Intra-Abdominal Hypertension

 

A 48 year old male was admitted to the ICU with rapidly evolving multi-organ dysfunction. He was in type I respiratory failure, hypotensive and had stage II acute kidney injury. He had been an inpatient recovering from a laparotomy for major urological surgery 5 days prior to his ICU admission. This was complicated by a major intraoperative haemorrhage.

The patient was commenced on treatment for presumed hospital acquired pneumonia. He was placed on mechanical ventilation and a noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. Over the following 24 hours the patient displayed worsening lung compliance in the context of adequate oxygenation and an atracurium infusion was started. Simultaneously the patient appeared to develop an ileus and he became anuric. Repeated clinical examination revealed an increasingly distended abdomen. A CT of the abdomen and pelvis showed a large left sided retroperitoneal haematoma with evidence of pelvico-ureteric leak on the left and an associated fluid collection. The patient was taken to theatre for urgent re-laparotomy.

At the conclusion of the operation, the surgical team was unable to close the abdomen due to significant bowel oedema. They accepted a laparostomy and returned the patient to ICU with a negative pressure wound dressing in-situ. Post-operatively, there was significant improvement in lung compliance, vasopressor requirement and urine output. Enteral feeding was quickly re-established. The abdomen was closed during the same hospital admission and the patient survived-to-discharge home. At no point was this patient’s intra-abdominal pressure measured.

 

Describe the management of intra-abdominal hypertension.

Christopher Westall

Intra-abdominal hypertension (IAH)- abdominal compartment syndrome (ACS) is a well-recognised cause of morbidity and mortality in critically ill patients, rising to prominence in the 1990s with increased early survival of patients with intra-abdominal pathology requiring emergent laparotomy (principally abdominal aortic aneurysm repair and blunt trauma).1,2 IAH/ ACS may be precipitated by a range of insults local (primary IAH) and distant (secondary IAH) to the abdomen.3 The syndrome encompasses a spectrum of severity and there are a range of treatment options, though with little high quality evidence to support these.

The World Society of the Abdominal Compartment Syndrome (WSACS) consensus guidelines recommend that intra-abdominal pressure (IAP) is measured using the trans-bladder technique in any critically ill patient with an associated risk factor for IAH. The normal value for IAP is <12mmHg. IAH is then categorized by increasing pressure increments from grade I (IAP 12-15mmHg) to grade IV (>25mmHg). Abdominal compartment syndrome is defined as sustained IAP >20mmHg associated with new organ dysfunction.3

The WSACS Consensus proposes a management algorithm for IAH/ ACS that is loosely analogous to commonly encountered algorithms for managing raised intracranial pressure The abdomen is considered a fixed compartment with intra-luminal and extra-luminal volumes that can be manipulated through neutral-negative fluid balance, nasogastric and colonic decompression and percutaneous drainage of ascites/collections. In this instance, however, the compliance of the “box”, the abdominal wall, can also be manipulated by patient position, ventilatory strategy and neuromuscular blockade. Decompressive [laparotomy] therapy is reserved for algorithm failure.

The efficacy of protocolised management of IAH/ACS has never been demonstrated. A single prospective observational study suggested reduction in morbidity and mortality using algorithm based management of IAH; the authors quoted an increase in survival-to-discharge rate from 50 to 72% (p= 0.015) across 6 years with improved rates of same-admission closure. However the study was single centre, recruiting patients only after the laparostomy, with substantial selection and observer bias. Furthermore it was unclear which parts of the protocol were effective.4 While the basic principles underlying the WCASC 2013 algorithm are sensible, it must be acknowledged that proposed therapies such as resuscitation with hypertonic fluids, diuretic-driven diuresis and ultrafiltration through renal replacement therapies have no evidence to support them and have potentially serious implications for the patient.

