Septal perforations are managed with a multitude of options. The treatment often depends on the severity of symptoms and the size of the perforations. Generally speaking anterior septal perforations are more bothersome and symptomatic. Posterior septal perforations, which mainly occur iatrogenically, are often managed with simple observation and are at times intended portions of skull base surgery. Septal perforations that are not bothersome can be managed with simple observation. While no septal perforation will spontaneously close, for the majority of septal perforations that are unlikely to get larger observation is an appropriate form of management. For perforations that bleed or are painful, initial management should include humidification and application of salves to the perforation edges to promote healing. Mucosalization of the perforation edges will help prevent pain and recurrent epistaxis and majority of septal perforations can be managed without surgery.

For perforations in which anosmia, or the loss of smell, and a persistent whistling are a concern the use of a sillicone septal button is a treatment option. These can be placed while the patient is awake and usually in the clinic setting. While complications of button insertion are minimal, the presence of the button can be bothersome to most patients.

For patients who desire definitive close, surgery is the only option. Prior to determining candidacy for surgical closure, the etiology of the perforation must be determined. Often this requires a biopsy of the perforation to rule out autoimmune causes. If a known cause such as cocaine is the offending agent, it must be ensured that the patient is not still using the irritant.

For those that are determined to be medically cleared for surgery, the anatomical location and size of the perforation must be determined. This is often done with a combination of a CT scan of the sinuses without contrast and an endoscopic evaluation by an Ear Nose and Throat doctor. Once dimensions are obtained the surgeon will decide if it is possible to close the perforation. Multiple approaches to access the septum have been described in the literature. While sublabial and midfacial degloving approaches have been described, the most popular today is the rhinoplasty approach. This can include both open and closed methods. The open method results in a scar on the columella, however, it allows for more visibility to the surgeon. The closed method utilizes an incision all on the inside of the nose. The concept behind closure includes bringing together the edges of mucosa on each side of the perforation with minimal tension. An interposition graft is also often used. The interposition graft provides extended stability and also structure to the area of the perforation. Classically, a graft from the scalp utilizing temporalis fascia was used. Kridel, et al., first described the usage of acellular dermis so that no further incisions are required; they reported an excellent closure rate of over 90%. Overall perforation closure rates are variable and often determined by the skill of the surgeon and technique used. Often surgeons who claim a high rate of closure choose perforations that are easier to close. An open rhinoplasty approach also allows for better access to the nose to repair any concurrent nasal deformities, such as saddle nose deformity, that occur with a septal perforation.

To treat a septal haematoma it is incised & drained to prevent avascular necrosis of the septal hyaline cartilage which depends on diffusion of nutrients from its attached nasal mucosa. Small hematomas can be aspirated with a wide-bore needle. Large hematomas are drained by an incision parallel to nasal floor. Systemic antibiotics are given after the incision and drainage to prevent local infection.

With the exception of a few case reports describing survival without surgery, the mortality of untreated Boerhaave syndrome is nearly 100%. Its treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation, and if there is significant fluid loss it should be replaced with IV fluid therapy since oral rehydration is not possible. Even with early surgical intervention (within 24 hours) the risk of death is 25%.

A nasal septum perforation is a medical condition in which the nasal septum, the cartilaginous membrane dividing the nostrils, develops a hole or fissure.

This may be brought on directly, as in the case of nasal piercings, or indirectly, as by long-term topical drug application, including intranasal ethylphenidate, methamphetamine, cocaine, crushed prescription pills, or decongestant nasal sprays, chronic epistaxis, excessive nose picking and as a complication of nasal surgery like septoplasty or rhinoplasty. Much less common causes for perforated nasal septums include rare granulomatous inflammatory conditions like granulomatosis with polyangiitis. It has been reported as a side effect of anti-angiogenesis drugs like bevacizumab.

Treatment for a nasal septal abscess is similar to that of other bacterial infections. Aggressive broad spectrum antibiotics may be used after the infected area has been drained of fluids.

Nasal septal hematoma is a condition affecting the nasal septum. It can be associated with trauma.

Because the septal cartilage has no blood supply of its own and receives all of its nutrients and oxygen from the perichondrium, an untreated septal hematoma may lead to destruction of the septum. Immediate drainage is necessary. Failure to recognise septal hematomas, or treat in a timely fashion, can cause a saddle nose deformity.

The primary aim of treatment of a newly formed oroantral communication is to prevent the development of an oroantral fistula as well as chronic sinusitis. The decision on how to treat OAC/OAF depends on various factors. Small size communications between 1 and 2 mm in diameter, if uninfected, are likely to form a clot and heal by itself later. Communications larger than this require treatments to close the defect and these interventions can be categorised into 3 types: surgical, non-surgical and pharmacological.

These interventions employ the principle of placement of materials into the defect without flap closure. These materials may act as a mechanical barrier and/or promote the healing process of the communication. Different materials, such as synthetic graft materials, xenografts, fibrin glue, synthetic absorbable implant and acrylic splints has all been reported as potential material to use.

