Methodological background and strategy for the 2012-2013 updated consensus definitions and clinical practice guidelines from the abdominal compartment society.

The Abdominal Compartment Society (www.wsacs.org) previously created highly cited Consensus Definitions/Management Guidelines related to intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). Implicit in this previous work, was a commitment to regularly reassess and update in relation to evolving research. Two years preceding the Fifth World Congress on Abdominal Compartment Syndrome, an International Guidelines committee began preparation. An oversight/steering committee formulated key clinical questions regarding IAH/ /ACS based on polling of the Executive to redundancy, structured according to the Patient, Intervention, Comparator, and Outcome (PICO) format. Scientific consultations were obtained from Methodological GRADE experts and a series of educational teleconferences were conducted to educate scientific review teams from among the wscacs. org membership. Each team conducted systematic or structured reviews to identify relevant studies and prepared evidence summaries and draft Grades of Recommendation Assessment, Development and Evaluation (GRADE) recommendations. The evidence and draft recommendations were presented and debated in person over four days. Updated consensus definitions and management statements were derived using a modified Delphi method. A writingcommittee subsequently compiled the results utilizing frequent Internet discussion and Delphi voting methods to compile a robust online Master Report and a concise peer-reviewed summarizing publication. A dedicated Paediatric Guidelines Subcommittee reviewed all recommendations and either accepted or revised them for appropriateness in children. Of the original 12 IAH/ACS definitions proposed in 2006, three (25%) were accepted unanimously, with four (33%) accepted by > 80%, and four (33%) accepted by > 50%, but required discussion to produce revised definitions. One (8%) was rejected by > 50%. In addition to previous 2006 definitions, the panel also defined the open abdomen, lateralization of the abdominal musculature, polycompartment syndrome, abdominal compliance, and suggested a refined open abdomen classification system. Recommendations were possible regarding intra-abdominal pressure (IAP) measurement, approach to sustained IAH, philosophy of protocolized IAP management and same-hospital-stay fascial closure, use of decompressive laparotomy, and negative pressure wound therapy. Consensus suggestions included use of non-invasive therapies for treating IAH/ACS, considering body position and IAP, damage control resuscitation, prophylactic open abdomen usage, and prudence in early biological mesh usage. No recommendations were made for the use of diuretics, albumin, renal replacement therapies, and utilizing abdominal perfusion pressure as a resuscitation-endpoint. Collaborating Methodological Guideline Development and Clinical Experts produced Consensus Definitions/Clinical Management statements encompassing the most contemporary evidence. Data summaries now exist for clinically relevant IAH/ACS questions, which will facilitate future scientific reanalysis.

Intra-abdominal hypertension and abdominal compartment syndrome in burns, obesity, pregnancy, and general medicine.

Intra-abdominal hypertension (IAH) is an important contributor to early organ dysfunction in trauma and sepsis. However, relatively little is known about the impact of intra-abdominal pressure (IAP) in general internal medicine, pregnant patients, and those with obesity or burns. The aim of this paper is to review the pathophysiologic implications and treatment options for IAH in these specific situations. A MEDLINE and PubMed search was performed and the resulting body-of-evidence included in the current review on the basis of relevance and scientific merit. There is increasing awareness of the role of IAH in different clinical situations. Specifically, IAH will develop in most (if not all) severely burned patients, and may contribute to early mortality. One should avoid over-resuscitation of these patients with large volumes of fluids, especially crystalloids. Acute elevations in IAP have similar effects in obese patients compared to non-obese patients, but the threshold IAP associated with organ dysfunction may be higher. Chronic elevations in IAP may, in part, be responsible for the pathogenesis of obesity-related co-morbid conditions such as hypertension, pseudotumor cerebri, pulmonary dysfunction, gastroesophageal reflux disease, and abdominal wall hernias. At the bedside, measuring IAP and considering IAH in all critical maternal conditions is essential, especially in preeclampsia/eclampsia where some have hypothesized that IAH may have an additional role. IAH in pregnancy must take into account the precautions for aorto-caval compression and has been associated with ovarian hyperstimulation syndrome. Recently, IAP has been associated with the cardiorenal dilemma and hepatorenal syndrome, and this has led to the recognition of the polycompartment syndrome. In conclusion, IAH and ACS have been associated with several patient populations beyond the classical ICU, surgical, and trauma patients. In all at risk conditions the focus should be on the early recognition of IAH and prevention of ACS. Patients at risk for IAH should be identified early through measurements of IAP. Appropriate actions should be taken when IAP increases above 15 mm Hg, especially if pressures reach above 20 mm Hg with new onset organ failure. Although non-operative measures come first, surgical decompression must not be delayed if these fail. Percutaneous drainage of ascites is a simple and potentially effective tool to reduce IAP if organ dysfunction develops, especially in burn patients. Escharotomy may also dramatically reduce IAP in the case of abdominal burns.

