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ABDOMINAL RIGIDITY

Rigidity of the abdomen is a sign of utmost importance, since in most cases it indicates serious intra-abdominal mischief requiring immediate operation.

It is the expression of a state of tonic contraction in the muscles of the abdominal wall. The responsible stimulus may be in the brain or basal ganglia, or in the territory of the six lower dorsal nerves that supply the abdominal wall. The extent of the rigidity will depend on the number of nerves involved, and its degree on the nature and duration of the stimulus.
The analysis in the table below may be considered.
The patient should be examined lying on the back with the whole abdomen and lower thorax exposed, but with the shoulders and legs well covered. The room must be warm. The examiner, seated on a level with the patient, should first watch the abdomen to see whether it moves with respiration or not, and whether one part moves more than another; at the same time, he or she may observe other things that will help in the diagnosis, such as asymmetry of the two sides, local swelling, or the movement of coils of bowel.

ABDOMINAL RIGIDITY

While watching – and later when examining – the examiner should engage the patient in conversation, encouraging him to talk in order to allay nervousness and to remove any part of the rigidity that is due to a voluntary contraction. Some nervous patients – especially if the room is cold – hold their abdomens intensely rigid, and can be induced to relax only after gentle persuasion; a request to take a few deep breaths, or to draw the knees up and keep the mouth open, will often help.
During this preliminary examination, one (well warmed) hand may be laid gently on the abdomen and passed over its surface with a light touch that cannot possibly hurt; this maneuver will help to allay the patient's anxiety still further and give the examiner an idea of the extent, intensity and constancy of the rigidity to be investigated later in more detail.

For a more exact examination, the observer should sit at the patient's side facing their head, and place both hands on the abdomen, examining comparable areas of both sides, simultaneously, and taking in turn the epigastrium, right and left hypochondria, umbilical region, both flanks as far back as the erector spinae (as the rigidity of a retrocaecal appendix may only affect the posterior part of the abdominal wall), the hypogastrium and both iliac fossae. First, the whole hand should be applied with light pressure; next, the fingers held flat should be pressed more firmly to estimate the extent of the rigidity and to discover deep tenderness; last, a detailed examination may be made in suspected areas with the firm pressure of one or two fingers. Evidence is not complete without percussion and auscultation. A rectal examination is indispensable.

After a leisurely examination with warm hands in a warm room, during which the physician has also been able to sum up the patient, their temperament, and whether they are really ill or not, the rigidity of anxiety or cold will have been dispelled or recognized .
The abdominal rigidity due to a lesion in the chest or chest wall usually involves a wide area limited to one side – a distribution most unusual with intra-abdominal mischief, which, if it has spread widely but not everywhere, tends to be limited to the upper or lower half. The extent and degree of rigidity in chest affections also vary widely during examination. Other things such as a flushed face, rapid respiration, movement of the alae nasi, or a temperature of more than 39 °C (102 °F) may suggest that the lesion is not abdominal, and a friction rub may be felt or heard in the chest.
Auscultation and rectal examination dispel any remaining doubts, as in chest conditions peristaltic sounds remain normal and there is no tenderness in Douglas's pouch.
Examination of the blood may show a high leucocytosis (up to 30,000 or 40,000 per mm3), whereas in peritonitis the count is rarely over 12,000 per mm3.
Chest X-rays (including a lateral film) will demonstrate the intrathoracic lesion.
Injuries of the abdominal wall, and particularly those caused by run-over accidents, lead to very marked rigidity of the injured segment. Here, the rigidity is not necessary to establish a diagnosis, as the injury is already known, but its degree and extent should be carefully noted. There must always be a doubt as
to whether the abdominal viscera are damaged as well as the walls, and this point can only be settled by careful observation. The patient is put to bed and kept warm, the pulse is charted every 15 minutes, and the abdomen is re-examined from time to time.
In the case of a mere contusion, the collapse will soon disappear, the abdomen will become less rigid, and the pulse rate will fall. If the contents of a hollow viscus have escaped, rigidity will extend beyond the area of the damaged muscles, and the signs of peritonitis will develop rapidly. An X-ray of the abdomen, in the
erect position, will demonstrate free gas beneath the diaphragm. If there is internal bleeding (e.g. from a ruptured spleen or liver), there is pallor and progressive elevation of the pulse, together with a falling blood pressure. Dullness in the flanks (especially on the left side, in rupture of the spleen) is often detected, as blood collects in the paracolic gutters.

