic ileus.
      6. Abnormal opaque shadows (gallstones, renal calculi, pancreatic calcification or calcified faecolith as seen in acute appendicitis) may be encountered.
      7. Obliteration of psoas shadow indicates retro­peritoneal haematoma or abscess.
    2. Supine abdominal X-ray: Look for shifting fluid levels.
    3. Left lateral decubitus film: Shows minimum amount of air in the peritoneal cavity. This X-ray is particularly useful if the patient is unable to remain in the erect position for minimum 10 minutes which in necessary to demonstrate air under the diaphragm.
  2. Contrast films
    1. If biliary pathology is suspected, oral cholecystogram or cholangiogram or endoscopic retrograde cholangio-pancreatography (ERCP) may be undertaken.
    2. ERCP is also useful for pancreatic pathology (should not be done in acute pancreatitis). Magnetic retrograde cholangio pancreatography (MRTB) detects biliary source of pancreatitis.
    3. If renal cause is suspected, IV pyelogram, may be done.
    4. In gastrointestinal pathology
      1. Barium meal (avoided in intestinal obstruction) is performed.
      2. Barium enema (avoided in perforation and peritonitis) done, when colonic obstruction is suspected, to identify the type and location. A patent appendix rules out acute appendicitis. Barium enema has to be done cautiously since the dangers of perforating an inflammatory lesion like diverticulitis or appendicitis or changing a partial colonic obstruction to complete obstruction, exist.
      3. Gastrografin (non-barium radio-opaque substance) may be useful to diagnose upper gastrointestinal tract pathology.
  3. Skiagram chest PA view and lateral views are useful particularly in acute abdomen due to extra-abdominal causes.
  4. X-ray of the spine at the suspected level (if necessary) is done.
 
ECG
ECG should be taken to rule out myocardial infarction as a cause of acute abdomen.
11
 
Special Investigations
  1. Ultrasound scanning is useful in gallstone, close loop obstruction and intussusception. Focussed high resolution ultrasound useful for appendicitis, diverticulitis.
  2. CT scanning is useful in acute pancreatitis or its compli­ca­tions, localisation of abscesses or detecting abdominal injuries like lacerations or subcapsular haematomas. Dual phase CT scanning with IV contrast may be beneficial.
  1. MRI with gadolinium is advocated if CT is contraindicated.
  1. Endoscopy (upper GI endoscopy or lower GI endo­scopy), sigmoidoscopy or colonoscopy should be reserved for discriminatory use.
  2. MRCP detects biliary source of pancreatitis.
  3. Culdocentesis and culdoscopy.
  4. Angiograms are useful in diagnosing subcapsular rupture of a solid organ or site of obstruction or bleeding in mesenteric vessels (not done routinely).
The clinician must exclude nonsurgical conditions arising from systemic diseases, be it thoracic or abdominal. If no definite diagnosis is established, laparotomy may be the only tool for the ultimate diagnosis. Of course, this has to be undertaken only when ‘wait and see’ policy for an optimum period does not yield any positive inference.
 
TREATMENT OF ACUTE ABDOMINAL PAIN
Successful treatment of acute abdominal pain depends entirely on precise diagnosis, a real challenge, since the list of both surgical and nonsurgical conditions is long, be it intra-abdominal or extra-abdominal. Most often an overlap of pain characteristics is encountered. It is further compounded either by a medical condition mimicking as “acute abdomen” or by its critical catastrophic nature. Hence, the clinician must be alert in identifying the origin of noxious stimulus for pain which may be due to inflammation, spasm, obstruction, or perforation/rupture. Other associated features also contribute substantially to the analysis of pain; be it arising de novo or transgressing from a chronic low type to an acute intense type.
 