Intra-abdominal hypertension and abdominal compartment syndrome in pancreatitis, paediatrics, and trauma.

Intra-abdominal hypertension (IAH) is an important contributor to early organ dysfunction among patients with trauma and sepsis. However, the impact of increased intra-abdominal pressure (IAP) among pediatric, pregnant, non-septic medical patients, and those with severe acute pancreatitis (SAP), obesity, and burns has been studied less extensively. The aim of this review is to outline the pathophysiologic implications and treatment options for IAH and abdominal compartment syndrome (ACS) for the above patient populations. We searched MEDLINE and PubMed to identify relevant studies. There is an increasing awareness of IAH in general medicine. The incidence of IAH and, to a lesser extent, ACS is high among patients with SAP. IAH should always be suspected and IAP measured routinely. In children, normal IAP in mechanically ventilated patients is approximately 7 ± 3 mm Hg. As an IAP of 10-15 mm Hg has been associated with organ damage in children, an IAP greater than 10 mm Hg should be considered IAH in these patients. Moreover, as ACS may occur in children at an IAP lower than 20 mm Hg, any elevation in IAP higher than 10 mm Hg associated with new organ dysfunction should be considered ACS in children until proven otherwise. Monitor IAP trends and be aware that specific interventions may need to be instituted at lower IAP than the current ACS definitions accommodate. Finally, IAH and ACS can occur both in abdominal trauma and extra-abdominal trauma patients. Early mechanical hemorrhage control and the avoidance of excessive fluid resuscitation are key elements in preventing IAH in trauma patients. IAH and ACS have been associated with many conditions beyond the general ICU patient. In adults and in children, the focus should be on the early recognition of IAH and the prevention of ACS. Patients at risk for IAH should be identified early during their treatment (with a low threshold to initiate IAP monitoring). Appropriate actions should be taken when IAP increases above 20 mm Hg, especially in patients developing difficulty with ventilation. Although on-operative measures should be instituted first, one should not hesitate to resort to surgical decompression if they fail.

A user's guide to intra-abdominal pressure measurement.

The intra-abdominal pressure (IAP) measurement is a key to diagnosing and managing critically ill medical and surgical patients. There are an increasing number of techniques that allow us to measure the IAP at the bedside. This paper reviews these techniques. IAP should be measured at end-expiration, with the patient in the supine position and ensuring that there is no abdominal muscle activity. The intravesicular IAP measurement is convenient and considered the gold standard. The level where the mid-axillary line crosses the iliac crest is the recommended zero reference for the transvesicular IAP measurement; moreover, marking this level on the patient increases reproducibility. Protocols for IAP measurement should be developed for each ICU based on the locally available tools and equipment. IAP measurement techniques are safe, reproducible and accurate and do not increase the risk of urinary tract infection. Continuous IAP measurement may offer benefits in specific situations in the future. In conclusion, the IAP measurement is a reliable and essential adjunct to the management of patients at risk of intra-abdominal hypertension.

What every ICU clinician needs to know about the cardiovascular effects caused by abdominal hypertension.