PERITONITIS
The most common and the most important cause of general abdominal rigidity is peritonitis, and it is a safe rule when meeting true rigidity to diagnose peritonitis until it can be excluded. Actually, rigidity means no more than that the parietal peritoneum lining the abdominal cavity is in contact with something different from the smooth surfaces that are its normal environment. The presence of rigidity therefore announces a change in the coelomic cavity that is probably infectious in origin.
When gallstone colic is followed by rigidity of the right rectus muscle, it means not only that a stone is blocking the cystic duct, but also that the wall of the gallbladder is inflamed. Intestinal obstruction of mechanical origin (such as that due to a band or
adhesion) gives colic referred to the umbilicus but no guarding of the muscles; local rigidity accompanying the clinical picture of intestinal obstruction indicates that there is also a local inflammatory focus such as a strangulated loop of bowel, while a more diffuse rigidity suggests changes such as thrombosis of the
superior mesenteric artery, affecting a large segment of bowel. In appendicitis, rigidity denotes that the infection has spread beyond the coats of the appendix.
The degree of rigidity varies with the nature of the irritant, the rapidity with which the peritoneum is attacked, and the area involved. At one extreme is the rigidity of a gastric or duodenal perforation, where the abdomen is suddenly flooded with gastric
contents. Here, the whole abdominal wall is fixed in a contraction that can best be described as board-like: there is no respiratory movement, and no yielding to the firmest pressure. At the other extreme is the relatively minor degree of rigidity that accompanies
the presence of small amounts of blood or urine in the peritoneal cavity; there is perhaps only a slightly increased resistance when the hands are pressed on the abdomen. Perforation of a gastric or duodenal ulcer produces the most intense rigidity; the escape of
amylase in acute pancreatitis leads to less rigidity, and the escape of other sterile fluids, urine for instance, or blood, still less. Bacterial invasion of the peritoneum produces marked rigidity.

The degree of muscle contraction also changes during the development of a case. The board-like abdominal wall of a perforation is considerably softer after 3–4 hours when the peritoneum has recovered from the shock of the first insult. The slight resistance apparent when sterile urine escapes from a ruptured bladder rapidly increases as infection occurs.
The extent of the rigidity usually corresponds to the area of peritoneum affected. The entire abdomen may be rigid, or it may affect only the upper or lower part, one side or a restricted part. Total rigidity should mean a total peritonitis, but because the peritoneum reacts immediately to invasion by forming adhesions that localize the mischief, a general peritonitis is only seen when an irritant or infected fluid is suddenly discharged in large quantities – as in duodenal perforation, pancreatitis or the bursting of a large abscess or distended viscus – or when the infection is brought by the bloodstream and reaches all parts
simultaneously. Occasionally, and particularly in children, the reaction to a sudden infection may be excessive and the muscles contract over a wide area in response to a purely local infection, for instance of the appendix, although this exaggerated response
quickly disappears. Conversely, the aged patient – with atrophic abdominal muscles – may exhibit only slight rigidity, even in generalized peritonitis.
Local peritonitis starts around some site of infection, and as it spreads it is guided by certain peritoneal watersheds, of which the most important is the attachment of the great omentum to the transverse colon, dividing the abdomen into supra- and infracolic
compartments: rigidity accompanies the infection.
Thus, localized rigidity is found over any inflamed organ, and as the infection and the guarding spread, they tend to involve the upper or the lower half of the abdomen as a whole. When we have mapped out the extent of the rigidity, we should – from a knowledge of the organs at that site and of the watersheds that
guide the spread of infection – be able, in conjunction with the history, to make a diagnosis.