Given that the efficacy of protocolised management of IAH/ACS is uncertain, is there then any evidence to support the measurement of IAP in every “at risk” patient, especially since the list of risk factors for IAH is so extensive that it is difficult to imagine a critically ill patient that is not at risk. This would not be without significant task-burden to critical care nursing staff, and as with any clinical index in ICU, risks morbidity from misinterpretation. There are only two small studies that have examined whether clinical examination can reliably predict intra-abdominal pressure; both small studies with significant methodological flaws and both conducted between 1996- 2000 when awareness of IAH was comparatively low. Importantly both studies compared examination to IAP measurement at pressures well below 20mmHg, where there is little evidence that specific intervention improves patient outcome, beyond highlighting that that patient is at risk of ACS.5,6

Decompressive laparotomy is recommended for the treatment of all patients with ACS refractory to medical therapy.3 In modern practice it is difficult to accurately assess the performance of this strategy in primary IAH/ACS, such is the absence of clinical equipoise. As many reviews acknowledge, the improvement in patient survival rates associated with primary laparostomy in abdominal trauma patients in the 1990s caused a fundamental paradigm shift from which it is now difficult to ethically justify alternative treatment strategies.1,2 That is to say that many patients with IAH/ ACS will now present to the ICU once decompressive laparostomy has either occurred or is imminently planned.

The benefits of decompressive laparotomy in secondary ACS are certainly less; data exists only for acute severe pancreatitis and sepsis associated with secondary peritonitis. While in both instances it must be acknowledged that laparostomy reduces IAP, like many interventions in a critically ill patient population, this does not translate into mortality benefit.7,8 As commentators note, laparostomy may often be performed because of a conceptual benefit of relook-laparotomy 48 hours later, rather than inability to close the abdomen or specific concerns regarding ACS.2 Indeed, regarding secondary peritonitis, there is good evidence that primary closure with on-demand re-laparotomy is non-inferior to laparostomy and planned re-laparotomy, and is associated with fewer surgeries and lower healthcare costs.9 This strategy is now [weakly] endorsed by the WCACS.3

One point that is widely agreed upon is the management of laparostomy. It appears universally agreed that negative pressure wound therapy (NPWT, i.e. “vac dressings”), with or without a form of dynamic retention system, is superior to previously popular methods such as bioprosthetic mesh and Bogota bag. The largest systematic review on the subject suggests that NPWT is associated with improved rates of primary delayed fascial closure (57.8%, 95% CI 50.8- 64.7) and mortality (22.3%, 95% CI 17.5- 27.5) with lower rates of entero-atmospheric fistulation (7.0%, 95% CI 5.0- 9.3) and abscess formation (4.2%, 95% CI 2.3- 6.9).10 This systematic review heavily influenced the most recent NICE review on the topic leading to endorsement of NPWT in clinical guideline IPG467, “Negative pressure wound therapy for the open abdomen” (2013).


Conclusion

The measurement of IAP in all at-risk critically ill patients is probably unnecessary and burdensome in resource terms. Critical care practitioners should have a low index of suspicion for ACS in their patients; if this develops then decompressive laparotomy is the treatment of choice (unless there is a large extra-luminal collection amenable to urgent drainage), particularly since modern laparostomy management appears to be associated with an increasingly low complication rate, if the abdomen cannot be closed.

The consensus guidelines for IAH/ACS remind us that attention to detail; such as ensuring that enteral nutrition is succeeding, that bowel care is optimal and that fluid balance is tightly controlled, may prevent numerous serious ICU-associated syndromes from ever developing.


References

1. Balogh ZJ, Lumsdaine W, Moore EE, Moore FA. Postinjury abdominal compartment syndrome: from recognition to prevention. Lancet,  2014; 384:1466-75

2. Leppaniemi AK. Laparostomy: why and when? Critical Care 2010; 14: 216. DOI: 10.1186/cc8857

3. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Keulenaer B, Duchesne J, Bjorck M, Leppaniemi A, Ejike JC, Sugrue M, et al.  Intra-abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med, 2013; 39:1190-1206

4. Cheatham ML, Safcsak KRN. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med,  2010; 38:402-407

5. Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg, 2000:43:207-11

6. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, Stewart A, Hillman K, Deane SA. Clinical examination is an inaccurate predictor of intra-abdominal pressure. World J Surg, 2002; 26:1428-31

7. Mentula P, Hienonen P, Kemppainen E, Puolakkainen P, Leppaniemi A. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg, 2010; 145:764-9

8. Robledo FA, Luque-de-Leon E, Suarez R, Sanchez P, de la Fuente M, Vargas A, Mier J. Open versus closed management of the abdomen in the surgical treatment of severe secondary peritonitis: a randomized clinical trial. Surg Infect (Larchmt), 2007; 8:63–72

