A 57-year-old woman with abdominal pain
Perforation of the gastrointestinal tract
Diverticulitis is the acute inflammation of one or more diverticula, which are small pouches created by herniation of the mucosa into the wall of the colon. The condition is caused by microscopic or macroscopic perforation of the diverticula. Microscopic perforation is usually self-limited (uncomplicated diverticulitis) and responds to conservative treatment, whereas macroscopic perforation can be associated with fecal or purulent peritonitis, abscess, enteric fistula, bowel obstruction, and stricture (complicated diverticulitis), in which case surgery may be necessary.
Patients with peritonitis due to free perforation present with generalized tenderness with rebound tenderness and guarding on abdominal examination. The abdomen may be distended and tympanic to percussion, with diminished or absent bowel sounds. Patients may have hemodynamic compromise.
Plain upright abdominal radiographs may show free air under the diaphragm. Computed tomography may show oral contrast outside the lumen and detect even small amounts of free intraperitoneal air (more clearly seen on a lung window setting).
Our patient initially presented with acute diverticulitis. She later developed diffuse abdominal tenderness with hypoactive bowel sounds. Bowel perforation is certainly a possibility at this stage, though it is usually not associated with abdominal bruising. She would need additional imaging to rule out this complication.
Other differential diagnoses to be considered in this patient with right lower-quadrant pain include acute appendicitis, incarcerated inguinal hernia, volvulus (particularly cecal volvulus), small-bowel obstruction, pyelonephritis, and gynecologic causes such as adnexal torsion, ruptured ovarian cyst, and tubo-ovarian abscess. Computed tomography helps to differentiate most of these causes.
Rectus sheath hematoma
Rectus sheath hematoma is relatively uncommon and often not considered in the initial differential diagnosis of an acute abdomen. This gives it the rightful term “a great masquerader.” It usually results from bleeding into the rectus sheath from damage to the superior (more common) or inferior epigastric arteries and occasionally from a direct tear of the rectus abdominis muscle. Predisposing factors include anticoagulant therapy (most common), advanced age, hypertension, previous abdominal surgery, trauma, paroxysmal coughing, medication injections, pregnancy, blood dyscrasias, severe vomiting, violent physical activity, and leukemia.11
Clinical manifestations include acute abdominal pain, often associated with fever, nausea, and vomiting. Physical examination may reveal signs of hypovolemic shock, a palpable nonpulsatile abdominal mass, and signs of local peritoneal irritation. The Carnett sign11 (tenderness within the abdominal wall that persists and does not improve with raising the head) and the Fothergill sign11 (a tender abdominal mass that does not cross the midline and remains palpable with tensing of the rectus sheath) may be elicited.
Computed tomography is more sensitive than abdominal ultrasonography in differentiating rectus sheath hematoma from an intra-abdominal pathology.11 In addition, computed tomography also helps to determine if the bleeding is active or not, which has therapeutic implications.
In our patient, rectus sheath hematoma is a possibility because of her ongoing anticoagulation, findings of localized abdominal bruising, and palpable right lower-quadrant mass, and it is high on the list of differential diagnoses. Rectus sheath hematoma should be considered in the differential diagnosis of lower abdominal pain particularly in elderly women who are on anticoagulation and in whom the onset of pain coincides with a paroxysm of cough.12 Women are twice as likely as men to develop rectus sheath hematoma, owing to their different muscle mass.13 In addition, anterior abdominal wall muscles are stretched during pregnancy.13
Abdominal compartment syndrome
Abdominal compartment syndrome has been classically associated with surgical patients. However, it is being increasingly recognized in critically ill medical patients, in whom detecting and treating it early may result in significant reduction in rates of morbidity and death.14
Abdominal compartment syndrome is of three types: primary, secondary, and recurrent. Primary abdominal compartment syndrome refers to the classic surgical patients with evidence of direct injury to the abdominal or pelvic organs through major trauma or extensive abdominal surgeries. Secondary abdominal compartment syndrome refers to its development in critically ill intensive care patients in whom the pathology does not directly involve the abdominal or pelvic organs.
Various medical conditions can culminate in abdominal compartment syndrome and result in multiorgan failure. Recurrent abdominal compartment syndrome refers to its development after management of either primary or secondary intra-abdominal hypertension or abdominal compartment syndrome.15 Clinicians thus must be aware of secondary and recurrent abdominal compartment syndrome occurring in critically ill patients.
