Abdominal compartment syndrome occurs when the abdomen becomes subject to increased pressure. Specific cause of abdominal compartment syndrome is not known, although some causes can be sepsis and severe abdominal trauma. Increasing pressure reduces blood flow to abdominal organs and impairs pulmonary, cardiovascular, renal, and gastro-intestinal (GI) function, causing multiple organ dysfunction syndrome and death.

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.

Abdominal compartment syndrome occurs when tissue fluid within the peritoneal and retroperitoneal space (either edema, retroperitoneal blood or free fluid in the abdomen) accumulates in such large volumes that the abdominal wall compliance threshold is crossed and the abdomen can no longer stretch. Once the abdominal wall can no longer expand, any further fluid leaking into the tissue results in fairly rapid rises in the pressure within the closed space. Initially this increase in pressure does not cause organ failure but does prevent organs from working properly - this is called intra-abdominal hypertension and is defined as a pressure over 12 mm Hg in adults. However, if the pressure continues to rise over 20 mm Hg and organs begin to fail, the syndrome has now progressed to the end stage of the highly fatal process termed abdominal compartment syndrome. These pressure measurements are relative. Small children get into trouble and develop compartment syndromes at much lower pressures while young previously healthy athletic individuals may tolerate an abdominal pressure of 20 mm Hg very well.

The underlying cause of the disease process is capillary permeability caused by the systemic inflammatory response syndrome (SIRS) that occurs in every critically ill patient. SIRS leads to leakage of fluid out of the capillary beds into the interstitial space in the entire body with a profound amount of this fluid leaking into the gut wall, mesentery and retroperitoneal tissue. (For a much more extensive discussion on the topic and physiology visit the Wikipedia section discussing intra-abdominal hypertension.)

- Peritoneal tissue edema secondary to diffuse peritonitis, abdominal trauma

- Fluid therapy due to massive volume resuscitation

- Retroperitoneal hematoma secondary to trauma and aortic rupture

- Peritoneal trauma secondary to emergency abdominal operations

- Reperfusion injury following bowel ischemia due to any cause

- Retroperitoneal and mesenteric inflammatory edema secondary to acute pancreatitis

- Ileus and bowel obstruction

- Intraabdominal masses of any cause

- Abdominal packing for control of bleeding

- Closure of the abdomen under undue tension

- Ascites / intraabdominal fluid accumulation

- Acute pancreatitis with abscesses formation

Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremities. When increased compression occurs in such a hollow space, organs will begin to collapse under the pressure. As the pressure increases and reaches a point where the abdomen can no longer be distended it starts to affect the cardiovascular and pulmonary systems. When abdominal compartment syndrome reaches this point without surgery and help of a silo the patient will most likely die. There is a high mortality rate associated with abdominal compartment syndrome.

NCS is associated with hematuria (which can lead to anemia) and abdominal pain (classically left flank or pelvic pain).

Since the left gonadal vein drains via the left renal vein it can also result in left testicular pain in men or left lower quadrant pain in women. Nausea and vomiting can result due to compression of the splanchnic veins. An unusual manifestation of NCS includes varicocele formation and varicose veins in the lower limbs. Another clinical study has shown that nutcracker syndrome is a frequent finding in varicocele-affected patients and possibly, nutcracker syndrome should be routinely excluded as a possible cause of varicocele and pelvic congestion.

Depending on the level of obstruction, bowel obstruction can present with abdominal pain, swollen abdomen, abdominal distension, vomiting, fecal vomiting, and constipation.

Bowel obstruction may be complicated by dehydration and electrolyte abnormalities due to vomiting; respiratory compromise from pressure on the diaphragm by a distended abdomen, or aspiration of vomitus; bowel ischemia or perforation from prolonged distension or pressure from a foreign body.

In small bowel obstruction, the pain tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation.

In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction.

The nutcracker syndrome (NCS) results most commonly from the compression of the left renal vein between the abdominal aorta (AA) and superior mesenteric artery (SMA), although other variants exist. The name derives from the fact that, in the sagittal plane and/or transverse plane, the SMA and AA (with some imagination) appear to be a nutcracker crushing a nut (the renal vein).

There is a wide spectrum of clinical presentations and diagnostic criteria are not well defined, which frequently results in delayed or incorrect diagnosis.

This condition is not to be confused with superior mesenteric artery syndrome, which is the compression of the third portion of the duodenum by the SMA and the AA.

