The patient is a female in her 70s with a history of hypothyroidism and unspecified dementia who presented to the emergency department (ED) from her skilled nursing facility (SNF) due to altered mental status and abdominal distention. Per report, the patient had recently been diagnosed with a small bowel obstruction via a plain film obtained at her SNF. She may have been treated with an enema in the days prior to presentation. On the morning of her arrival, the patient had increasing abdominal distention with severe pain. She subsequently became altered, prompting transfer to the ED. Her blood sugar was within normal limits prior to transfer.
Vitals: T 97.4 HR 103 BP 133/107 RR 33 SpO2 93% on RA
Physical Exam: Exam reveals an ill-appearing elderly female that is not responsive to verbal or painful stimuli. Her eyes are open with a fixed rightward gaze deviation. Pupils are equal, round, and reactive to light bilaterally. Her upper extremities are contracted upwards. She is tachypneic but her lungs are clear to auscultation bilaterally. Cardiovascular exam reveals a tachycardic rate with a regular rhythm and no murmurs appreciated. Her abdomen is markedly distended and rigid. No significant lower extremity edema. No obvious signs of traumatic injury.
BUN/Creatinine: 39/1.6 WBC: 2.7 H/H: 15/49 Lactate: 10.4 VBG: 7.09/63/21 Troponin: 0.05 BNP: 178 EKG: Sinus tachycardia
IV access was obtained and fluid resuscitation was initiated. Based on the patient’s history and physical exam, there was concern for small bowel obstruction or other intra-abdominal pathology with resultant sepsis. Additionally, given the patient’s neurological exam, there was concomitant concern for status epilepticus versus intracerebral hemorrhage or ischemic stroke. She was given 10 mg of intramuscular midazolam without improvement of her mental status and was felt to not be protecting her airway. As such, she was intubated and loaded with levetiracetam. Plain films of the chest and abdomen revealed pneumoperitoneum. She was started on piperacillin/tazobactam for her presumed sepsis. She became progressively hypotensive requiring push-dose vasopressors. Prior to being admitted to the acute care surgery service, a CT of the head was obtained which ruled-out intracranial hemorrhage. The patient was transferred to the surgical intensive care unit pending medical stabilization and a goals of care discussion with family.
The patient eventually underwent exploratory laparotomy, where she was found to have a sigmoid volvulus with infarction and perforation, cecal infarction with perforation, and abdominal compartment syndrome. She underwent a total colectomy. She was monitored with continuous electroencephalogram without evidence of seizures or non-convulsive status epilepticus. Her mental status did not improve. An MRI of the head and neck was obtained demonstrating bilateral cerebral and cerebellar infarcts. Her family ultimately pursued comfort care given her poor prognosis, and she was transferred to hospice.
ABDOMINAL COMPARTMENT SYNDROME
Abdominal compartment syndrome is a rare but likely under-recognized clinical condition. Defined as intra-abdominal pressure greater than 20 mmHg with associated end-organ damage, abdominal compartment syndrome can be seen after recent surgery or due to any number of intra-abdominal pathologies. Few studies exist that find agreement upon the true incidence and prevalence of the disease process, ranging from 1% to 14% depending on the exact etiology of the condition.[2,3] Although the precise incidence is unknown, it carries a high rate of morbidity and mortality, making early recognition by the ED physician paramount.
Patients presenting to the ED with abdominal compartment syndrome are typically critically ill, and therefore are not often able to provide a history, as seen with the above patient. If they are able to, they will often be experiencing abdominal pain and bloating, difficulty breathing, and lightheadedness. On physical examination, they will have a distended abdomen that is tender to palpation and possibly rigid or peritonitic if infarction and perforation has occurred. In critically ill patients, decreased urine output, increased ventilation requirements, hypotension, tachycardia, and a lactic acidosis in the setting of a distended abdomen should raise suspicion for abdominal compartment syndrome.
Abdominal compartment syndrome can be classified into primary or secondary causes. In general, a primary cause is from trauma or a direct medical or surgical etiology, whereas a secondary cause is typically iatrogenic from aggressive fluid resuscitation in sepsis and burn patients. Consider abdominal compartment syndrome if the patient has had any recent abdominal surgery or recent treatment of the pathologies listed in the table above (Figure 1).