The effects of increased intra-abdominal pressure (IAP) on cardiovascular function are well recognized and include a combined negative effect on preload, afterload and contractility. The aim of this review is to summarize the current knowledge on this topic. The presence of intra-abdominal hypertension (IAH) erroneously increases barometric filling pressures like central venous (CVP) and pulmonary artery occlusion pressure (PAOP) (since these are zeroed against atmospheric pressure). Transmural filling pressures (calculated by subtracting the pleural pressure from the end-expiratory CVP value) may better reflect the true preload status but are difficult to obtain at the bedside. Alternatively, since pleural pressures are seldom measured, transmural CVP can also be estimated by subtracting half of the IAP from the end-expiratory CVP value, since abdominothoracic transmission is on average 50%. Volumetric preload indicators, such as global and right ventricular end-diastolic volumes or the left ventricular end-diastolic area, also correlate better with true preload. When using functional hemodynamic monitoring parameters like stroke volume variation (SVV) or pulse pressure variation (PPV) one must bear in mind that increased IAP will increase these values (via a concomitant increase in intrathoracic pressure). The passive leg raising test may be a false negative in IAH. Calculation of the abdominal perfusion pressure (as mean arterial pressure minus IAP) has been shown to be a better resuscitation endpoint than IAP alone. Finally, it is re-assuring that transpulmonary thermodilution techniques have been validated in the setting of IAH and abdominal compartment syndrome. In conclusion, the clinician must be aware of the different effects of IAH on cardiovascular function in order to assess the volume status accurately and to optimize hemodynamic performance.

Awareness and knowledge of intra-abdominal hypertension and abdominal compartment syndrome: results of an international survey.

BACKGROUND: Surveys have demonstrated a lack of physician awareness of intra-abdominal hypertension and abdominal compartment syndrome (IAH/ACS) and wide variations in management of these conditions, with many intensive care units (ICUs) reporting that they do not measure intra-abdominal pressure (IAP). We sought to determine the association between publication of the 2006/2007 World Society of the Abdominal Compartment Syndrome (WSACS) Consensus Definitions and Guidelines and IAH/ACS clinical awareness and management. METHODS: The WSACS Executive Committee created an interactive online survey with 53 questions, accessible from November 2006 until December 2008. The survey was endorsed by the WSACS, the European Society of Intensive Care Medicine (ESICM) and the Society of Critical Care Medicine (SCCM). A link to the survey was emailed to all members of the supporting societies. Participants of the 3rd World Congress on Abdominal Compartment Syndrome meeting (March 2007, Antwerp, Belgium) were also asked to complete the questionnaire. No reminders were sent. Based on 13 knowledge questions an overall score was calculated (expressed as percentage). RESULTS: A total of 2244 of the approximately 10,000 clinicians sent the survey responded (response rate, 22.4%). Most of the 2244 respondents (79.2%) completing the survey were physicians or physicians in training and the majority were residing in North America (53.0%). The majority of responders (85%) were familiar with IAP/IAH/ACS, but only 28% were aware of the WSACS consensus definitions for IAH/ACS. Three quarters of respondents considered the cut-off for IAH to be at least 15 mm Hg, and nearly two thirds believed the cut-off for ACS was higher than the currently suggested consensus definition (20 mm Hg). In 67.8% of respondents, organ dysfunction was only considered a problem with IAP of 20 mm Hg or higher. IAP was measured most frequently via the bladder (91.9%), but the majority reported that they instilled volumes well above the current guidelines. Surgical decompression was frequently used to treat IAH/ACS, whereas medical management was only attempted by about half of the respondents. Decisions to decompress the abdomen were predominantly based on the severity of IAP elevation and presence of organ dysfunction (74.4%). Overall knowledge scores were low (43 ± 15%), respondents that were aware of the WSACS had a better score compared to those who were not (49.6% vs. 38.6%, P < 0.001). CONCLUSIONS: This survey showed that although most responding clinicians claim to be familiar with IAH and ACS, knowledge of published consensus definitions, measurement techniques, and clinical management are inadequate.

The polycompartment syndrome: a concise state-of-the-art review.