Signs and symptoms include early satiety, nausea, vomiting, extreme "stabbing" postprandial abdominal pain (due to both the duodenal compression and the compensatory reversed peristalsis), abdominal distention/distortion, burping (eructation), external hypersensitivity or tenderness of the abdominal area, reflux, and heartburn. In infants, feeding difficulties and poor weight gain are also frequent symptoms.

In some cases of SMA syndrome, severe malnutrition accompanying spontaneous wasting may occur. This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms.

"Food fear" is a common development among patients with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver (pressure applied below the umbilicus in cephalad and dorsal direction) elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a supine (face up) position.

Patients with MALS reportedly experience abdominal pain, particularly in the epigastrium, which may be associated with eating and which may result in anorexia and weight loss.The pain can be in the left or right side, but usually where the ribs meet. Other signs are persistent nausea, lassitude (especially after a heavy meal) and exercise intolerance. Diarrhea is a common symptom, some experience constipation. While some experience vomiting, not everyone does. Exercise or certain postures can aggravate the symptoms. Occasionally, physical examination reveals an abdominal bruit in the mid-epigastrium.

Complications of MALS result from chronic compression of the celiac artery. They include gastroparesis and aneurysm of the pancreaticoduodenal arteries.

Superior mesenteric artery (SMA) syndrome is a gastro-vascular disorder in which the third and final portion of the duodenum is compressed between the abdominal aorta (AA) and the overlying superior mesenteric artery. This rare, potentially life-threatening syndrome is typically caused by an angle of 6°–25° between the AA and the SMA, in comparison to the normal range of 38°–56°, due to a lack of retroperitoneal and visceral fat (mesenteric fat). In addition, the aortomesenteric distance is 2–8 millimeters, as opposed to the typical 10–20. However, a narrow SMA angle alone is not enough to make a diagnosis, because patients with a low BMI, most notably children, have been known to have a narrow SMA angle with no symptoms of SMA syndrome.

SMA syndrome was first described in 1861 by Carl Freiherr von Rokitansky in victims at autopsy, but remained pathologically undefined until 1927 when Wilkie published the first comprehensive series of 75 patients. According to a 1956 study, only 0.3% of patients referred for an upper-gastrointestinal-tract barium studies fit this diagnosis, making it one of the rarest gastrointestinal disorders known to medical science. Recognition of SMA syndrome as a distinct clinical entity is controversial, due in part to its possible confusion with a number of other conditions, though it is now widely acknowledged.

SMA syndrome is also known as Wilkie's syndrome, cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion.

It is distinct from Nutcracker syndrome, which is the entrapment of the left renal vein between the AA and the SMA, although it is possible to be diagnosed with both conditions.

Chilaiditi syndrome is a rare condition when pain occurs due to transposition of a loop of large intestine (usually transverse colon) in between the diaphragm and the liver, visible on plain abdominal X-ray or chest X-ray.

Normally this causes no symptoms, and this is called Chilaiditi's sign. The sign can be permanently present, or sporadically. This anatomical variant is sometimes mistaken for the more serious condition of having air under the diaphragm (pneumoperitoneum) which is usually an indication of bowel perforation, possibly leading to surgical interventions.

Chilaiditi syndrome refers only to complications in the presence of Chilaiditi's sign. These include abdominal pain, torsion of the bowel (transverse colon volvulus) or shortness of breath.

Causes of small bowel obstruction include:

- Adhesions from previous abdominal surgery (most common cause)

- Barbed sutures.

- Pseudoobstruction

- Hernias containing bowel

- Crohn's disease causing adhesions or inflammatory strictures

- Neoplasms, benign or malignant

- Intussusception

- Volvulus

- Superior mesenteric artery syndrome, a compression of the duodenum by the superior mesenteric artery and the abdominal aorta

- Ischemic strictures

- Foreign bodies (e.g. gallstones in gallstone ileus, swallowed objects)

- Intestinal atresia

After abdominal surgery, the incidence of small bowel obstruction from any cause is 9%. In those where the cause of the obstruction was clear, adhesions are the single most common cause (more than half).

It is estimated that in 10-24% of normal, asymptomatic individuals the median arcuate ligament crosses in front of (anterior to) the celiac artery, causing some degree of compression. Approximately 1% of these individuals exhibit severe compression associated with symptoms of MALS. The syndrome most commonly affects individuals between 20 and 40 years old, and is more common in women, particularly thin women.

Diffuse tightness and tenderness over the entire belly of the tibialis anterior that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients suffering from this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms.

The exact cause is not always known, but it may occur in patients with a long and mobile colon (dolichocolon), chronic lung disease such as emphysema, or liver problems such as cirrhosis and ascites. Chilaiditi's sign is generally not associated with symptoms, and is most commonly an incidental finding in normal individuals.

