Index
It occurs when the antimesenteric wall of the intestine protrudes through a defect in the abdominal wall.
This is different from other types of abdominal hernias. Only one intestinal wall protrudes through the defect, so the lumen of the intestine is incompletely contained in the fault. At the same time, the rest remains in the peritoneal cavity.
If such a hernia becomes necrotic and subsequently shrinks during hernia repair, perforation and peritonitis may occur.
A Richter’s hernia can cause strangulation and necrosis in the absence of intestinal obstruction. It is a relatively rare but dangerous type of hernia.
Richter’s hernia has also been seen at laparoscopic port sites, usually when the fascia is not closed for ports larger than 10mm.
A high index of suspicion is required in the postoperative period, as this sinister problem can closely mimic the more benign complications, such as bruising at the port site.
Pathology
In contrast to most other types of hernias, only the antimesenteric wall of the intestine herniates without compromising all of the lumens. This hernia is usually through a minor, firm defect in the abdominal wall.
Although any part of the intestine can be affected, the terminal ileum is the most affected. Richter’s hernias can occur in:
- Femoral ring (36-88%).
- Inguinal ring (12-36%).
- Incisional hernia of the abdominal wall (4-25%).
- Rare: umbilical, ventral, Spigelian, supravesical, sacral foramen, petit’s triangle, retrosternal and diaphragmatic.
- Trocar ports for laparoscopic surgery.
Richter and Sir Frederick Treves hernia
Richter’s hernia can be defined as an abdominal hernia in which only part of the circumference of the intestine is trapped and strangled in the hernial orifice.
The segment of the intestine involved is almost always the lower portion of the ileum, one but any part of the intestinal tract, from the stomach 2 to the colon, including the appendix, can be imprisoned.
The precondition for the formation of this particular hernia, as established by Richter, is determined by the size and consistency of the hernial orifice:
It must be large enough to trap the intestinal wall but small enough to prevent protrusion of a complete cycle of the intestine, and the margin of the hernial ring must be firm or, in Richter’s words, “possess strong elastic force.”.
According to others, the presence of a tight ring is a prerequisite for strangulation and compromised blood circulation, eventually leading to ischemia and gangrene of the affected intestine.
Richter’s hernias tend to progress more rapidly to gangrene than common strangulated ones. This can be seen in Horbach’s series, which found 45 Richter’s hernias among 146 strangulated hernias.
Of these 45, he found necrosis of the intestinal wall in 31 (69%); Among 101 common strangulated hernias, he found intestinal necrosis in only 25 (25%).
This can be explained not only by the firm constrictive ring that exerts direct pressure on the intestine wall but also by the anatomical peculiarity that, as a general rule, it is the free edge of the intestine opposite the intestine mesentery with the predominance of terminal arterioles that is involved.
The time factor can also explain it. In most cases, when it is less than two-thirds of the gut wall circumference, the lumen of the gut remains free, and there is no alarming intestinal obstruction.
This insidious pathologic feature of Richter’s hernia often leads to late or even misdiagnosis, allowing intestinal necrosis to develop.
Treatment is resection and anastomosis. Mortality increases with delay in surgical intervention. This hernia is rare, but not so rare as to be just a curiosity.
Furthermore, the dramatic increase in laparoscopic surgery, creating a new site for the development of Richter’s hernia, will undoubtedly be followed by the rise in its incidence.
As our knowledge of this type of hernia increases, the diagnosis will be made more quickly. The condition will be suspected more often, thus avoiding the serious consequences of delayed treatment.
The first description of a Richter hernia case was made by Fabricius Hildanus (1560-1634) in 1606.
Because this case illustrates a typical clinical presentation of a perforated Richter’s hernia, and because a correct citation and interpretation of his fascinating and detailed report could not be found in all the articles that refer to him, we offer the following translation of his source in Latin:
- “Gangrene resulting from an intestinal hernia with perforation and subsequent healing.”
Margarete of Gléresse, a 63-year-old noblewoman who suffered from a right inguinal hernia for 17 years, had been bothered by severe pain since December 1597.
After finally breaking through the abdominal wall, the intestine caused not minor pain and, at the same time, inflammation and other heavy symptoms. I called her in January 1598; I found the right groin region affected with gangrene.