9. van Ruler O, Mahler CW, Boer KR, Reuland EA, Gooszen HG, Opmeer BC, de Graaf PW, Lamme B, Gerhards MF, Steller EP, van Till JW, et al. Comparison of on-demand vs planned relaparotomy strategy in patients with severe peritonitis: a randomized trial. JAMA, 2007; 298:865-73

10. Quyn AJ, Johnston C, Hall D, Chambers A, Arapova N, Ogston S, Amin AI. The open abdomen and temporary abdominal closure systems- historical evolution and systematic review. Colorectal Dis, 2012; 14: e429–38

 

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Faecal Peritonitis: The Role of Laparostomy

A 68-year-old previously fit woman was admitted with left lower abdominal pain and signs of cardiovascular shock. She had had a 2 day history of crampy left lower abdominal pain and altered bowel habit. Clinically she had a diagnosis of bowel perforation with generalised peritonitis. She was exhibiting signs of shock with a pronounced tachycardia and a reduced systolic blood pressure.

She was started on fluid resuscitation and intravenous antibiotics. After her cardiovascular system stabilised she was taken to the operating theatre where she had a laparotomy. A sigmoid perforation was found with four quadrant faecal contamination. A Hartmann’s procedure was performed. A laparostomy was decided upon at the first instance, and was covered with a VAC dressing.

She was transferred to the intensive care unit (ICU) still intubated and ventilated.

Her condition rapidly worsened on the ICU. She required vasopressor support intra-operatively and her requirements rapidly escalated. She seemed to stabilse over the next 36 hours. Her condition then worsened and she was taken back to theatre for a washout of her peritoneal cavity. A number of collections were found and further soiling of her abdomen was evident. Her condition remained the same for the next 12 hours but then started to show an improvement again. She continued to make a good response to treatment over the next 3-4 days. She had another washout at 4 days. She was extubated on day 5 and invasive monitoring and cardiovascular support was no longer needed.

 

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A 65-year-old woman was admitted with a two-day history of feeling non-specifically unwell, severe upper abdominal pain, anorexia and vomiting. On examination she was tachycardic, hypotensive with epigastric tenderness and guarding. Admission amylase was 1024 mmol/L. A diagnosis of acute pancreatitis was made and she was admitted for conservative management with IV fluids and analgaesia. Her initial Ranson score was 3 placing her at moderate risk of of death. Abdominal ultrasound scanning showed a swollen pancreas with a small amount of free fluid but no gallstones or obstruction to the biliary system. Over the next twelve hours she deteriorated on the ward, developing type 1 respiratory failure for which she was referred to intensive care.

On admission to ITU she was semi-electively intubated and ventilated. A low-dose infusion of noradrenaline required to achieve adequate mean arterial pressure. A CT scan showed inflammatory changes and free fluid around the pancreas with possible early pseudocyst formation but no necrotic areas. Two hours after admission she became pyrexial at 39.5°C with a modest increase in her noradrenaline requirements. Peripheral blood cultures were taken and empirical imipenem started following discussion with microbiology. Subsequent repeated microbiological cultures of blood, ascitic fluid, urine and sputum were negative. A nasojejunal tube was passed to allow enteral feeding.

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An elderly man was admitted after a Hartman’s procedure with primary closure for a perforated sigmoid diverticulum with four quadrant peritonitis. Postoperatively, he remained ventilated and noradrenaline dependent. His intra-abdominal pressures gradually rose from 15 to 24mmHg. Urine output was poor, and he required peak pressures of 28cmH2O to achieve 6ml/kg tidal volumes. Vasopressor requirements gradually increased and a diagnosis of abdominal compartment syndrome was made. Medical management was attempted with fluid resuscitation, increased sedation, aspiration of nasogastric tube and neuromuscular blockade. However this did not improve the intra-abdominal pressures so the patient returned to theatre laparostomy and VAC dressing. On return from theatre, intra-abdominal pressures stabilised between 12 and 15mmHg. Noradrenaline requirements fell and urine output improved. The abdomen was closed on day 5 and he was discharged from ICU on day 10.

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