Immediate Management
  1. When the diagnosis is in doubt, it is rewarding “to look and see, than to wait and see”; re-examine the abdomen and observe for any progression of symp­toms, without risking undue delay. Simultaneously, appropriate radiological investigation or ultrasound examination may be undertaken.
  2. The opinion of the surgical colleague shall be sought to assess the real need for any immediate surgical intervention, preferably after eliminating medical conditions (avoid unnecessary delay in operation or unjustifiable surgery, which is equally harmful).
  3. Since many acute abdominal conditions are associated with fluid and electrolyte imbalances, appropriate intravenous fluid therapy is instituted, monitoring haemodynamic status. It is better not to give anything orally. Pass nasogastric tube (“Drip and Suck”).
  4. Shock, if present, is treated with inotropic agents when volume replacement fails to restore adequate circulation (Vital signs are to be monitored. Refer to Chapter titled ‘Shock’).
  5. Analgesics: Narcotic analgesics must be withheld, pending diagnosis, since the valuable diagnostic signs may be masked, delaying the necessary therapy. Analgesics without sedation may be considered. However, the pitfall of disappearance of pain, worsening the disease and endangering patient’s life must be kept in mind while offering symptomatic relief for pain. The temptation is better resisted.
  6. Antispasmodics: If the pain is due to colic and if severe, suitable antispasmodics like atropine, propan the line, hyoscine, dicyclomine, drotaverine are beneficial. It should be borne in mind that disappear­ance of pain may mislead the clinician and in the meanwhile, the disease may worsen.
  7. If acid peptic disease is suspected, antacids, H2 receptor antagonists, proton pump inhibitors and/or anticholinergics may be considered.
  8. Nasogastric tube is inserted for decompression so as to prevent any further distension or aspiration pneumonia during anaesthesia. Fluid aspirated continuously must be measured for purposes of optimum fluid administration. (In paralytic ileus fluid is yellow and of less quantity, i.e. 1-2 L/d as against intestinal obstruction, it is dark brown or black and or more quantity. It is to be managed with appropriate fluid and electrolyte replacement).
  9. If any history of constipation is forthcoming, flatus tube is passed or soap and water enema considered. No purgatives shall be given.
  10. Antibiotics: They are better withheld till diagnosis is fairly settled, since they may conceal the true perspective of the disease or even its complications.
 
SPECIFIC TREATMENT FOR SPECIFIC DISEASES
 
Intra-abdominal
 
Inflammations
Acute peritonitis: Treatment of peritonitis depends upon whether it is primary (spontaneous) which is rare, or secondary to acute infection or perforation of viscus, and includes control of infection, correction of fluid imbalance, 12restoring, normal intestinal motility and maintaining nutrition.
  1. Preoperative supportive measures are:
    1. Bed rest in Fowler position.
    2. Start appropriate fluid therapy immediately (normal saline and/or Ringer lactate); parenteral feeding may be required.
    3. Associated shock should be combated (oxygen therapy with or without inotropic agents).
    4. Nasogastric suction to be done. Nothing is given by mouth. Oral intake is allowed only when suction is discontinued.
    5. Establish adequate urinary output (fluid requirements are to be estimated from the urinary output and nasogastric aspirations).
    6. Effective antibiotics are initiated as soon as the diagnosis is made (blood cultures may be obtained and type-specific antibiotic better administered).
    7. Analgesics: Narcotic analgesics like morphine are valuable once diagnosis is definite.
    8. If paralytic ileus is persistent, intestinal decompression is done by Miller-Abbott’s tube (The long intestinal tube is pushed into small bowel-duodenum).
  2. Operative: Surgical removal of the source of contami­nation like inflamed appendix, perforated bowel or gallbladder, together with peritoneal toilet and lavage. Intestinal decompression may be employed.
     The sequel of peritonitis is localised abscess formation at the primary site either in the subphrenic or pelvic region, which is treated by surgical drainage; supplemented with appropriate antibiotics and metronidazole parenterally.
  3. Postoperative: Necessary preoperative measures must be continued. Blood transfusion may be required for anaemia.
Peptic ulcer (Refer to Chapters ‘Dyspepsia and Haema­temesis’)
Treatment of perforation of peptic ulcer includes insertion of nasogastric tube and emptying the stomach, antibiotics, combating shock are the nonsurgical measures. Laparotomy and simple closure is routine measure hitherto. But vagotomy and gastroenterostomy or partial gastrectomy are preferred when general condition is good in the absence of purulent peritonitis.
 
Biliary Tract
  1. Biliary colic
    1. Anticholinergic drugs like dicyclomine hydrochloride relieve smooth muscle spasm.
    2. Narcotic analgesics (morphine—10 mg IM) may be required, though they cause spasm of the sphincter of Oddi which can be countered by simultaneous administration of atropine (0.6 mg IM). Pentazocine (30 mg) or buprenorphine (0.3 mg) are other parenteral alternatives.
    3. Low fat diet.
  2. Acute cholecystitis
    1. Bed rest.
    2. Nasogastric suction especially if the vomiting persists.
    3. Pain is relieved using analgesics (morphine or pentazocine).
    4. Maintain fluid balance.
    5. Antibiotics (cephalosporin and metronidazole).
    6. Prompt cholecystectomy is undertaken if the pain and tenderness spread with tachycardia, otherwise an elective cholecystectomy planned after complete recovery usually 2–3 months later.
  3. Cholangitis
    1. Appropriate antibiotics are chosen.
    2. Biliary drainage may be attempted (Refer to Chapter titled ‘Jaundice’).
 
