Secondary Intra-abdominal Hypertension Research Articles

Fluid Management, Intra-Abdominal Hypertension and the Abdominal Compartment Syndrome: A Narrative Review.

Background: General pathophysiological mechanisms regarding associations between fluid administration and intra-abdominal hypertension (IAH) are evident, but specific effects of type, amount, and timing of fluids are less clear. Objectives: This review aims to summarize current knowledge on associations between fluid administration and intra-abdominal pressure (IAP) and fluid management in patients at risk of intra-abdominal hypertension and abdominal compartment syndrome (ACS). Methods: We performed a structured literature search from 1950 until May 2021 to identify evidence of associations between fluid management and intra-abdominal pressure not limited to any specific study or patient population. Findings were summarized based on the following information: general concepts of fluid management, physiology of fluid movement in patients with intra-abdominal hypertension, and data on associations between fluid administration and IAH. Results: We identified three randomized controlled trials (RCTs), 38 prospective observational studies, 29 retrospective studies, 18 case reports in adults, two observational studies and 10 case reports in children, and three animal studies that addressed associations between fluid administration and IAH. Associations between fluid resuscitation and IAH were confirmed in most studies. Fluid resuscitation contributes to the development of IAH. However, patients with IAH receive more fluids to manage the effect of IAH on other organ systems, thereby causing a vicious cycle. Timing and approach to de-resuscitation are of utmost importance, but clear indicators to guide this decision-making process are lacking. In selected cases, only surgical decompression of the abdomen can stop deterioration and prevent further morbidity and mortality. Conclusions: Current evidence confirms an association between fluid resuscitation and secondary IAH, but optimal fluid management strategies for patients with IAH remain controversial.

Case Report: Tachycardia, Hypoxemia and Shock in a Severely Burned Pediatric Patient

BackgroundSeverely burned children are at high risk of secondary intraabdominal hypertension and abdominal compartment syndrome (ACS). ACS is a life-threatening condition with high mortality and requires an effective, minimally invasive treatment to improve the prognosis when the condition is refractory to conventional therapy.Case presentationA 4.5-year-old girl was admitted to our hospital 30 h after a severe burn injury. Her symptoms of burn shock were relieved after fluid resuscitation. However, her bloating was aggravated, and ACS developed on Day 5, manifesting as tachycardia, hypoxemia, shock, and oliguria. Invasive mechanical ventilation, vasopressors, and percutaneous catheter drainage were applied in addition to medical treatments (such as gastrointestinal decompression, diuresis, sedation, and neuromuscular blockade). These treatments did not improve the patient's condition until she received continuous renal replacement therapy. Subsequently, her vital signs and laboratory data improved, which were accompanied by decreased intra-abdominal pressure, and she was discharged after nutrition support, antibiotic therapy, and skin grafting.ConclusionACS can occur in severely burned children, leading to rapid deterioration of cardiopulmonary function. Patients who fail to respond to conventional medical management should be considered for continuous renal replacement therapy.

Melatonin prevents secondary intra-abdominal hypertension in rats possibly through inhibition of the p38 MAPK pathway

Exogenous administration of melatonin has been demonstrated to down-regulate inflammatory responses and attenuate organ damage in various models. However, the salutary effect of melatonin against secondary intra-abdominal hypertension (IAH) remains unclear. This study sought to test the influence of melatonin on secondary IAH in a pathophysiological rat model and the underlying mechanisms involved. Before resuscitation, male rats underwent a combination of induced portal hypertension, applying an abdominal restraint device, and hemorrhaging to mean arterial pressure (MAP) of 40mmHg for 2h. After blood reinfusion, the rats were treated with lactated Ringer solution (LR) (30mL/h), melatonin (50mg/kg) +LR, and SB-203580 (10μmol/kg)+LR. LR was continuously infused for 6h. MAP, the inferior vena cava pressure and urine output were monitored. Histopathological examination, immunofluorescence of tight junction proteins, and transmission electron microscopy were administered. Intestinal permeability, myeloperoxidase activity, malondialdehyde, glutathione peroxidase, and levels of TNF-a, IL-2, and IL-6, were assessed. The expression of extracellular signal-regulated kinase, p38, c-Jun NH2-terminal kinase, translocation of nuclear factor kappa B subunit, signal transducers and activators of transcription and tight junction proteins were detected by Western blot. We found that melatonin inhibited the inflammatory responses, decreased expression of p38 MAPK, attenuated intestinal injury, and prevented secondary IAH. Moreover, administration of SB203580 abolished the increase in p38 MAPK and also attenuated intestinal injury. These data indicate that melatonin exerts a protective effect in intestine in secondary IAH primarily by attenuating the inflammatory responses which are in part attributable to p38 MAPK inhibition.

