Effects of Increased Renal Parenchymal Pressure on Renal Function

Doty, James M.; Saggi, Bob H.; Blocher, Charles R.; Fakhry, Itaf; Gehr, Todd W.B.; Sica, Domenic A.; Sugerman, Harvey J.

doi:10.1097/00005373-200005000-00010

Cited by 138 publications

(84 citation statements)

References 14 publications

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“…Our results are in line with the previous literature reporting renal [19][20][21][22] and hepatic [21] dysfunction (Tables 1, 2, Figs 1, 2). Toens et al [23] used a porcine model with IAP ~30 mm Hg for 24 h, induced by CO 2 insufflation, and observed necrosis in the central vein of the liver, as well as tubular and glomerular necrosis.…”

Section: Impact Of Intra-abdominal Hypertension On the Liver Kidneyssupporting

confidence: 93%

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Lima¹,

Silva²,

Capelozzi³

et al. 2017

Anaesthesiol Intensive Ther

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Background: Abdominal compartment syndrome (ACS) sometimes occurs in critically ill patients following damage control surgery. The purpose of the present study was to develop a model of ACS and to evaluate its pathologic impact on liver, kidney, and lung morphology. Methods: Twenty Wistar rats (mass 300-350 g) were randomly divided into four groups: 1) intra-abdominal hypertension (IAH): a laparotomy was performed and the abdomen packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery. After 3 hours of protective mechanical ventilation, the animals were euthanized and the liver, kidney and lungs removed to examine the degree of tissue damage. Results: IAH resulted in the following: oedema and neutrophil infiltration in the kidney; necrosis, congestion, and microsteatosis in the liver; and alveolar collapse, haemorrhage, interstitial oedema, and neutrophil infiltration in the lungs. Furthermore, IAH was associated with greater cell apoptosis in the kidney, liver and lungs compared to sham surgery. HYPO led to oedema and neutrophil infiltration in the kidney. The combination of IAH and HYPO resulted in all the aforementioned changes in lung, kidney and liver tissue, as well as exacerbation of the inflammatory process in the kidney and liver and kidney cell necrosis and apoptosis. Conclusions: Intra-abdominal hypertension by itself is associated with kidney, liver and lung damage; when combined with hypovolemia, it leads to further impairment and organ damage.

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Section: Impact Of Intra-abdominal Hypertension On the Liver Kidneyssupporting

confidence: 93%

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Lima¹,

Silva²,

Capelozzi³

et al. 2017

Anaesthesiol Intensive Ther

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“…[8][9][10] The main suggested mechanism is increased intra-abdominal pressure and compression of the inferior vena cava causing renal congestion and compromised venous return. 11,12 Fluid accumulation also dilutes Scr and delays AKI diagnosis. Macedo et al indicated that 50% of the time AKI diagnosis was missed or delayed in the ICU because of fluid accumulation and suggested the formula used in our study to improve early recognition and severity assessment.…”

Section: Discussionmentioning

confidence: 99%

“…Another limitation of our study is the lack of intra-abdominal pressure measurement. Fluid overload-induced intra-abdominal hypertension plays a significant role in the pathophysiology of renal injury predisposing to a prerenal state 11,12 and further worsening the preexisting injury. Measurement of intra-abdominal pressure usually requires urinary catheter insertion, which is not the standard of care for all ICU admissions.…”

mentioning

confidence: 99%

Acute kidney injury adjusted to volume status in critically ill patients: recognition of delayed diagnosis, restaging, and associated outcomes

Yacoub

Khoury

Douaihy

et al. 2016

IJNRD

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Abstract:Critically ill patients receive a significant amount of fluids leading to a positive fluid balance; this dilutes serum creatinine resulting in an overestimated glomerular filtration rate. The goal of our study is to identify undiagnosed or underestimated acute kidney injury (AKI) in the intensive care unit (ICU). It will also identify the morbidity and mortality associated with an underestimated AKI. We reviewed records of patients admitted to our institution (Staten Island University Hospital) between 2012 and 2013 for more than 2 days. Patients with end stage renal disease were excluded. AKI was defined using the Acute Kidney Injury Network criteria. The following formula was used to identify and restage patients with AKI: adjusted creatinine = serum creatinine × [(hospital admission weight (kg) 0.6 + Σ (daily cumulative fluid balance (L)) / hospital admission weight × 0.6]. The primary outcome identified newly diagnosed AKI and those who were restaged. The secondary outcome identified associated morbidities. Seven-hundred and thirty-three out of 1,982 ICU records reviewed, were used. Two-hundred and fifty-seven (mean age 69.8±14.9) had AKI, out of which 15.9% were restaged using the equation. Comparison of mean by Student's t-test showed no difference between patients who were restaged. Similarly, chi-square revealed no differences between both arms, except mean admission weight (lower in patients who were restaged), fluid balance on days 1, 2, and 3 (higher in the restaged arm), and the presence of congestive heart failure (more prevalent in the restaged arm). Of note, the mean cost of stay was US$150,562.82 vs $197,174.63 for same stage vs restaged, respectively, however, without statistical significance (P=0.74). Applying the adjustment equation showed a modest (15.9%) increase in the AKI staging slightly impacting outcomes (mortality, length, and cost of stay) without statistical significance.