A compartment syndrome is defined as an increase in the compartmental pressure to such an extent that the viability of the tissues and organs within the compartment are threatened. The term describes a syndrome and not a disease, and as such there are many diseases and underlying pathophysiological processes that may lead to such a scenario. The aim of this review is to give a state-of-the-art overview on the current knowledge on different compartment syndromes and how they may interact. Suggested definitions are included. There are four major compartments in the human body: the head, chest, abdomen, and the extremities. Initially, the term multicompartment syndrome was suggested when more than one compartment was affected. But this led to confusion as the term multi- or multiple compartment syndromes is mostly used in relation to multiple limb trauma leading to compartment syndrome requiring fasciotomy. Only recently was the term 'polycompartment syndrome' coined to describe a condition where two or more anatomical compartments have elevated pressures. When more than one compartment is affected, an exponential detrimental effect on end-organ function to both immediate and distant organs can occur. Within each compartment, the disease leading towards a compartment syndrome can be primary or secondary. The compliance of each compartment is the key to determining the transmission of a given compartmental pressure from one compartment to another. The intra-abdominal pressure helps to explain the severe pathophysiological condition occurring in patients with cardiorenal, hepatopulmonary and hepatorenal syndromes. Initial treatment of a compartment syndrome should be focused on the primary compartment and is based on three principles: lowering of compartmental pressure, supporting organ perfusion, and optimisation and prevention of specific adverse events. Clinicians need to be aware of the existence of the polycompartment syndrome and the interactions of increased compartmental pressures between compartments.

Matching positive end-expiratory pressure to intra-abdominal pressure improves oxygenation in a porcine sick lung model of intra-abdominal hypertension.

INTRODUCTION: Intra-abdominal hypertension (IAH) causes atelectasis, reduces lung volumes and increases respiratory system elastance. Positive end-expiratory pressure (PEEP) in the setting of IAH and healthy lungs improves lung volumes but not oxygenation. However, critically ill patients with IAH often suffer from acute lung injury (ALI). This study, therefore, examined the respiratory and cardiac effects of positive end-expiratory pressure in an animal model of IAH, with sick lungs. METHODS: Nine pigs were anesthetized and ventilated (48 +/- 6 kg). Lung injury was induced with oleic acid. Three levels of intra-abdominal pressure (baseline, 18, and 22 mmHg) were randomly generated. At each level of intra-abdominal pressure, three levels of PEEP were randomly applied: baseline (5 cmH2O), moderate (0.5 × intra-abdominal pressure), and high (1.0 × intra-abdominal pressure). We measured end-expiratory lung volumes, arterial oxygen levels, respiratory mechanics, and cardiac output 10 minutes after each new IAP and PEEP setting. RESULTS: At baseline PEEP, IAH (22 mmHg) decreased oxygen levels (-55%, P <0.001) and end-expiratory lung volumes (-45%, P = 0.007). At IAP of 22 mmHg, moderate and high PEEP increased oxygen levels (+60%, P = 0.04 and +162%, P <0.001) and end-expiratory lung volume (+44%, P = 0.02 and +279%, P <0.001) and high PEEP reduced cardiac output (-30%, P = 0.04). Shunt and dead-space fraction inversely correlated with oxygen levels and end-expiratory lung volumes. In the presence of IAH, lung, chest wall and respiratory system elastance increased. Subsequently, PEEP decreased respiratory system elastance by decreasing chest wall elastance. CONCLUSIONS: In a porcine sick lung model of IAH, PEEP matched to intra-abdominal pressure led to increased lung volumes and oxygenation and decreased chest wall elastance shunt and dead-space fraction. High PEEP decreased cardiac output. The study shows that lung injury influences the effects of IAH and PEEP on oxygenation and respiratory mechanics. Our findings support the application of PEEP in the setting of acute lung injury and IAH.

Comparing intra-abdominal pressures in different body positions via a urinary catheter and nasogastric tube: a pilot study.

OBJECTIVES: Intra-abdominal pressure (IAP) is most commonly measured via the bladder with the patient in the supine position. In the ICU, patients are nursed with the head of the bed elevated at 30° (HOB30) to reduce the risk of ventilator-associated pneumonia. This study investigated whether gastric pressure at HOB30 can be used as a surrogate measure of IAP via the bladder in the supine position. METHODS: A prospective observational study was conducted in a single-centre intensive care unit. A total of 20 patients were included. IAP was recorded simultaneously via the bladder catheter (bladder pressure, IBP) and via nasogastric tube (gastric pressures, IGP) in the supine and HOB30 position. Each patient had three sets of IAP measurements performed at least 4 h apart. RESULTS: In the supine position, mean IBP was 12.3 ± 4.5 mmHg compared to IGP of 11.8 ± 4.7 mmHg. The bias between the two groups was 0.5 and precision of 3.7 (LA, -6.8 to 7.5 mmHg). At 30 degrees, mean IBP was 15.8 ± 4.9 mmHg compared to IGP of 13.1 ± 6.1 mmHg. The bias between both groups was 2.7 with a precision of 5.5 (LA, -8.0 to 13.5). Comparing IBP in the supine position with IGP at 30° showed a bias of -0.8 and precision of 5.6 (LA, -10.1 to 11.6 mmHg). CONCLUSION: IAP measured via a nasogastric tube was less influenced by changing the body position from supine to HOB30 than was bladder pressure.