After having scarified the tumor and done other necessary things for the gangrene to heal, there was calloused and calloused flesh falling off the break.
Consequently, aches, swelling, fever, fainting, nausea, and vomiting vanished. But for about two months, the intestine’s contents, ileum or coecum, were excreted through the fistula.
However, to the great amazement of those present, the ailing woman regained good health with God’s help and was perfectly healed from the rupture without any residual fistula or hernia.
Hildanus then cites several prominent men as witnesses to this miracle cure. He concludes from his observation that intestinal wounds are not always incurable, which at the time was still incredible.
In the complete edition of her works from 1646 11, she notes that the noblewoman lived until 1613 when she died of the plague.
Causes of Richter’s hernia
This hernia occurs when only the antimesenteric border of the intestine herniates through the fascial defect (it involves only a portion of the circumference of the intestine). Its small size makes it more challenging to diagnose.
They develop strangulated tissue because the opening in the abdominal wall is small and well-formed.
When a part of the intestinal wall finds its way through the opening, the tissue becomes trapped (imprisoned) and pinches. Loss of blood causes gangrene (tissue death), leading to life-threatening medical conditions.
Richter’s hernia can occur with any of several abdominal hernias.
Methods
Case study No. 1
Twenty-one patients with strangulated hernias were admitted to the hospital. In four patients (19%), a typical strangulated hernia was present; in 17 patients (81%), a Richter’s hernia was present.
One patient was admitted twice with a recurrent Richter hernia the second time. The approximate mean age of patients with Richter’s hernia was 45 years (25-65).
Case study No. 2
Sixteen of the 18 patients (89%) had a perforated Richter’s hernia: in 11, there was an enterocutaneous fistula in the groin; in one, the hernia perforated through the labia majora.
Surgical anatomy and repair technique
Richter hernia (partial enterocele) is the protrusion and strangulation of only part of the circumference of the antimesenteric border of the intestine through a minor rigid defect in the abdominal wall.
The first case was reported in 1606 by Fabricius Hildanus. August Gottlieb Richter gave the first definition of a partial enterocele in 1785. Sir Frederick Treves discriminated it from the Littre hernia (Meckel’s diverticulum hernia).
These hernias are often diagnosed in the sixth and seventh decades of life. They comprise 10% of strangulated hernias. Their common sites are the femoral ring, the inguinal ring, and incisional trauma.
The intestine most often trapped part is the distal ileum, but any part of the intestinal tube can be imprisoned. These hernias progress more rapidly to gangrene than other strangulated hernias, and obstruction is less common.
The standard gold technique for repair is the preperitoneal approach, followed by laparotomy and resection if perforation is suspected.
Richter’s hernia history
In his famous Treatise on the Ruptures in 1785, August Gottlob Richter (1742-1812) gave the first comprehensive description of hernias in which only part of the circumference of the intestine is strangled, calling them “small ruptures.”
The vocabulary of this hernia was later confused because many English authors described it without a unique name or mentioned it as Littre’s hernia.
Only 100 years later, in 1887, the famous London surgeon Sir Frederick Treves distinguished this type of hernias from the hernia of a Meckel diverticulum, classically described by Littre.
Treves credited Richter with the distinction of giving the first scientific description of this particular lesion. They suggested the term Richter’s hernia “(in part) because with Richter must rest the main credit of establishing the individuality of this lesion.”
After more than a century, Treves’ unprecedented scholarly contribution to the subject remains the cornerstone of modern understanding.
He provided a detailed clinical description based on his own surgical experience. Still, he also comprehensively addressed the subject, citing 52 authors since 1606 in his analytical and historical review of the issue.
Then, modestly, he proposed that Richter, and not himself, deserve namesake recognition for this hernia. All of this exemplifies his honest and scientific approach to research and medicine.
With the two notable events in his life that made him famous: the rescue of the “Elephant Man” and King Edward VII’s life-saving appendicitis intervention on the eve of the coronation, we must not forget his role as a pioneering physician.
During his distinguished career, his outstanding contributions to anatomy and surgery are evidenced by his authorship of more than 250 medical books and articles.