Intestinal
  1. Acute appendicitis
    1. Appendectomy is the treatment of choice, though early cases recover spontaneously with or without antibiotics.
    2. Nasogastric suction prevents distension of the stomach.
    3. Fluids are given if necessary.
    4. Antibiotics and analgesics are withheld preferably before operation though they are mandatory at the time of surgery and thereafter.
    5. If appendicular mass is present without other abdominal signs, conservative treatment is preferred.
    6. Surgical intervention is necessary when pulse rate rises, pain spreads and gastric aspirations are copious.
  2. Acute gastroenteritis
    1. Fluid replacement and appropriate antibiotics like ciprofloxacin are administered.
    2. Loperamide is beneficial in controlling diarrhoea.
    3. If any food poisoning is suspected, stomach wash is given and the contents are to be kept for analysis.
  3. Diverticulitis
    1. High fibre diet with bran and bulky laxatives help constipation.
    2. Treatment of acute diverticulitis includes bed rest, nasogastric suction (nothing by mouth), intra-venous fluids, antibiotics like cefuroxime, and metronidazole and antispasmodics. If severe, blood transfusion may be needed.
    3. If unresponsive surgery is undertaken (colectomy and end-to-end anastomosis).
    4. If obstructive features or any complications occur after the acute attack, elective surgery is indicated.
  4. 13Colitis
    1. Treatment of acute catarrhal colitis is same as acute gastroenteritis.
    2. Ischaemic colitis may subside with conservative management.
    3. Surgery may be necessary in a few cases, if peritonitis or stricture develops.
  5. Intestinal colic: Since the colic is due to distension and spasm of the bowel, antispasmodics like dicyclomine or atropine relieve the spasm and the distension by passing a flatus tube. Apart from this, the underlying cause of the intestinal colic (ranging from improper diet to intestinal obstruction) must be carefully explored and treated accordingly.
 
Acute Pancreatitis
  1. Nothing by mouth for 48 hours.
  2. Nasogastric suction till distension subsides and peristalsis returns.
  3. Pain is relieved with narcotic analgesics except morphine as it causes spasm of sphincter of Oddi (Pain is servere in necrotising paincreatitis).
  4. Volume is repleted and oxygen administered to relieve hypoxia (refer Chapter ‘Shock’). If shock lung (acute respiratory distress syndrome) results. Mechanical ventilation and positive and-expiratory pressure (peep) must be established.
  5. Antibiotics like imipenem is highly beneficial. Third generation cephalosporins with quinolone; metronidazole and flucanozole are alternatives for secondary infection. Probiotics prevent infections.
  6. Acid suppression with PPIs or H2 receptor to antagonists are recommended for stress ulceration.
  7. Parenteral nutrition suggested to avoid secretary stimulation.
  8. Specific therapy with gavexate; mexilate (antiproteases). Octreotide (antisecretary). Lexipafant (antiplatelet activating factor) may have amelorating effects.
  9. Endoscopic therapy: Emergency ERCP (within 72 hours) for acute biliary pancreatitis advocated.
  10. Treatment of complications:
    1. Pancreas:
      1. Pancreatic abscess—needs draining.
      2. Pancreatic necrosis—laparotomy and drainage. Necrotising pancreatitis indicates severity.
      3. Recurrent pancreatic oedema—near total pancreatectomy).
      4. Pancreatic pseudocyst (resolves within 4 weeks, surgery is required for rapidly enlarging pancreatic pseudocyst).
      If pseudocyst ruptures pancreatic ascites results.
    2. Gastrointestinal
      1. GI bleeding from gastric varices due to splenic vein thrombosis.
      2. Bowel necrosis
      3. Obstructive Jaundice.
    3. Systemic:
      1. Acute respiratory distress syndrome.
      2. Acute tubular necrosis.
      3. Shock.
      4. Pleural effusion.
      5. Hypocalcaemia hypomagnesaemia, hyper­glycaemia appropriately treated.
 
Pyelonephritis
Refer to Chapter titled ‘Haematuria’.
 