Intra-abdominal pressure may be measured by specialized pressure transducer instruments that can be passed into the stomach by a nasogastric route, into the colon from the rectum, or into the bladder using a Foley catheter. Measurement of intravesicular pressure by Foley catheter has become the standard method of screening. Intra-abdominal hypertension exists when the pressure is sustained at greater 12 mmHg. As stated above, abdominal compartment syndrome is recognized as an elevated abdominal pressure that is greater than 20 mmHg with evidence of end-organ damage.
To better understand abdominal compartment syndrome, one must appreciate the physiology of the process that leads to it. Intra-abdominal pressure is related to a patient’s body mass index and can be influenced by any recent abdominal surgeries or disease processes. A prospective study looking to determine normal intra-abdominal pressure found a range of 0.2-16.2 mmHg with a mean pressure of 6.5 mmHg. Different stages of intra-abdominal hypertension exist, ranging from normal for that individual towards a pathological increase towards abdominal compartment syndrome. The most obvious consequences of this pathology are the effects on the intra-abdominal organs.
When intra-abdominal pressure rises, the abdominal perfusion pressure is reduced, leading to end-organ dysfunction (Figure 2). This is frequently exacerbated by the fact that these patients are often critically ill and have low MAPs to begin with, further reducing the abdominal perfusion pressure. This has multiple pathophysiologic effects, the majority of which have been studied in animal models.
In the abdominal compartment, increasing pressures leads to reduced perfusion of the abdominal viscera. This can result in progressive bowel ischemia, infarction, and perforation, as well as a significant lactic acidosis, all of which were seen in the presented patient. The lactic acidosis is worsened by the fact that there is reduced hepatic perfusion and therefore inadequate lactate clearance. In addition, intestinal edema and necrosis can lead to subsequent bacterial translocation, sepsis, and multi-system organ dysfunction.
Increased abdominal pressure also leads to compression of the renal veins, causing an increase in renal pressure and acute kidney injury. As the intra-abdominal pressure increases, the patient will become progressively oliguric and may progress to anuria. In addition, the patient generally has reduced cardiac output with subsequent activation of the renin-angiotensin-aldosterone system (RAAS), leading to renal vasoconstriction and further kidney injury.
Abdominal compartment syndrome also leads to cardiopulmonary and neurologic effects. These patients are typically hypovolemic and with the high abdominal pressure can have compression of the inferior vena cava with reduction in preload, all leading towards reduced cardiac output. Activation of the RAAS system also causes increased systemic vascular resistance. Intra-thoracic pressure can become elevated with a reduction in compliance and difficulty with ventilation. Cerebral venous outflow can be obstructed due to the increased intra-thoracic pressure, leading to a significant increase in intracranial pressure.
ED treatment of abdominal compartment syndrome primarily involves recognition of the disease process and resuscitation of these often critically ill patients. Unfortunately, excessive fluid resuscitation can lead to increased intra-abdominal pressures due to third spacing. Some sources report that iatrogenic abdominal compartment syndrome can occur with only 5-7 liters of crystalloid in the first 24 hours of presentation. Therefore, judicious fluid administration is recommended. Recent studies suggest that targeting certain abdominal perfusion pressure goals may help guide resuscitation. While not yet prospectively validated, maintaining an abdominal perfusion pressure of 50-60 mmHg has been shown to be associated with increased survival in these patients.
As vascular flow to the intestines is compromised due to increasing abdominal pressures, bacterial translocation can occur. Consequently, patients with abdominal compartment syndrome are at increased risk of intra-abdominal infections. ED providers are therefore encouraged to consider empiric antibiotic coverage for abdominal flora. While awaiting definitive intervention, gastric and colonic decompression can be performed by placement of nasogastric or rectal tubes. Likewise, if the patient has abdominal ascites, paracentesis can be used to help alleviate the pressure.
Surgical management and decompression is completed by laparotomy. Practice patterns vary, with some surgeons waiting for intra-abdominal pressure to exceed 20 mmHg, whereas others will perform surgery if there is any end-organ damage present, or if the abdominal perfusion pressure is reduced. Temporary abdominal closure is common to prevent recurrence, with patients typically being brought back to the operating room within 48-72 hours to attempt primary closure.