He also takes into account his tireless energy and immense ability to work as a surgeon at London Hospital while leading a life of almost Spartan simplicity.
Along with his literary skills and humanitarian commitment, he must be recognized as a shining example of holistic medicine and personal excellence.
Recent literature reveals little new information on the incidence and sites of Richter’s hernia. It confirms the classic reports by Treves, Frankau, and Gillespie et al., which remain the best sources of information except for Africa.
Based on these large series, the general rule can be derived that approximately 10% of strangulated hernias are Richter’s hernias (5-15%).
Typically, Richter’s hernia patients are between 60 and 80, but cases have even been reported in infants.
The preference for the femoral hernial site is manifested in the distribution of sex. In whites, women are generally overrepresented: 58% in the series by Treves and 57% in the series by Kadirov et al.
Richter’s hernia can occur in any common hernial site, but it seems more likely in small hernial rings with tight margins.
In whites, the most common site is the femoral ring (36-88%), followed by the inguinal canal (12-36%) and incisional hernia of the abdominal wall (4-25%).
Rare sites have also been described, such as umbilical, obturator, supravesical, Spigelian, Petit’s triangle, sacral foramen, Morgagni, and internal or traumatic diaphragmatic hernias.
The increasing popularity of laparoscopic surgery has led to a possible new site for the development of a Richter’s hernia:
Since the first description of a Richter’s hernia through a laparoscopic incision in 1977, similar case reports have been published more and more.
The conditions for the development of a Richter’s hernia appear to be ideally met by the size and quality of the insertion sites of laparoscopic instruments, especially those with a diameter of 10-20 mm.
The situation is different in Central Africa, where Richter’s hernias occur frequently.
Symptoms of Richter’s hernia
Making the diagnosis of Richter’s hernia can be difficult due to seemingly harmless initial symptoms and few clinical findings; the diagnosis may remain presumptive until it is confirmed at surgery.
The first mild symptoms, such as vague abdominal pain and slight discomfort, may not be appreciated, leading to a late diagnosis.
Nausea and vomiting may be present, but they are generally less common and less severe than in the usual form of strangulation because the obstruction is rarely complete.
The clinical and radiological signs of ileus are present in approximately 10% of patients; in the absence of complete mechanical obstruction, this may be due to paralysis.
Local signs may be absent or inconspicuous, and, if present, they are easily overlooked or misinterpreted.
The most consistent physical finding remains tenderness or swelling over a possible hernial orifice. The underlying erythema should increase the index of suspicion.
Diagnosis and tests
In addition to the patient’s history and careful physical examination, radiology may help establish the diagnosis. The value of ultrasound and computed tomography in individual patients is indisputable.
However, the diagnosis can generally be suspected on clinical grounds.
The crucial point is to keep this condition in mind, just as gallstone ileus should be considered in obese patients with unexplained subacute symptoms and signs of intestinal obstruction.
radiographic characteristics
Computed tomography
A focal bulge of the antimesenteric wall of an intestinal loop is a minor defect in the abdominal wall.
Ultrasound
Ultrasound can identify the fascial defect and the part of the intestine that enters the hernial sac.
Clinical picture and its course
The clinical picture and course can vary considerably depending on the location and mode of herniation and entrapment. However, cases can be divided into four main groups based on clinical responses:
- The obstructive group: The dominant clinical presentation of intestinal obstruction leads to early diagnosis and treatment, resulting in an excellent prognosis.
- The danger group: in which the symptoms are vague and nonspecific: initial examinations with or without contrast do not reveal an imminent disaster, and the subsequent delay in surgery is the main responsible for the high rates of death and complications;
- The postnecrotic group: in which local strangulation and perforation lead to the formation of an enterocutaneous fistula, similar to that described by Fabricius Hildanus 400 years ago; the fistula can close spontaneously or remain chronic; Y
- The “unfortunate perforation” group: The postnecrotic abscess, due to unfortunate anatomical constellations, accidentally finds its way into another compartment, resulting in a prominent spot with severe septic / toxic burden or peritonitis; both would lead to a high mortality rate.
Complications of a Richter’s hernia
When the tumor is small, it is challenging to examine, but when it is large enough, it presents only the characteristics of a common strangulated hernia.