Incidence and prognosis of intra-abdominal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literature.

Burn patients are at high risk for secondary intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) due to capillary leak and large volume fluid resuscitation. Our objective was to examine the incidence the incidence of IAH and ACS and their relation to outcome in mechanically ventilated (MV) burn patients. This observational study included all MV burn patients admitted between April 2007 and December 2009. Various physiological parameters, intra-abdominal pressure (IAP) measurements and severity scoring indices were recorded on admission and/or each day in ICU. Transpulmonary thermodilution parameters were also obtained in 23 patients. The mean and maximum IAP during admission was calculated. The primary endpoint was ICU (burn unit) mortality. Fifty-six patients were included. The average Simplified Acute Physiology Score (SAPS II) and Sequential Organ Failure Assessment (SOFA) scores were 43.4 (± 15.1) and 6.4 (± 3.4), respectively. The average total body surface area (TBSA) affected by burns was 24.9% (± 24.9), with 33 patients suffering inhalational injuries. Forty-four (78.6%) patients developed IAH and 16 (28.6%) suffered ACS. Patients with ACS had higher TBSAs burned (35.8 ± 30 vs. 20.6 ± 21.4%, P = 0.04) and higher cumulative fluid balances after 48 hours (13.6 ± 16L vs. 7.6 ± 4.1 L, P = 0.03). The TBSA burned correlated well with the mean IAP (R = 0.34, P = 0.01). Mortality was notably high (26.8%) and significantly higher in patients with IAH (34.1%, P = 0.014) and ACS (62.5%, P < 0.0001). Most patients received more fluids than calculated by the Parkland Consensus Formula while, interestingly, non-survivors received less. However, when patients with pure inhalation injury were excluded there were no differences. Non-surgical interventions (n = 24) were successful in removing body fluids and were related to a significant decrease in IAP, central venous pressure (CVP) and an improvement in oxygenation and urine output. Non-resolution of IAH was associated with a significantly worse outcome (P < 0.0001). Based on our preliminary results we conclude that IAH and ACS have a relatively high incidence in MV burn patients compared to other groups of critically ill patients. The percentage of TBSA burned correlates with the mean IAP. The combination of high CLI, positive (daily and cumulative) fluid balance, high IAP, high EVLWI and low APP suggest a poor outcome. Non-surgical interventions appear to improve end-organ function. Non-resolution of IAH is related to a worse outcome.

Role of permissive hypotension, hypertonic resuscitation and the global increased permeability syndrome in patients with severe hemorrhage: adjuncts to damage control resuscitation to prevent intra-abdominal hypertension.

Secondary intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are closely related to fluid resuscitation. IAH causes major deterioration of the cardiac function by affecting preload, contractility and afterload. The aim of this review is to discuss the different interactions between IAH, ACS and resuscitation, and to explore a new hypothesis with regard to damage control resuscitation, permissive hypotension and global increased permeability syndrome. Review of the relevant literature via PubMed search. The recognition of the association between the development of ACS and resuscitation urged the need for new approach in traumatic shock management. Over a decade after wide spread application of damage control surgery damage control resuscitation was developed. DCR differs from previous resuscitation approaches by attempting an earlier and more aggressive correction of coagulopathy, as well as metabolic derangements like acidosis and hypothermia, often referred to as the 'deadly triad' or the 'bloody vicious cycle'. Permissive hypotension involves keeping the blood pressure low enough to avoid exacerbating uncontrolled haemorrhage while maintaining perfusion to vital end organs. The potential detrimental mechanisms of early, aggressive crystalloid resuscitation have been described. Limitation of fluid intake by using colloids, hypertonic saline (HTS) or hyperoncotic albumin solutions have been associated with favourable effects. HTS allows not only for rapid restoration of circulating intravascular volume with less administered fluid, but also attenuates post-injury oedema at the microcirculatory level and may improve microvascular perfusion. Capillary leak represents the maladaptive, often excessive, and undesirable loss of fluid and electrolytes with or without protein into the interstitium that generates oedema. The global increased permeability syndrome (GIPS) has been articulated in patients with persistent systemic inflammation failing to curtail transcapillary albumin leakage and resulting in increasingly positive net fluid balances. GIPS may represent a third hit after the initial insult and the ischaemia reperfusion injury. Novel markers like the capillary leak index, extravascular lung water and pulmonary permeability index may help the clinician in guiding appropriate fluid management. Capillary leak is an inflammatory condition with diverse triggers that results from a common pathway that includes ischaemia-reperfusion, toxic oxygen metabolite generation, cell wall and enzyme injury leading to a loss of capillary endothelial barrier function. Fluid overload should be avoided in this setting.