The perforation may heal in a few weeks, or may take up to a few months. Some perforations require intervention. This may take the form of a paper patch to promote healing (a simple procedure by an ear, nose and throat specialist), or surgery (tympanoplasty). However, in some cases, the perforation can last several years and will be unable to heal naturally.

Hearing is usually recovered fully, but chronic infection over a long period may lead to permanent hearing loss. Those with more severe ruptures may need to wear an ear plug to prevent water contact with the ear drum.

In simple cases of obstruction, where there are no complications, a variety of non-surgical and surgical techniques are used to remove the enterolith. These include crushing the enterolith and milking it back to the stomach or forward to the colon, surgical removal via an uninvolved segment of the gastrointestinal tract, and resection of the involved segment.

Esophageal rupture is a rupture of the esophageal wall. Iatrogenic causes account for approximately 56% of esophageal perforations, usually due to medical instrumentation such as an endoscopy or paraesophageal surgery. In contrast, the term Boerhaave syndrome is reserved for the 10% of esophageal perforations which occur due to vomiting.

Spontaneous perforation of the esophagus most commonly results from a full-thickness tear in the esophageal wall due to a sudden increase in intraesophageal pressure combined with relatively negative intrathoracic pressure caused by straining or vomiting (effort rupture of the esophagus or Boerhaave's syndrome). Other causes of spontaneous perforation include caustic ingestion, pill esophagitis, Barrett's esophagus, infectious ulcers in patients with AIDS, and following dilation of esophageal strictures.

In most cases of Boerhaave's syndrome, the tear occurs at the left postero-lateral aspect of the distal esophagus and extends for several centimeters. The condition is associated with high morbidity and mortality and is fatal without treatment. The occasionally nonspecific nature of the symptoms may contribute to a delay in diagnosis and a poor outcome. Spontaneous effort rupture of the cervical esophagus, leading to localized cervical perforation, may be more common than previously recognized and has a generally benign course. Preexisting esophageal disease is not a prerequisite for esophageal perforation but it contributes to increased mortality.

This condition was first documented by the 18th-century physician Herman Boerhaave, after whom it is named. A related condition is Mallory-Weiss syndrome which is only a mucosal tear.

In case of iatrogenic perforation common site is cervical esophagus just above the upper sphincter whereas spontaneous rupture as seen in Boerhaave's syndrome perforation commonly occurs in the lower (1/3)rd of esophagus.

A perforated eardrum or punctured eardrum is a rupture or perforation (hole) of the eardrum which can occur as a result of otitis media (ear infection), trauma (e.g. by trying to clean the ear with sharp instruments), explosion, loud noise or surgery (accidental creation of a rupture). Flying with a severe cold can also cause perforation due to changes in air pressure and blocked eustachian tubes resulting from the cold. This is especially true on landing.

Potential complications of a nasal septal abscess include cavernous sinus thrombophlebitis, septal perforation, or saddle deformity due to cartilage necrosis.

Equine enteroliths are found by walking pastures or turning over manure compost piles to find small enteroliths, during necroscopy, and increasingly, during surgery for colic. Therefore, the incidence of asymptomatic enteroliths is unknown.

Equine enteroliths typically are smoothly spherical or tetrahedral, consist mostly of the mineral struvite (ammonium magnesium phosphate), and have concentric rings of mineral precipitated around a nidus.

Enteroliths in horses were reported widely in the 19th century, infrequently in the early 20th century, and now increasingly. They have also been reported in zebras: five in a zoo in California and one in a zoo in Wisconsin. Struvite enteroliths are associated with elevated pH and mineral concentrations in the lumen. In California, struvite enteroliths are associated also with a high proportion of alfalfa in the feed and less access to grass pasture. This association has been attributed to the cultivation of alfalfa on serpentine soils, resulting in high concentrations of magnesium in the alfalfa.

Pneumoperitoneum is (abnormal presence of air or other gas) in the peritoneal cavity, a potential space within the abdominal cavity. The most common cause is a perforated abdominal viscus, generally a perforated peptic ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or abdominal trauma. A perforated appendix seldom causes a pneumoperitoneum.

In the mid-twentieth century, an "artificial" pneumoperitoneum was sometimes intentionally administered as a treatment for a hiatal hernia. This was achieved by insufflating the abdomen with carbon dioxide. The practice is currently used by surgical teams in order to perform laparoscopic surgery.

A perforated ulcer, is a condition in which untreated ulcer can burn through the wall of the stomach (or other areas of the gastrointestinal tract), allowing digestive juices and food to leak into the abdominal cavity. Treatment generally requires immediate surgery. The ulcer is known initially as a peptic ulcer before the ulcer burns through the full thickness of the stomach or duodenal wall. A diagnosis is made by taking an erect abdominal/chest X-ray (seeking air under the diaphragm). This is in fact one of the very few occasions in modern times where surgery is undertaken to treat an ulcer. Many perforated ulcers have been attributed to the bacterium "Helicobacter pylori". The incidence of perforated ulcer is steadily declining, though there are still incidents where it occurs. Causes include smoking and nonsteroidal anti-inflammatory drugs (NSAIDs). A perforated ulcer can be grouped into a stercoral perforation which involves a number of different things that causes perforation of the intestine wall. The first symptom of a perforated peptic ulcer is usually sudden, severe, sharp pain in the abdomen. The experience is typically so intense that most people precisely recall the exact moment the pain began. The pain is typically at its maximum immediately and persists. It is characteristically made worse by any movement, and greatly intensifies with coughing or sneezing.