A small hernia in the femoral canal, the most common site of Richter’s hernia, is sometimes masked by body fat or an enlarged lymph node or is mistaken for acute lymphadenitis.
If local gangrene of the intestinal wall occurs, the classic signs of inflammation appear (painful swelling, redness of the overlying skin, and local heat).
This tumor may be inconspicuous in the initial stage and may appear as a local abscess or subcutaneous emphysema caused by an anaerobic infection.
If a hernia pierces the inguinal canal in the scrotum, which corresponds to an advanced stage, grotesque scrotal abscesses with gangrene may develop.
These are generally fatal due to the high toxin load. Similarly, gangrenous inflammation of the vulva can occur.
If surgery is done too late or not done, natural healing can occur in the form of drainage through an enterocutaneous fistula.
The venous circulation of the incarcerated hernia is damaged, resulting in intestinal infarction and gangrene. Hernial sac perforation can progress to an enterocutaneous fistula if left untreated.
If the perforation occurs after the necrotic segment has receded into the abdomen, abscess formation or fecal peritonitis could be the sequelae.
Under certain conditions (a self-limited septic process, a low-output fistula, and a free intestinal passage), the fistula can close spontaneously, but it can persist for months.
Perforation in another compartment, such as the scrotum, vulva, thighs, or peritoneal cavity, can also occur, producing a severe clinical course with considerable morbidity and a high mortality rate.
Treatment
There is only one treatment: surgery. Richter’s hernias in the groin without apparent signs of perforation can be managed like common inguinal hernias.
Preliminary attempts at manual reduction should be avoided because the viability of the hernial sac can be determined by direct inspection only.
Laparotomy is often necessary to properly treat the bowel defect in perforated hernias. Segmental resection is avoided, and the fault is closed after careful debridement of the margins.
This is possible in most cases where the area involved does not exceed half (sometimes even two-thirds) of the circumference of the intestine. However, the rule regarding strangulation (“When in doubt, resection”) must be adhered to.
This is especially true in patients with chronic enterocutaneous fistulas or significant inflammation of the affected bowel segment, which could compromise free intestinal passage and lead to anastomotic leakage.
The primary goal in these patients should be to reduce the systemic toxin load of herniated gangrenous tissues and prevent contaminated material from spilling into the peritoneal cavity.
To achieve these goals, the hernia is initially approached from its inner aspect through a laparotomy to ensure control of both the intestine and vascular supply before the release of the hernia.
In patients with necrotizing infections of the surrounding tissue (for example, the scrotal abscesses seen in Lokichokio), a two-stage approach may be preferred:
Debridement and drainage of the abscess followed by bowel and hernia repair when the infection has subsided.
A preperitoneal or midline approach is used with perforated inguinal or femoral hernias.
With advantages and disadvantages, in any case, the surgeon, however, should always keep in mind that early surgery and careful bowel management are much more critical to the result.
Obliteration of the hernial orifice by suture should never be omitted if the recurrence of a Richter hernia is to be avoided.
The gangrenous area is invaginated, and the margins are sutured together. After a few days, the necrotic part will shed inside the intestine while the joined margins fuse.
This procedure, also suggested by Littler Jones in 1904 and Cattell, proved fast, reliable, and well-tolerated in patients.
Conclusion
Richter’s hernia is associated with a surprisingly high mortality rate, as shown throughout the medical literature.
The reduction in the mortality rate from 62.2% reported by Treves to the 21.4% found by Kadirov et al. emphasizes the severity of this condition.
Regardless of the availability of sophisticated diagnostic facilities, the prognosis can be significantly improved only by including this misleading disease in the differential diagnosis of uncharacteristic abdominal pain, specifically in patients with a history of laparoscopic surgery.
According to Kadirov et al., imaging modalities, such as computed tomography or water-soluble contrast studies, are of doubtful utility in the early diagnosis of Richter’s hernia.
The small, trapped segment of the intestinal wall would be difficult to visualize on CT, and contrast studies would not be revealed in the early stages when patency is still present.
Therefore, during the clinical examination, awareness remains the key to proper diagnosis and timely surgery.