Melanocortin-4 receptor agonists alleviate intestinal dysfunction in secondary intra-abdominal hypertension rat model

BackgroundIntra-abdominal hypertension (IAH) is a potentially life-threatening disease. Melanocortin-4 (MC4) receptor activation exhibits life-saving properties. The aim of the present study was to examine whether treatment with the MC4 receptor agonist RO27-3225 ameliorates intestinal injury in IAH rats. MethodsA total of 72 male Sprague–Dawley rats were randomized into six groups. Group 1 was the sham group. Group 2, the sham + RO group, received RO27-3225 (180 μg/kg, intraperitoneally). IAH was induced in group 3, the IAH group, by blood draw (mean arterial pressure = 30 mm Hg for 90 min) followed by shed blood and/or Ringer solution reinfusion. Intra-abdominal pressure was increased to 20 mm Hg by injecting air into the peritoneal cavity. Group 4, the RO group, was administered RO27-3225 at 5 min after blood draw. Groups 5 and 6 were the chlorisondamine (Chl) and HS024 groups, in which the rats were pretreated with the nicotinic acetylcholine receptor antagonist Chl or selective MC4 receptor antagonist (HS024), respectively, at 2 min before RO27-3225 was administered. ResultsRO27-3225 restored mean arterial pressure, reduced tumor necrosis factor-α, and interleukin-1β messenger RNA expression increased by IAH, alleviated histologic damage, and improved superoxide dismutase activity in the intestine. Compared with the IAH group, the levels of intestinal fatty acid-binding protein, intestinal edema and intestinal permeability were lower in the RO group. Furthermore, the RO27-3225 treatment increased the expression of Rho-associated coiled–coil-containing protein kinase 1 and phosphorylated myosin light chain. Chl and HS024 abrogated the protective effects of RO27-3225. ConclusionsThese data indicate that the MC4 receptor agonist counteracts the intestinal inflammatory response, ameliorating intestinal injury in experimental secondary IAH by MC4 receptor-triggered activation of the cholinergic anti-inflammatory pathway. It may represent a promising strategy for the treatment of IAH in the future.

Fluid therapy and perfusional considerations during resuscitation in critically ill patients with intra-abdominal hypertension.

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are consistently associated with morbidity and mortality among the critically ill or injured. Thus, avoiding or potentially treating these conditions may improve patient outcomes. With the aim of improving the outcomes for patients with IAH/ACS, the World Society of the Abdominal Compartment Syndrome recently updated its clinical practice guidelines. In this article, we review the association between a positive fluid balance and outcomes among patients with IAH/ACS and how optimisation of fluid administration and systemic/regional perfusion may potentially lead to improved outcomes among this patient population.Evidence consistently associates secondary IAH with a positive fluid balance. However, despite increased research in the area of non-surgical management of patients with IAH and ACS, evidence supporting this approach is limited. Some evidence exists to support implementing goal-directed resuscitation protocols and restrictive fluid therapy protocols in shocked and recovering critically ill patients with IAH. Data from animal experiments and clinical trials has shown that the early use of vasopressors and inotropic agents is likely to be safe and may help reduce excessive fluid administration, especially in patients with IAH. Studies using furosemide and/or renal replacement therapy to achieve a negative fluid balance in patients with IAH are encouraging. The type of fluid to be administered in patients with IAH remains far from resolved. There is currently insufficient evidence to recommend the use of abdominal perfusion pressure as a resuscitation endpoint in patients with IAH. However, it is important to recognise that IAH either abolishes or increases threshold values for pulse pressure variation and stroke volume variation to predict fluid responsiveness, while the presence of IAH may also result in a false negative passive leg raising test.Correct fluid therapy and perfusional support during resuscitation form the cornerstone of medical management in patients with abdominal hypertension. Controlled studies determining whether the above medical interventions may improve outcomes among those with IAH/ACS are urgently required.