Matching positive end-expiratory pressure to intra-abdominal pressure prevents end-expiratory lung volume decline in a pig model of intra-abdominal hypertension.

OBJECTIVE: Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. In a previous experimental study, positive end-expiratory pressures of up to 15 cm H2O did not prevent end-expiratory lung volume decline caused by intra-abdominal hypertension. Therefore, we examined the effect of matching positive end-expiratory pressure to the intra-abdominal pressure on cardio-respiratory parameters. DESIGN: Experimental pig model of intra-abdominal hypertension. SETTING: Large animal facility, University of Western Australia. SUBJECTS: Nine anesthetized, nonparalyzed, and ventilated pigs (48 ± 7 kg). INTERVENTIONS: Four levels of intra-abdominal pressure (baseline, 12, 18, and 22 mm Hg) were generated in a randomized order by inflating an intra-abdominal balloon. At each level of intra-abdominal pressure, three levels of positive end-expiratory pressure were randomly applied with varying degrees of matching the corresponding intra-abdominal pressure: baseline positive end-expiratory pressure (= 5 cm H2O), moderate positive end-expiratory pressure (= half intra-abdominal pressure in cm H2O + 5 cm H2O), and high positive end-expiratory pressure (= intra-abdominal pressure in cm H2O). MEASUREMENTS: We measured end-expiratory lung volume, arterial oxygen levels, respiratory mechanics, and cardiac output 5 mins after each new intra-abdominal pressure and positive end-expiratory pressure setting. MAIN RESULTS: Intra-abdominal hypertension decreased end-expiratory lung volume and PaO2 (-49% [p < .001] and -8% [p < .05], respectively, at 22 mm Hg intra-abdominal pressure compared with baseline intra-abdominal pressure) but did not change cardiac output (p = .5). At each level of intra-abdominal pressure, moderate positive end-expiratory pressure increased end-expiratory lung volume (+119% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) while minimally decreasing cardiac output (-8%, p < .05). High positive end-expiratory pressure further increased end-expiratory lung volume (+233% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) but led to a greater decrease in cardiac output (-26%, p < .05). Neither moderate nor high positive end-expiratory pressure improved PaO2 (p = .7). Intra-abdominal hypertension decreased end-expiratory transpulmonary pressure but did not alter end-inspiratory transpulmonary pressure. Intra-abdominal hypertension decreased total respiratory compliance through a decrease in chest wall compliance. Positive end-expiratory pressure decreased the respiratory compliance by reducing lung compliance. CONCLUSIONS: In a pig model of intra-abdominal hypertension, positive end-expiratory pressure matched to intra-abdominal pressure led to a preservation of end-expiratory lung volume, but did not improve arterial oxygen tension and caused a reduction in cardiac output. Therefore, we do not recommend routine application of positive end-expiratory pressure matched to intra-abdominal pressure to prevent intra-abdominal pressure-induced end-expiratory lung volume decline in healthy lungs.

Intra-abdominal measurement techniques: is there anything new?

Intra-abdominal pressure (IAP) measurements are essential to the diagnosis and management of intra-abdominal hypertension (IAH) and abdominal compartment syndrome. A variety of IAP measurement techniques have been described. The intravesicular or "bladder" technique remains the gold standard. This commentary reviews each of the different techniques for IAP measurement and discusses their clinical application. It also explores how IAP is affected by changes in body position, body mass index, and positive end-expiratory pressure (PEEP). IAP should be measured every 4 to 6 hours in patients with risk factors for IAH. Putting patients in the semirecumbent position changes the IAP measurement significantly. The role of prone positioning in unstable patients with IAH remains unclear. PEEP has a small effect on IAP.

Nonoperative management of intra-abdominal hypertension and abdominal compartment syndrome: evolving concepts.