Absence or laxity of the ligament suspending the transverse colon or of the falciform ligament are also thought to contribute to the condition. It can also be associated with relative atrophy of the medial segment of the left lobe of the liver. In this case, the gallbladder position is often anomalous as well – it is often located anterior to the liver, rather than posterior.

A compartment syndrome is an increased pressure within a muscular compartment that compromises the circulation to the muscles.

The first symptom of compartment syndrome is pain. Loss of function and decreased pulses or pulselessness, however, are late signs. According to Shears, paresthesia in the distribution of the nerves transversing the affected compartment has also been described as relatively early sign of compartment syndrome, and later is followed by anesthesia (Shears, 2006).

- Pain is often reported early and almost universally. The description is usually of deep, constant, and poorly localized pain out of proportion with the findings on physical examination (often incorrectly described as pain out of proportion to the injury). The pain is aggravated by passively stretching the muscle group within the compartment or actively flexing it (though this finding is not specific to compartment syndrome alone) and is not relieved by analgesia up to and including morphine.

- Paresthesia (altered sensation e.g., "pins & needles") in the cutaneous nerves of the affected compartment is another typical sign.

- Paralysis of the limb is usually a late finding. The compartment may also feel very tense and firm (pressure). Some find that their feet and even legs fall asleep. This is because compartment syndrome prevents adequate blood flow to the rest of the leg.

- A lack of pulse rarely occurs in patients, as pressures that cause compartment syndrome are often well below arterial pressures and pulse is only affected if the relevant artery is contained within the affected compartment.

- Tense and swollen shiny skin, sometimes with obvious bruising of the skin.

- Congestion of the digits with prolonged capillary refill time.

Acute limb ischaemia can occur in patients through all age groups. Patients that smoke and have diabetes mellitus are at a higher risk of developing acute limb ischaemia. Most cases involve people with atherosclerosis problems.

Symptoms of acute limb ischaemia include:

- Pain

- Pallor

- Paresthesias

- Perishingly cold

- Pulselessness

- Paralysis

These symptoms are called "the six P's'"; they are commonly mis-attributed to compartment syndrome. One more symptom would be the development of gangrene. Immediate medical attention should be sought with any of the symptoms.

In late stages, paresthesia is replaced by anesthesia due to death of nerve cells.

In some cases, gangrene can occur within six hours of ischaemia.

The symptoms of chronic exertional compartment syndrome (CECS) are brought on by exercise and consist of a sensation of extreme tightness in the affected muscles followed by a painful burning sensation if exercise is continued. After exercise is ceased, the pressure in the compartment will decrease within a few minutes, relieving painful symptoms. Symptoms will occur at a certain threshold of exercise which varies from person to person but is rather consistent for a given individual and can range anywhere from 30 seconds of running to about 10–15 minutes of running. CECS most commonly occurs in the lower leg, with the anterior compartment being the most frequently affected compartment. Foot drop is a common symptom of CECS.

Most SCLS patients report having flu-like symptoms (like a runny nose), or else gastro-intestinal disorders (diarrhea or vomiting), or a general weakness or pain in their limbs, but others get no particular or consistent warning signs ahead of their episodes. They subsequently develop thirst and lightheadedness and the following conditions measurable in a hospital emergency-room setting:

- hemoconcentration (elevated hematocrit or hemoglobin readings, with hematocrit levels >49% in men and >43% in women, not because of an absolute increase in them but because of the leak of plasma);

- very low blood pressure (profound arterial hypotension, with systolic blood pressure levels <90 mm Hg);

- albumin deficiency (hypoalbuminemia measuring <3.0 g/dL);

- partial or generalized edema, and cold extremities;

- a paraprotein in the blood (an MGUS in approximately 80% of cases).

Affected individuals typically experience limited relief from standard pain relieving medication, with the exception of some neuroleptic agents. Patients frequently experience 'pseudovisceral' phenomena or symptoms of altered autonomic nervous system function including nausea, bloating, abdominal swelling, loss of appetite with consecutively lowered body weight or an altered defecation process.

Pain is typically related to tensing the abdominal wall muscles, so any type of movement is prone to aggravate pain. Lying quietly can be the least painful position. Most patients report that they cannot sleep on the painful side.

Postcholecystectomy syndrome describes the presence of abdominal symptoms after surgical removal of the gallbladder (cholecystectomy), 2 years after the surgery.

Symptoms of postcholecystectomy syndrome may include:

- Dyspepsia, nausea, and vomiting.