Pelvic Inflammatory Disease
The preferred regimen of ceftriaxone 2 g IV 12 hourly (or equivalent of cephalosporin) followed by doxycycline (100 mg BD for two weeks) relieves symptoms caused by commonly incriminated organisms like N.gonorrhoeae, Chlamydia and preserves the tubal function.
Alternative choice is clindamycin (900 mg IV 8th hourly) and gentamicin (1.5 mg/kg 8 hourly) followed by doxycycline (100 mg BD for two weeks).
Surgery is necessary for ruptured tube-ovarian abscess or drainage of the pelvic mass pointing to cul-de-sac.
 
Acute Mesenteric Lymphadenitis
Short bouts of periumbilical pain lasting few minutes may be relieved by bed rest. Most of these infections mimic appendicitis. If operation is performed, inflamed lymph nodes and bowel are apparent. Some prefer to do appendectomy under such circumstances. If it is due to filariasis, treat with diethylcarbamazine, and antibiotics.
 
Mechanical (Colics—Obstruction and Acute Distension)
 
Intestinal Obstruction
Treatment of intestinal obstruction includes decompression by gastrointestinal suction, replacement of fluid and electrolytes and supplementing with antibiotics before relieving the obstruction surgically. Small intestine obstruction and paralytic ileus can be managed conservatively (nasogastric decompression till flatus is passed) in the initial stages at least, whereas strangulation and large bowel obstruction need immediate surgery. If the small intestine is strangulated, blood-stained fluid in the peritoneal cavity is removed by suction, and the strangulated segment is resected followed by anastomosis. Pyridostigmine (60–240 mg TDS) is useful in paralytic ileus. If the obstruction is in the large intestine (usually due to 14malignancy), appropriate surgical measures depending on the site of obstruction and general condition of the patient, either hemicolectomy, ileotransverse enterostomy or left iliac colostomy, are to be undertaken.
Sigmoid volvulus is treated by sigmoidoscopy and a soft rubber tube is coaxed into the twisted loop to deflate the gut, failing which deflations is attempted after laparotomy followed by resection and end-to-end anastomosis.
 
Biliary Obstruction (Symptomatic Cholelithiasis)
Sympto­matic treatment is indicated with antispasmodics and narcotic analgesics for biliary colic. Administer antibiotics if cholangitis is associated. If the biliary colic is recurrent, surgery is imperative (cholecystectomy and choledo­chostomy if necessary and endoscopic papillotomy with calculus extraction).
Gallstone induced pancreatitis or gallstone ileus due to stone ulcerating into the gut and obstructing is treated appropriately (Refer to Chapter titled ‘Jaundice’).
Medical dissolution with Ursodeoxy-cholic acid (8–15 mg/kg/24 h orally for 2 years) recommended for small stones, which are radiolucent, and noncalcified.
Lithotripsy is not favoured because of high recurrence:
 
Ureteric Colic
  • Renal colic and Dietl’s crisis (Refer to Chapter titled ‘Haematuria’).
 
Torsion of Ovarian Cyst
  • Appropriate incision is made and the cyst removed. When ruptured ovarian cyst leads to peritonitis, it may be treated accordingly.
 
Ruptured Graafian Follicle
  • Symptomatic treatment with analgesics suffice, if there is no evidence of associated pathology.
 
Ectopic Pregnancy
  • Haemorrhagic shock associated with ruptured tubal pregnancy is combated by blood transfusion besides surgery. Attempts must be made to control haemorrhage by salpingectomy or salpingostomy (removal of the products of conception and ligating bleeding points). However, excision of the implanted ovum and preservation of tube indicated in unruptured tubal pregnancy or tubal abortion.
 
Omental Torsion
  • Treatment of omental torsion includes ligating the pedicle above the twist and removal of the mass. Bacterial peritonitis which may follow is treated appropriately.
 
Vascular
 
Mesenteric Angina and Infarction
 
Mesenteric Angina (Abdominal Angina)
  • Due to chronic intestinal ischaemia is rare and treatment is symptomatic.
    When the diagnosis is obvious at laparotomy, superior mesenteric embolectomy is attempted or the artery is re-anastomosed to the aorta along with resection of the affected bowel. Blood transfusion may be given and anticoagulants may be started one day after opera­tion. In case intestinal obstruction occurs, treat accordingly. Occlusion of inferior mesenteric artery leads to ischaemic colitis (vide supra).
 
Splenic Infarction
  • Bed rest and sedation may suffice. If a septic infarct results in an abscess, splenectomy is required.
 