The normal intra-abdominal pressure is around 5 to 7 mm Hg, even in most critically ill patients. Persistent elevation, ie, higher than 12 mm Hg, is referred to as intra-abdominal hypertension.16–18 Intra-abdominal hypertension is subdivided into four grades:
- Grade I: 12–15 mm Hg
- Grade II: 16–20 mm Hg
- Grade III: 21–25 mm Hg
- Grade IV: > 25 mm Hg.
The World Society of the Abdominal Compartment Syndrome (WSACS) defines abdominal compartment syndrome as pressure higher than 20 mm Hg along with organ damage.18 It may or may not be associated with an abdominal perfusion pressure less than 60 mm Hg.18
Risk factors associated with abdominal compartment syndrome include conditions causing decreased gut motility (gastroparesis, ileus, and colonic pseudo-obstruction), intra-abdominal or retroperitoneal masses or abscesses, ascites, hemoperitoneum, acute pancreatitis, third-spacing due to massive fluid resuscitation with transfusions, peritoneal dialysis, and shock.18,19
Physical examination has a sensitivity of only 40% to 60% in detecting intra-abdominal hypertension.20 The gold-standard method of measuring the intra-abdominal pressure is the modified Kron technique,18 using a Foley catheter in the bladder connected to a pressure transducer. With the patient in the supine position, the transducer is zeroed at the mid-axillary line at the level of the iliac crest, and 25 mL of normal saline is instilled into the bladder and maintained for 30 to 60 seconds to let the detrusor muscle relax.15 Pressure tracings are then recorded at the end of expiration. Factors that are known to affect the transbladder pressure include patient position, respiratory movement, and body mass index, and should be taken into account when reading the pressure recordings.15,21 Other techniques that can be used include intragastric, intra-inferior vena cava, and intrarectal approaches.15
The WSACS recommends that any patient admitted to a critical care unit or in whom new organ failure develops should be screened for risk factors for intra-abdominal hypertension and abdominal compartment syndrome. If a patient has at least two of the risk factors suggested by WSACS, a baseline intra-abdominal pressure measurement should be obtained. Patients at risk for intra-abdominal hypertension should have the intra-abdominal pressure measured every 4 to 6 hours. However, in the face of hemodynamic instability and worsening multiorgan failure, the pressure may need to be measured hourly.18
Clinicians managing patients in the intensive care unit should think of intra-abdominal pressure alongside blood pressure, urine output, and mental status when evaluating hemodynamic status. Clinical manifestations of abdominal compartment syndrome reflect the underlying organ dysfunction and include hypotension, refractory shock, decreased urine output, intracranial hypertension, progressive hypoxemia and hypercarbia, elevated pulmonary peak pressures, and worsening of metabolic acidosis.22
Treatment. The standard treatment for primary abdominal compartment syndrome is surgical decompression. According to WSACS guidelines, insertion of a percutaneous drainage catheter should be advocated in patients with gross ascites and in whom decompressive surgery is not feasible. A damage-control resuscitation strategy used for patients undergoing damage-control laparotomy has been found to increase the 30-day survival rate.23 A damage-control resuscitation strategy consists of increasing the use of plasma and platelet transfusions over packed red cell transfusions, limiting the use of crystalloid solutions in early fluid resuscitation, and allowing for permissive hypotension.
Secondary abdominal compartment syndrome is treated conservatively in most cases, since patients with this condition are very poor surgical candidates owing to their comorbidities.18 However, in patients with progressive organ dysfunction in whom medical management has failed, surgical decompression should be considered.18 Medical management of secondary abdominal compartment syndrome depends on the underlying etiology. Strategies include nasogastric or colonic decompression, use of prokinetic agents, paracentesis in cases with gross ascites, and maintaining a cumulative negative fluid balance. The WSACS does not recommend routine use of diuretics, albumin infusion, or renal replacement strategies. Pain should be adequately controlled to improve abdominal wall compliance.18,24 Neuromuscular blockade agents may be used to aid this process. Neostigmine may be used to treat colonic pseudo-obstruction when other conservative methods fail. Use of enteral nutrition should be minimized.18
Our patient might have abdominal compartment syndrome, but a definitive diagnosis cannot be made at this point without measuring the intra-abdominal pressure.