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are associated with significant morbidity and mortality. Nonoperative medical management strategies play an important role in the current treatment of IAH and ACS. There are five medical treatment options to be considered to reduce elevated intra-abdominal pressure (IAP): 1) improvement of abdominal wall compliance; 2) evacuation of intraluminal contents; 3) evacuation of abdominal fluid collections; 4) optimization of systemic and regional perfusion; and 5) correction of positive fluid balance. Nonsurgical management is an important treatment option in critically ill patients with raised IAP.

Does femoral venous pressure measurement correlate well with intrabladder pressure measurement? A multicenter observational trial.

PURPOSE: To investigate if femoral venous pressure (FVP) measurement can be used as a surrogate measure for intra-abdominal pressure (IAP) via the bladder. METHODS: This was a prospective, multicenter observational study. IAP and FVP were simultaneously measured in 149 patients. The effect of BMI on IAP was investigated. RESULTS: The incidences of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) were 58 and 7% respectively. The mean APACHE II score was 22 ± 10, SAPS 2 score 42 ± 20, and SOFA score 9 ± 4. The mean IAP was 11.2 ± 4.5 mmHg versus 12.7 ± 4.7 mmHg for FVP. The bias and precision for all measurements were -1.5 and 3.6 mmHg respectively with the lower and upper limits of agreement being -8.6 and 5.7. When IAP was above 20 mmHg, the bias between IAP and FVP was 0.7 with a precision of 2.0 mmHg (lower and upper limits of agreement -3 and 4.6 respectively). Excluding those with ACS, according to the receiver operating curve analysis FVP = 11.5 mmHg predicted IAH with a sensitivity and specificity of 84.8 and 67.0% (AUC of 0.83 (95% CI 0.81-0.86) with P < 0.001). FVP = 14.5 mmHg predicted IAP above 20 mmHg with a sensitivity of 91.3% and specificity of 68.1% (AUC 0.85 (95% CI 0.79-0.91), P < 0.001). Finally, at study entry, the mean IAP in patients with a BMI less then 30 kg/m(2) was 10.6 ± 4.0 mmHg versus 13.8 ± 3.8 mmHg in patients with a BMI ≥ 30 kg/m(2) (P < 0.001). CONCLUSIONS: FVP cannot be used as a surrogate measure of IAP unless IAP is above 20 mmHg.

The role of femoral venous pressure and femoral venous oxygen saturation in the setting of intra-abdominal hypertension: a pig model.

Femoral venous access is frequently used in critically ill patients. Because raised intra-abdominal pressure (IAP) is also frequently found in this group of patients, we examined the impact of IAP and positive end-expiratory pressure (PEEP) on femoral venous pressure (FVP) and femoral venous oxygen saturation (Sfvo2) in an animal model. Thirteen adult pigs received standardized anesthesia and ventilation. Randomized levels of IAP (3 [baseline], 18, and 26 mmHg) were applied, with levels of PEEP (5, 8, 12, and 15 cmH2O) applied randomly at each IAP level. We measured bladder pressure (IAP), superior vena cava pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, FVP, mixed venous oxygen saturation (Svo2), and Sfvo2. We found that FVP correlated well with IAP (FVP = 4.1 + [0.12 × PEEP] + [1.00 × IAP]; R = 0.89, P < 0.001) with a moderate bias and precision of 5.0 and 3.8 mmHg, respectively. Because the level of agreement did not meet the recommendations of the World Society of Abdominal Compartment Syndrome, FVP cannot currently be recommended to measure IAP, and further clinical trials are warranted. However, a raised FVP should prompt the measurement of the bladder pressure. Femoral venous oxygen saturation did correlate neither with Svo2 nor with abdominal perfusion pressure. Therefore, Sfvo2 is of no clinical use in the setting of raised IAP.

Burkholderia pseudomallei sepsis presenting with pericardial effusion and tamponade.

Severe septicaemia secondary to melioidosis carries a high mortality. Although melioidosis can involve most tissues and organs, pericardial involvement is rare. We report a 40-yearold woman with melioidosis with pericardial involvement but no contiguous pulmonary involvement. She developed acute pericardial tamponade but was successfully treated with surgery and medical therapy. This is the first case in Australia or New Zealand of melioid sepsis presenting with pericarditis and subsequent cardiac tamponade. We review the literature on cardiac involvement in melioidosis.