- Flatulence, bloating, and diarrhea.

- Persistent pain in the upper right abdomen.

Symptoms occur in about 5 to 40 percent of patients who undergo cholecystectomy, and can be transient, persistent or lifelong. The chronic condition is diagnosed in approximately 10% of postcholecystectomy cases.

The pain associated with postcholecystectomy syndrome is usually ascribed to either sphincter of Oddi dysfunction or to post-surgical adhesions. A recent study shows that postcholecystectomy syndrome can be caused by biliary microlithiasis.

Approximately 50% of cases are due to biliary causes such as remaining stone, biliary injury, dysmotility, and choledococyst. The remaining 50% are due to non-biliary causes. This is because upper abdominal pain and gallstones are both common but are not always related.

Chronic diarrhea in postcholecystectomy syndrome is a type of bile acid diarrhea (type 3). This can be treated with a bile acid sequestrant like cholestyramine, colestipol or colesevelam, which may be better tolerated.

Acute limb ischaemia (ALI) occurs when there is a sudden lack of blood flow to a limb.

Acute limb ischaemia is caused by embolism or thrombosis, or rarely by dissection or trauma. Thrombosis is usually caused by peripheral vascular disease (atherosclerotic disease that leads to blood vessel blockage), while an embolism is usually of cardiac origin. In the United States, ALI is estimated to occur in 14 out of every 100,000 people per year. With proper surgical care, acute limb ischaemia is a highly treatable condition; however, delayed treatment (beyond 6 to 12 hours) can result in permanent disability, amputation, and/or death.

The New Latin term "ischaemia" as written, is a British version of the word "ischemia", and stems from the Greek terms "ischein" 'to hold'; and "haima" 'blood'. In this sense, ischaemia refers to the inhibition of blood flow to/through the limb.

Capillary leak syndrome is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning. Pharmaceuticals, including the chemotherapy medication gemcitabine, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks. These conditions and factors are sources of secondary capillary leak syndrome.

Systemic capillary leak syndrome (SCLS, or Clarkson's disease), or primary capillary leak syndrome, is a rare, grave and episodic medical condition observed largely in otherwise healthy individuals mostly in middle age. It is characterized by self-reversing episodes during which the endothelial cells which line the capillaries, usually of the extremities, separate for one to three days, causing a leakage of plasma mainly into the muscle compartments of the arms and legs. The abdomen, the central nervous system, and the organs (including the lungs) are typically spared, but the extravasation in the extremities is sufficiently massive to cause circulatory shock and compartment syndromes, with a dangerous hypotension (low blood pressure), hemoconcentration(thickening of the blood) and hypoalbuminemia (drop in albumin, a major protein) in the absence of other causes for such abnormalities. SCLS is thus a limb- and life-threatening illness, because each episode has the potential to cause damage to limb muscles and nerves, as well as to vital organs due to limited perfusion. It is often misdiagnosed as polycythemia, polycythemia vera, hyperviscosity syndrome, or sepsis.

Hiatal hernia has often been called the "great mimic" because its symptoms can resemble many disorders. Among them, a person with a hiatal hernia can experience dull pains in the chest, shortness of breath (caused by the hernia's effect on the diaphragm), heart palpitations (due to irritation of the vagus nerve), and swallowed food "balling up" and causing discomfort in the lower esophagus until it passes on to the stomach. In addition, hiatal hernias often result in heartburn but may also cause chest pain or pain with eating.

In most cases however, a hiatal hernia does not cause any symptoms. The pain and discomfort that a patient experiences is due to the reflux of gastric acid, air, or bile. While there are several causes of acid reflux, it occurs more frequently in the presence of hiatal hernia.

In newborns, the presence of Bochdalek hernia can be recognised from symptoms such as difficulty breathing fast respiration, increased heart rate.

Anterior cutaneous nerve entrapment syndrome (ACNES) is a nerve entrapment condition that causes chronic pain of the abdominal wall. It occurs when nerve endings of the lower thoracic intercostal nerves (7–12) are 'entrapped' in abdominal muscles, causing a severe localized nerve (neuropathic) pain that is usually experienced at the front of the abdomen.

ACNES syndrome is frequently overlooked and unrecognized, although the incidence is estimated to be 1:2000 patients.

The relative unfamiliarity with this condition often leads to significant diagnostic delays and misdiagnoses, often resulting in unnecessary diagnostic interventions and futile procedures. Physicians often misdiagnose ACNES as irritable bowel syndrome or "functional disorders", as symptoms of the condition are not dispositive.