Surgical intervention is nearly always required in form of exploratory laparotomy and closure of perforation with peritoneal wash. Occasionally they may be managed laparoscopically.

Conservative treatment including intravenous fluids, antibiotics, nasogastric aspiration and bowel rest is indicated only if the person is nontoxic and clinically stable.

Distal or sigmoid, fecalomas can often be disimpacted digitally or by a catheter which carries a flow of disimpaction fluid (water or other solvent or lubricant). Surgical intervention in the form of sigmoid colectomy or proctocolectomy and ileostomy may be required only when all conservative measures of evacuation fail.

Organ perforation is a complete penetration of the wall of a hollow organ in the body, such as the gastrointestinal tract in the case of gastrointestinal perforation. It mainly refers to accidental or pathologic perforation, rather than intentional penetration during surgery.

Types include gastrointestinal perforation and uterine perforation.

Stercoral ulcer is an ulcer of the colon due to pressure and irritation resulting from severe, prolonged constipation due to large bowel obstruction. It is most commonly located in the rectum. Individuals with this condition are at risk for stercoral perforation.

Diverticular disease is when problems occur due to diverticulosis, a condition defined by the presence of pouches in the wall of the large intestine (diverticula). This includes diverticula becoming inflamed (diverticulitis) or bleeding. Colonic perforation due to diverticular disease may be classified using the Hinchey Classification.

Uterine perforation is a potential complication of any intrauterine procedure. It may be associated with injury to surrounding blood vessels or viscera such as the bladder or intestine. If not diagnosed at the time of the procedure it can occasionally result in massive hemorrhage or sepsis; however, the majority of uterine perforations are sub-clinical and safely resolve by themselves without treatment and do not cause any significant long-term damage. Risk factors include cervical stenosis during trans-cervical procedures or decreased strength of the myometrial wall as in pregnancy or menopause.

Fecal impaction and attempts at removal can have severe and even lethal effects, such as the rupture of the colon wall by catheter or an acute angle of the fecaloma (stercoral perforation), followed by septicemia. A small fecalith is one cause of both appendicitis and acute diverticulitis. It may also lead to stercoral perforation, a condition characterized by bowel perforation due to pressure necrosis from a fecal mass or fecaloma.

In medicine, Valentino's syndrome is pain presenting in the right lower quadrant of the abdomen caused by a duodenal ulcer with perforation through the retroperitoneum.

It is named after Rudolph Valentino who presented with right lower quadrant pain which turned out to be perforated peptic ulcer. He subsequently died from an infection inspite of surgery to repair the perforation. The pain is caused by gastric and duodenal fluids that tend to settle in the right paracolic gutter causing peritonitis and RLQ pain.

Patients with perforated Valentino's syndrome usually present with a sudden onset of severe, sharp abdominal pain which is reminiscent of appendicitis. Most patients describe generalized pain; a few present with severe epigastric pain. As even slight movement can tremendously worsen their pain, these patients assume a fetal position. Abdominal examination usually discloses generalized tenderness, rebound tenderness, guarding, and rigidity. However, the degree of peritoneal findings is strongly influenced by a number of factors, including the size of perforation, amount of bacterial and gastric contents contaminating the abdominal cavity, time between perforation and presentation, and spontaneous sealing of perforation.

These patients may also demonstrate signs and symptoms of septic shock, such as tachycardia, hypotension, and anuria. Not surprisingly, these indicators of shock may be absent in elderly or immunocompromised patients or in those with diabetes. Patients should be asked if retching and vomiting occurred before the onset of pain.

When present, pneumoperitoneum can often be seen on projectional radiography, but small amounts are often missed, and CT scan is nowadays regarded as a criterion standard in the assessment of a pneumoperitoneum. CT can visualize quantities as small as 5 cm³ of air or gas.

Signs that can be seen on projectional radiography are the "double wall sign" (also called "Rigler's sign") and the "football sign".

The "double wall sign" marks the presence of air on both sides of the intestine. However, a false double wall sign can result from two loops of bowel being in contact with one another. The sign is named after Leo George Rigler. It is not the same as Rigler's triad.

The "football sign" is when the abdomen appears as a large oval radiolucency reminiscent of an American football on a supine projectional radiograph. The football sign is most frequently seen in infants with spontaneous or iatrogenic gastric perforation causing pneumoperitoneum. It is also seen in bowel obstruction with secondary perforation, as in Hirschprung disease, midgut volvulus, meconium ileus and intestinal atresia. Iatrogenic causes like endoscopic perforation may also give football sign.