A new model for the study of secondary intra-abdominal hypertension in rats

BackgroundTo build a new and appropriate model of secondary intra-abdominal hypertension (IAH) in rats. MethodsA total of 32 female Sprague–Dawley rats were randomized into four groups. Group I: the rats were hemorrhaged to a mean arterial pressure (MAP) of 40 mm Hg for 1 h and portal hypertension was induced by partial ligation of the portal vein 1 h later; Group II: after inducing portal hypertension, hemorrhagic shock of MAP of 40 mm Hg was induced and maintained for 1 h; Group III: after inducing portal hypertension, hemorrhagic shock of MAP of 40 mm Hg was induced and maintained for 2 h; Group IV: after inducing portal hypertension, hemorrhagic shock of MAP of 40 mm Hg was induced and maintained for 2 h, and a specially designed abdominal restraint device was used. After these procedures, respectively, the collected blood was reinfused and lactated Ringer solution was continuously infused until the secondary IAH model was established. ResultsNo models were built in Groups I, II, and III. One rat died in Group IV after portal vein ligation, and all the remaining rats successfully developed IAH; the success rate was 87.5%. During the resuscitation period, the average time was 5.26 ± 0.59 h and the average total infusion volume was 665.5 ± 86.04 mL/kg. ConclusionA rat model of secondary IAH was successfully established by resuscitation after a combination of inducing portal hypertension, hemorrhaging to a MAP of 40 mm Hg for 2 h, and using an abdominal restraint device. All these criteria mimic key etiological factors for the development of secondary IAH.

Primary and secondary intra-abdominal hypertension—different impact on ICU outcome

To investigate the differences in incidence, time course and outcome of primary versus secondary intra-abdominal hypertension (IAH), and to evaluate IAH as an independent risk factor of mortality in a presumable risk population of critically ill patients. Prospective observational study. General intensive care unit of a university hospital. A total of 257 mechanically ventilated patients at presumable risk for the development of IAH were studied during their ICU stay and followed up for 90-day survival. Repeated measurements of intra-abdominal pressure (IAP). IAP was measured intermittently, via bladder. IAH (sustained or repeated IAP > or = 12 mmHg) developed in 95 patients (37.0%). Primary IAH was observed in 60 and secondary IAH in 35 patients. Patients with secondary IAH demonstrated a significant increase of mean IAP during the first three days (mean DeltaIAP was 2.2 +/- 4.7 mmHg), whilst IAP decreased (mean DeltaIAP -1.1 +/- 3.7 mmHg) in the patients with primary IAH. The patients with IAH had a significantly higher ICU- (37.9 vs. 19.1%; P = 0.001), 28-day (48.4 vs. 27.8%, P = 0.001), and 90-day mortality (53.7 vs. 35.8%, P = 0.004) compared to the patients without the syndrome. Patients with secondary IAH had a significantly higher ICU mortality than patients with primary IAH (P = 0.032). Development of IAH was identified as an independent risk factor for death (OR 2.52; 95% CI 1.23-5.14). Secondary IAH is less frequent, has a different time course and worse outcome than primary IAH. Development of IAH during ICU period is an independent risk factor for death.

Abdominal Compartment Syndrome

Compartment syndrome is a pathophysiological term, comprising a variety of tissues and organ alterations, due to a higher than normal pressure in an anatomically detached space (compartment). In the human body, areas denoted as compartments include the orbital globe, the sub and epidural space, the abdomen, pleura, pericardium, and others. Compartment syndrome was described initially in limbs. Abdominal compartment syndrome is defined as an intra-abdominal pressure above 20 mmHg with evidence of organ failure. Abdominal compartment syndrome develops when the intra-abdominal pressure rapidly reaches certain pathological values, within several hours (intra-abdominal hypertension is observed), and lasts for 6 or more hours. The key to recognizing abdominal compartment syndrome is the demonstration of elevated intra-abdominal pressure which is performed most often via the urinary bladder, and it is considered to be the "gold standard." Multiorgan failure includes damage to the cardiac, pulmonary, renal, neurological, gastrointestinal, abdominal wall, and ophthalmic systems. The gut is the most sensitive to intra-abdominal hypertension, and it develops evidence of end-organ damage before alterations are observed in other systems. The surgical decompression of the abdomen remains the treatment of choice of abdominal compartment syndrome; this usually improves the organ changes, and is followed by one of the temporary abdominal closure techniques in order to prevent secondary intra-abdominal hypertension.