Emergency General Surgery,  Trauma Surgery

Pricking the Big Red Balloon

It’s gonna blow!!!

Common exclamation in action movies

Hi everybody!!! Here we are again…

Well, let’s not lose time, and go straight to our clinical scenario…

Your night colleague just told you that 5 patients are waiting for an emergency operation because the vascular colleagues spent the entire night in the operating room for a ruptured aortic aneurysm… Not the best start for a Monday morning…

A few hours later, the intensivist calls you because the patient who underwent the open repair of the ruptured aortic aneurysm during the night has a very distended abdomen. He is a 56 yo male, and his vitals are far from normal…

The patient is tubed, has high peak pressures, MAP of 60 mmHg on inotropes, and a capillary refill of 4 seconds. 

The last blood gas reported: pH 7.25; pO2 93; pCO2 28; HCO3 21; Lac 40; BE -18.

A contrast-enhanced abdominal CT scan has already been done and it showed no signs of acute bleeding, but diffuse free fluid.

The blood tests showed: Hb 11 g/dL, WBC 20’000 mm3; Plt 250’000; Creat 4 mg/dL; INR 2; elevated CPK and BUN.

On exploration, the abdomen is diffusely distended and tense, hypertympanic, and without bowel movements. No muscular defense reaction is provoked, but the patient is fully sedated and relaxed. 

So? Why the hell did the intensivist call you for?

Introduction

When we speak about abdominal compartment syndrome (ACS) we cannot avoid pointing out some definitions first:

  • Intra-abdominal pressure (IAP): under normal conditions, it is usually 5-7 mmHg, but it may be altered by BMI;
  • Abdominal perfusion pressure (APP): mean arterial pressure minus intra-abdominal pressure;
  • Intra-abdominal hypertension (IAH): defined as IAP >12 mmHg.

Intra-abdominal hypertension may have different timing and etiologies:

  • It may be acute when it develops within hours due to a traumatic event, operations, bleeding, or a complication. It often leads to an ACS.
  • It could be subacute when the development is within days because of intestinal obstruction, acute pancreatitis with diffuse intra-abdominal edema, intra-abdominal collections… It may develop an ACS.
  • It may be chronic when it develops within months. It is usually the consequence of pregnancy, obesity, or retroperitoneal neoplasia. Even if it is considered a risk factor for the uprise of an ACS, it cannot evolve into it by itself though.

Furthermore, the IAH may be classified according to the IAP into 4 grades:

  1. Grade 1 – IAP 12-15 mmHg
  2. Grade 2 – IAP 16-20 mmHg
  3. Grade 3 – IAP 21-25 mmHg
  4. Grade 4 – IAP >25 mmHg

The ACS is a critical condition derived from a sustained IAH, usually with a IAP >20 mmHg, leading to the onset of a new organ failure. This state uprises when the APP is below the critical limit of 60 mmHg. It may be primary, subordinate to an intra-abdominal pathology, or secondary, due to an extra-abdominal pathology.

The prevalence of IAH in critical patients is around 32%, and that of ACS is 4%.

Pathophysiology & Clinical Presentation

The onset of IAH will impair many different organs/systems, thus determining an ACS:

  • Cardiovascular: diaphragmatic hypomobility with reduction of cardiac mobility; inferior vena cava (IVC) compression with decreased venous return, reduction of preload with venous hypertension in the lower body, meaning an increased risk of deep venous thrombosis;
  • Respiratory: increased intrathoracic pressure, decreased pulmonary compliance, increased peak inspiratory pressure, decreased PaO2, and increased PaCO2.
  • Renal: increased intrarenal pressure because of the increased pressure inside the IVC with activation of the Renin-Angiotensin system leading to the production of the antidiuretic hormone and, consequently, to a decreased urinary output.
  • Gastrointestinal: decreased venous return, mesenteric edema, hypoperfusion, lactic acidosis, which is worsened by the decreased ability of the liver of clearing lactates.
  • Central nervous system: increased venous pressure with intracranial hypertension and, subsequently, cerebral hypoperfusion.