Budd-Chiari Syndrome
  • Streptokinase followed by anticoagulants indicated. If it is infective in origin, appropriate antibiotics must be administered. A meso­atrial shunt may be considered in a blocked inferior vena cava. However, peritoneal-jugular shunt for ascites or portacaval anastomosis or mesocaval shunt for portal hypertension recommended. Liver transplantation may be required in progressive hepatic failure.
 
Sickle Cell Crisis
  • Pain associated with infarction crisis in sickle cell anaemia is relieved by narcotic analgesics followed by non-addictive analgesics. Dehydration is corrected which may also help to relieve pain. Antibiotics administered in the presence of infection. Mesenteric infarction may be treated as above. Pulmonary micro­embolism and pseudo-toxaemia syndrome (the hazards of associated pregnancy) may require heparin therapy. Urgent blood transfusion may be needed in Aplastic crisis, and exchange transfusion in sequestration.
 
Ruptured Ectopic Pregnancy
  • Vide supra.
 
Ruptured Graafian Follicle
  • Vide supra.
 
Ruptured Spleen
  • Treatment consists of resuscitation, immediate laparotomy and splenectomy.
15
 
Ruptured Mesentery (Mesenteric Apoplexy)
  • Immediate laparotomy, locating the site of bleeding and ligating the bleeding artery is imperative. Resection of the segments of bowel may be required, if its blood supply is impaired.
 
Ruptured Aortic Aneurysm
  • Immediate laparotomy is mandatory. Aorta proximal to aneurysm is taken control off, to stop bleeding. Replace the aneurysmal segment with a prosthesis.
 
Abdominal
 
Bornholm Disease
  • Epidemic myalgia due to coxsackie B virus infection is treated with analgesics and NSAIDs (rarely requires narcotic analgesics).
 
Nerve Entrapment
  • It may necessitate exploration and mobilisation of the nerve.
 
Haematoma of Rectus Sheath
  • Locate and evacuate the haematoma.
 
Abdominal Hernias
  • Appropriate operative treatment is undertaken (herniotomy, herniorrhaphy).
 
Referred Pain
  1. Myocardial infarction (Refer to Chapter titled ‘Chest Pain’).
  2. Diaphragmatic pleurisy (Refer to Chapter titled ‘Chest Pain’).
  3. Spinal lesions and hip joint disease (Refer to Chapter ‘Low Backache’).
 
Extra-abdominal
 
Cardiopulmonary
Refer to Chapter titled ‘Chest Pain’.
 
Neurological
Refer to Chapter titled ‘Low Backache’.
 
Genital Torsion of the Testicle
Untwist the testis gently in the right direction till pain is relieved. If unsuccessful, exploration of the scrotum and fixation of the testis is to be done without risking delay. If the testis is not viable, orchidectomy is to be done.
 
Metabolic
  1. Diabetic ketoacidosis: (Refer to Chapter titled ‘Coma’).
  2. Acute porphyria: Treatment includes infusion of glucose 30 g/h and correction of electrolyte imbalance. If unresponsive within two days, haematin is infused twice a day for about four days (4 mg/kg body weight). Nausea, pain, seizures are controlled appropriately. Tachycardia and hyper­tension treated with propranolol. The precipitating factors are better avoided.
  3. C’1 esterase inhibitor deficiency: It is treated either by danazol which raises the inhibitor levels or with epsilon aminocaproic acid which decreases plasmin activity.
 
Alcohol and Metals
  1. Acute pancreatitis (Vide supra).
  2. Lead poisoning treatment consists of:
    1. Fluids: Maintain fluid balance to ensure adequate urine flow.
    2. Chelation therapy: Calcium sodium edetate (25 mg/kg twice daily IV in saline) and dimercaprol (3 mg/kg IM every four hours) for five days. Interrupt for two days and repeat for another five days if necessary. This may be followed by oral D-penicillamine (up to 500 mg/d) for about 1–2 months.
    3. Symptomatic treatment for convulsions with diazepam, and cerebral oedema with dexamethasone and mannitol.
    4. Remove permanently from exposure to lead.
 
Hip Joint Disease
  • Acute bursitis rest, hot fomentations and avoidance of pressure are helpful for inflammation. Needle puncture may be done and purulent infections demand incision and drainage whereas tuberculosis needs excision and antituberculous treatment.
 
Psychogenic
After eliminating confidently the organic causes of abdominal pain by a comprehensive examination, psychiat­ric assessment is to be done. Appropriate psycho­therapy behavioural therapy, systemic desensitisation and physical drug therapy with anxiolytic drugs are instituted. This may be supplemented by educating the patient about his illness and dealing with psychosocial problems.
16
zoom view
17
zoom view