The influence of natural subdivisions in guiding intraperitoneal extension must always be taken into account. Infections in the right supracolic compartment tend to pass down between the ascending colon and the right abdominal wall, while one in the pelvis is guided by the pelvic mesocolon to the left side of the abdomen as it ascends. Thus, rigidity in the right iliac fossa may indicate a leaking duodenal ulcer, and rigidity in the left may be due to a pelvic appendix.
Since the diagnosis of peritonitis in most cases means immediate operation, every effort must be made to confirm the diagnosis, particularly by the simple tests of percussion, auscultation and rectal examination. Percussion may reveal the outline of some dilated hollow organ, such as the caecum; it may disclose free gas that has escaped from a perforation as a shifting circle of resonance or a tympanitic note where liver dullness should be; it may map out an abnormal area of dullness where there is an abscess or a collection of blood; or it may indicate
free fluid in the peritoneum. Auscultation is even more important, as peristalsis ceases with peritonitis: in a normal abdomen, peristaltic sounds can be heard every 4–10 seconds; in obstruction, they are increased in loudness, pitch and frequency; but in peritonitis, there is complete silence. Rectal examination almost always reveals tenderness when there is intra-abdominal infection, even if it is distant and localized.
Other signs must be mentioned: the patient lies still, sometimes with the knees drawn up, and resists interference. The abdomen gradually becomes distended, tense and tympanitic. The tongue is brown and dry. Vomiting is to be expected at the onset of any abdominal catastrophe, but it usually ceases, except in intestinal obstruction. With advancing peritonitis, it reappears, and the vomit becomes first bile-stained, later brownish and faecal-smelling, and is allowed to dribble from the corner of the mouth in contrast to the projectile vomiting of obstruction. There may be diarrhea at
first, but absolute constipation soon succeeds it. The temperature tends to fall; the pulse is small and rapid, rising progressively. In late stages, the sunken cheeks, wide eyes and anxious expression of the patient form a characteristic feature – the Hippocratic facies.
These signs are indications of a peritonitis discovered too late, and are the heralds of approaching death.
Abdominal rigidity, abdominal silence, rectal tenderness and a rising pulse are a tetrad that calls for immediate definitive treatment.
A more detailed diagnosis is usually possible when the history and other signs are taken together, but a consideration of all the alternatives is out of the question in this section. Abdominal paracentesis with a fine needle may clinch the presence of pus, blood or urine in the peritoneal cavity, but a false-negative tap may delay rather than aid diagnosis. A list of the more common conditions associated with rigidity may, however, help the inquiry:

• Stomach or duodenum
– Perforation of peptic ulcer
• Gallbladder
– Acute cholecystitis
– Rupture of the gallbladder
• Pancreas
– Acute pancreatitis
• Small intestine
– Strangulation of a loop
– Traumatic perforation
– Mesenteric vascular thrombosis or embolism
– Meckel's diverticulitis
– Acute ileitis
• Large intestine
– Appendicitis
– Volvulus
– Diverticulitis with perforation
• Peritoneum
– Acute blood-borne peritonitis
⚬ Streptococcal
⚬ Pneumococcal
⚬ Gonococcal
• Female reproductive organs
– Twisted ovarian cyst
– Ruptured ectopic pregnancy
– Acute salpingitis
– Torsion or red degeneration of a fibroid
– Perforation of the uterus or posterior fornix of vagina in attempted abortion
• Spleen and/or liver
– Traumatic rupture
• Aorta
– Ruptured aneurysm

Perforation of a peptic ulcer is characterized by the most sudden onset, the worst agony and the most extreme abdominal rigidity that the physician is ever likely to see. Radiation of pain to the right shoulder tip (referred pain from diaphragmatic irritation) may be experienced. Immediately afterwards, the patient is motionless and speechless, in a state of obvious collapse. A few hours later, pain, rigidity and shock have all diminished, and only the dramatic history of sudden onset and persistent abdominal and rectal tenderness may remain to indicate the seriousness of the condition.
Acute pancreatitis is rarely accompanied by the severe pain described in textbooks, or indeed by pain as bad as that of gallstone colic. The abdominal rigidity is more marked in the upper abdomen but is not profound. On the other hand, the patient shows a degree of toxaemia out of all proportion to the physical signs in the abdomen. The diagnosis is confirmed by a considerable rise in the serum amylase. A ruptured ectopic pregnancy may simulate a lower abdominal peritonitis, but the signs of bleeding predominate and rigidity is not well marked. If the patient is a woman of child-bearing age who is known to have missed a period, the onset of abdominal pain and pallor suggest the diagnosis. Extravasated blood will be felt in the pelvis, together with acute tenderness on vaginal and rectal examinations. The diagnosis is confirmed by the urinary pregnancy test (positive beta human chorionic gonadotrophin (hCG)) and, if necessary, by pelvic ultrasonography.
Blue discoloration of the skin around the umbilicus - Cullen's sign - may be associated with rigidity. This discoloration is due to extravasated blood coming forward from the retroperitoneal space. The sign is seen in ruptured kidney, leaking abdominal aneurysm and acute pancreatitis. Occasionally, it is seen in ruptured ectopic pregnancy, when the blood gains entry to the subperitoneal space through the broad ligament. Although pancreatitis may produce this sign, it is more common to see a green discoloration in the loins (Grey Turner's sign).

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Detailed medical information on more common causes of acute abdomen

Intestinal Pain

Acute Appendicitis

Peritoneal Pain

Pain from Vascular Causes

Retroperitoneal Pain

Abdominal Pain from Intoxication

Acute appendicitis in children


Toxicological risk during lactation

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