The symptoms in an awake patient are aspecifics: dyspnea, diffuse abdominal pain, and generalized malaise. On the other side, signs of ACS are abdominal distension and diffuse pain, progressive oliguria, hypoventilation, tachypnea, acute respiratory failure, hypotension, tachycardia with hypoperfusion, and peripheral edema. 

Diagnosis

The final diagnosis is clinical.

Unfortunately, there are no radiological exams that can identify an ACS. Ultrasound may help to evaluate the volemic status of the patient, but nothing more. What is helpful is the evaluation of the IAP through a urinary catheter, as shown in the figure below. The image shows the special graduate connector with which it is possible to calculate the IAP.

Intra-abdominal pressure should be measured every 12 hours in all patients at risk of developing IAH/ACS and every 4-6 hours once IAH/ACS has been detected or if organ failure uprises.

Remember that this evaluation is not trustable in patients with diffuse pelvic adhesions, pelvic packing/fractures/hematomas, or neurogenic bladder.

Management

Once IAP has increased above its standard value, we need to bring it back within its normal range to avoid the onset of an ACS.

Possible ways to decrease the IAP are: 

  • Reducing the intestinal content (e.g. nasogastric tube, rectal decompression, enemas, prokinetics…);
  • Evaluating the presence of occupying space lesions that may be addressed directly (e.g. percutaneous drainage of intra-abdominal collections);
  • Improving the abdominal wall compliance (e.g sedation, proper analgesia, neuromuscular blockade, avoiding prone position, retrieving compressive elements);
  • Optimizing fluid therapy and resuscitation (i.e. maintaining MAP >60 mmHg without over-fluid resuscitation, fluid restriction, diuretics, hemodialysis/ultrafiltration).

Now, imagine we have done everything of the above on our patient, but he/she still has a high IAP (>20 mmHg) and he/she develops a new organ failure… What can we do?
We need to decompress the abdomen with a laparotomy to “create space” and release the IAH. We won’t be able to close the abdomen during the first operation, so we’ll have to leave it open, fashioning a so-called open abdomen (if you want to read more about the open abdomen).

Here is a useful flow-chart for the management of the ACS:

Now, if we follow the flow-chart, we know how to manage our poor patient:

The IAP is 30 mmHg even after the balanced resuscitation given by the intensivists. So, we have an unstable patient with multiple new organ dysfunctions and, thanks to the (unnecessary) CT scan, we know he’s not bleeding. We need to release the intra-abdominal pressure. 

Therefore, you decide to go to the OR where a laparotomy is carried out. You find a very edematous bowel and almost 1 L of serous fluid. Luckily, the patient, after the release, starts getting better and better (even though slowly… We are not God!!!). The choice now is one, and only one: leave the abdomen open… 

As always, we really hope this post was of some help to you…

See you next time!

Namasté…

References

  1. Gestring M. Abdominal compartment syndrome in adults. UpToDate. Published on March 24, 2021. Accessed on May 27, 2021. Available at [https://www.uptodate.com/contents/abdominal-compartment-syndrome-in-adults/]
  2. Martin N, et al. Management of the open abdomen in adults. UpToDate. Published on April 22, 2021. Accessed on May 27, 2022. Available at [https://www.uptodate.com/contents/management-of-the-open-abdomen-in-adults/]
  3. Kirkpatrick AW, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013;29:1190-206.
  4. S. Navarro. Síndrome Compartimental. Rev Hispanoam Hernia 2016;4:39-41.
  5. Montalvo-Jave E, et al.  Síndrome compartimental abdominal: conceptos actuales y manejo. Revista de Gastroenterología de México 2020;85:443-51.
  6. Sánchez-Mirallesa A, et al. Síndrome compartimental abdominal y síndrome de distrés intestinal agudo. Med Intensiva 2013;37:99-109.
  7. Farkas J. Abdominal compartment syndrome. EMCrit. Published on September 27, 2021. Accessed on May 27, 2022. Available at [https://emcrit.org/ibcc/abdominal-compartment-syndrome/].

How to Cite This Post

Marrano E, Bellio G. Pricking the Big Red Balloon. Surgical Pizza. Published on June 25, 2022. Accessed on September 24, 2022. Available at [https://surgicalpizza.org/emergency-surgery/pricking-the-big-red-balloon/].

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