Abdominal compartment syndrome should be suspected in patients presenting critically ill with a distended abdomen and any of the possible etiologies listed above. Diagnosis is made by measurement of the intra-abdominal pressure using an intra-vesicular pressure transducer, with a pressure greater than 20 mmHg and associated end-organ damage. Definitive management is by surgical decompression. Morbidity and mortality from abdominal compartment syndrome is high, with one prospective observational study finding a 36% mortality rate at one month, increasing to 55% at one year.[13 While abdominal compartment syndrome is rare in the ED, mortality increases with time, making the interventions by the ED provider crucial in improving patient outcomes.
PROCEDURE: MEASUREMENT OF INTRA-ABDOMINAL PRESSURE
In cases of suspected abdominal compartment syndrome, measurement of the intra-abdominal pressure is a crucial step in the diagnosis and management of these often critically ill patients. Early identification of elevated intra-abdominal pressures by the emergency medicine provider can be life and organ saving. Measurement of a patient’s bladder pressure is the current standard of care for diagnosis of this rare disease process and should be considered in patients with severe abdominal distension and a tense or rigid abdomen.
There are many different ways to perform this procedure, and certain Foley catheters have the capability to obtain this measurement without additional supplies. Nonetheless, these are often difficult to find in the emergency department (ED), and locating them may lead to dangerous delays in patient care. Therefore, the following is a description of how to obtain this measurement with supplies that can quickly be found in the ED (Image 1).
- Foley catheter kit
- Sterile gloves
- Kelly forceps
- 60 mL syringe filled with sterile saline
- Three-way stopcock
- Arterial line pressure transducing tubing
- 1 L normal saline
- Pressure bag
- Insert a Foley catheter and allow drainage of urine.
- Prepare a standard arterial line set-up and prime it using the 1 L bag of saline.
- Connect the stopcock attached to a 60 mL syringe of saline to the end of the arterial line tubing.
- Lie patient flat.
- Clean Foley catheter access port with an alcohol swab.
- Connect the three-way stopcock to the Foley catheter access port (Image 2).
- Zero the pressure transducer at the level of the iliac crest in the mid-axillary line.
- Clamp the drainage bag of the Foley catheter just distal to the culture aspiration port using the Kelly forceps (Image 3).
- Instill 60 mL of sterile saline into the bladder via the stopcock. Turn the stopcock off to the syringe and open to the patient upon completion of this.
- Briefly unclamp the distal Foley to allow all air in the proximal collection tubing to pass into the distal tubing, then reclamp.
- Allow 60 seconds for detrusor muscle relaxation prior to obtaining measurements.
- The bladder pressure should be taken at end-exhalation with the patient completely flat in the supine position. Ensure a good waveform prior to recording the measurement.
- Unclamp Foley when complete and remove pressure transducing tubing. If strict measurement of urine output is necessary for the patient, subtract 60 mL from the total urine output.
Normal intra-abdominal pressure is less than or equal to 5 mmHg. Intra-abdominal hypertension occurs at pressures greater than 12 mmHg, while abdominal compartment syndrome is diagnosed at pressures greater than 20 mmHg in the setting of organ dysfunction. Ideally, bladder pressures should be obtained in paralyzed patients in order to ensure complete relaxation of the abdominal muscles. However, this is often unrealistic and not feasible. With appropriate instruction, accurate numbers can be obtained in alert patients. Complete supine positioning is also recommended, as measurements will be artificially elevated if the head of bed is at all elevated. Ultimately, it can be helpful to obtain serial measurements using the same technique and positioning in order to assess for clinically significant changes in intra-abdominal pressures and to help guide response to treatment.
"Abdominal Compartment Syndrome" Authored by Shaun Harty, MD
"Procedure: Measurement of Intra-Abdominal Pressure" Authored by Jessica Baez, MD
Posted by Matthew Scanlon, MD
- Malbrain, M. L. N. G., Cheatham, M. L., Kirkpatrick, A., Sugrue, M., Parr, M., De Waele, J., Balogh, Z., et al. (2006). Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Medicine, 32(11), 1722–1732. doi:10.1007/s00134-006-0349-5
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