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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ICP Monitoring and Acute Liver Failure

ICP Monitoring and Acute Liver Failure

A 28-year-old lady presented to the medical team jaundiced with cramping upper abdominal pain and multiple episodes of vomiting over the previous day. She admitted ingesting Paracetamol 8 grams 3 days previously (staggered throughout the day) ostensibly to treat a frontal headache. She had been commenced on Citalopram 1 week previously for depression but denied taking any intentional overdose. On examination, she was slightly drowsy but GCS 15. HR 109, BP 136/92. Sats 98%on air. Her chest was clear, she was warm peripherally but jaundiced with some epigastric and RUQ tenderness on palpation. Her urine output was 10-20ml/hr.

Full Blood Count revealed Hb 152, WCC 24.7, Plats 301. She was in acute liver failure with Bil 189, AST 22970, ALT 13040, ALP 426 and coagulopathic with PT 82, APTT 72, Fib 0.7 Urea 5.7, Cr 193. Paracetamol and Salicylate were not detected. She was not acidotic with H+ 35, OCI2 3.7, pO2 17, Bic 20, BE –3. Lactate 7.1.

She was commenced on N-acetylcysteine and transferred to Critical Care. She was reviewed by the Hepatobiliary surgical team and placed on the super-urgent list for liver transplant. 

On Day 2, she became encephalopathic with GCS E3M5V5 and she was intubated and ventilated.Her PT had increased to 168 (INR >15) and she became anuric. She commenced FFP and Cryoprecipitate transfusions that improved her PT to 17, APTT 34 and Fibrinogen 1.5. An Intracranial Pressure (ICP) monitor was inserted and an opening pressure of 19mmHg was found. 2 hours post-insertion, it was noticed that her right pupil had increased in size from 2mm to 4mm and was poorly reactive. ICP remained at 16 and pCO2 4.1.

A brain CT showed a large haematoma in the right frontal region around the ICP bolt (which was not in the brain parenchyma but sitting in the skull) and mass effect with 5mm midline shift. There was also some lack of grey-white matter differentiation and sulcal effacement in keeping with diffuse oedema and mass effect.

INR was 1.7 and so further FFP was given. She was discussed with the neurosurgical registrar (in a separate hospital) who advised they would not drain at present but he would discuss with his Consultant and call back. 

Soon after, her right pupil increased to 8mm and the left to 7mm. Repeat CT brain showed slightly increased right frontal haematoma with 6mm midline shift and global oedematous cortical changes but no herniation. The ICP readings were thought to be inaccurate due to proximal placement and she was medically treated for raised ICP with hypertonic saline, mannitol and then therapeutic hypothermia. Despite this treatment, her pupils were fixed and dilated and so a thiopentone infusion was commenced.

The neurosurgeons advised that they would insert a further ICP monitor when INR <1.3 and so further FFP was given. An ICP bolt was inserted and the opening pressure was >120.

Discussions between the ICU, hepatobiliary and neurosurgical teams confirmed that she had a non-survivable injury and so this was discussed with her family. She was rewarmed, paralysis and then sedation were discontinued, brain stem death testing took place and she was extubated in the presence of her family. She died on Day 3 and was referred to the Coroner for further investigation.

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Management of Refractory Intracranial Hypertension

A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.

Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.

There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.

On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.

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Medical Management of Abdominal Compartment Syndrome

Medical Management of Abdominal Compartment Syndrome

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.

What non-surgical strategies can be used to reduce intra-abdominal pressure?

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Decompressive Laparotomy in Abdominal Compartment Syndrome

Decompressive Laparotomy in Abdominal Compartment Syndrome

A 55 yr old man developed severe necrotizing pancreatitis with multiorgan failure. One week into his illness he had developed multiple intra-abdominal collections and had high intra-abdominal pressures. Initial conservative management failed, percutaneous drainage of his collections failed to reduce the abdominal pressures, and he underwent decompressive laparotomy.

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Intraabdominal Hypertension & Abdominal Compartment Syndrome

Intraabdominal Hypertension & Abdominal Compartment Syndrome

A 35 year old was admitted following a simultaneous kidney pancreas transplant. The procedure had been complicated and she had received a large volume transfusion and crystalloid infusion.Her initial intraabdominal pressures were elevated at 22cmH2O on admission to the intensive care. It continued to escalate over the next 48 hours peaking at 29. She was managed with sedation, NG tube and abdominal perfusion pressures kept above 60mmHg. The tranplanted pancreas remained functional, but the renal transplant showed delayed graft function. On day 4 there was a reduction in her abdominal pressure and her urine output correspondingly increased.

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ICP Monitoring in Non-Traumatic Intracranial Haemorrhage

ICP Monitoring in Non-Traumatic Intracranial Haemorrhage

A middle aged man had a sudden collapse with no precipitating features. His GCS on presentation was 3, with unequal but reactive pupils and CT brain showed a large subarachnoid bleed with midline shift. Neurosurgical opinion was to observe for clinical improvement, after which an intervention might be indicated. He was sedated on ICU and his MAP maintained above 80mmHg with noradrenaline. Nimodipine was commenced and mannitol was administered. After 24 hours he had a sedation hold and he began to localise and open eyes spontaneously. He was transferred to the neurosurgical unit.

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