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“…Kardiyak debide düşme ve direkt renal basıya bağlı renal disfonksiyon gelişmektedir. [12] Artmış İAB splanknik ve hepatik dolaşımda hipoperfüzyona yol açmaktadır. İAB artışında hemodinamik belirtilerin ortaya çıkmasından çok önce viseral dolaşımın bozulduğu gösterilmiştir.…”

Section: Discussionunclassified

Can high risk diseases for increasing intraabdominal pressure be treated more efficiently under intravesical pressure measurement?

Divarcı¹,

Ergün²,

Karapınar³

et al. 2013

Ulus Travma Acil Cerrahi Derg

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ÖZET AMAÇ: Karıniçi basınç artışına bağlı ilerleyici organ yetersizliği gelişebilmektedir. Travma, adheziv ileus, karın ön duvarı defektleri ve septik şokta sıvı resüsitasyonu çocukluk çağında karıniçi basınç artışına neden olabilen hastalıklardan bazılarıdır. Bu hastalıkların tedavisi karıniçi (intraabdominal) basınç (İAB) ölçümü kontrolü altında daha güvenle yapılabilir mi? GEREÇ VE YÖNTEM: Aralık 2009 -Ekim 2010 tarihleri arasında ileriye yönelik bir çalışma uygulandı. İAB saptanmasında intravezikal basınç (İVB) ölçümü kullanıldı. Tedavi stratejilerinin belirlenmesinde karıniçi hipertansiyon (İAB >12 mmHg) ve abdominal kompartman sendromu (İAB >15 mmHg + yeni gelişen organ disfonksiyonu) eşik değerler olarak kullanıldı. BULGULAR:Abdominal travma (n=14), karın ön duvarı defektleri (n=8), septik şokta sıvı resüsitasyonu (n=7) ve adheziv ileuslu (n=6) 35 hasta çalışmaya alındı. Travmalı hastaların %14'ünde AKS saptandı ve cerrahi gerekti. İAH/AKS karın ön duvarı defektli hastaların %38'inde defektin kapatılması sonrasında saptandı ve kapatma stratejileri değiştirildi. Septik şokta sıvı resüsitasyonu sırasında hastaların %43'ünde İAH gözlendi ve dekompresif girişimler uygulandı. İAH/AKS saptanan adheziv ileuslu üç hastada (%50) cerrahi girişim kararında basınç yüksekliklerinin katkısı oldu. SONUÇ:İntravezikal basınç ölçümü, izlem ve tedavileri sırasında İAB artışına yol açabilen hastalıkların tedavilerinin yönlendirilmesi ve girişim gerekliliğinin karar verilmesinde önemli katkılar sağlayabilmektedir. Riskli hastalık gruplarında İVB ölçümü, kolay ve güvenle uygulanabilecek yardımcı bir yöntemdir.Anahtar sözcükler: Abdominal kompartman sendromu; çocuk; ileus; intraabdominal basınç; karıniçi hipertansiyon; intravezikal basınç ölçümü; karın ön duvarı defekti; septik şokta sıvı resüsitasyonu; travma. GİRİŞKarıniçi basınç artışı çeşitli mekanizmalarla ilerleyici organ işlev bozukluğu yaratabilen klinik bir durumdur. Artmış karıniçi (intraabdominal) basınç (İAB) majör damarlara basıya bağlı kardiyak debiyi düşürmekte, diyafragmanın yükselmesine neden olarak pulmoner oksijenizasyonu bozmakta ve dolaşım bozukluğu sonucunda renal yetersizliğe neden olabilmektedir (Şekil 1). Sonuçta gelişen çoklu organ yetersizliği tablosu, çocuklarda yüksek oranda mortaliteye yol açabilen abdominal kompartman sendromu (AKS) olarak adlandırılmaktadır (%50-60). [1][2][3] İntravezikal basınç (İVB) ölçümü, İAB'nin saptanmasında klinik kullanımı kolay ve güvenilir bir yöntem olması nedeniyle öncelikle tercih edilmektedir.[4] Çocuklarda çeşitli klinik durumların izlem ve tedavileri sırasında İAB artışı gelişebilmek-tedir. Abdominal travma, karın ön duvarı defektleri, adheziv bağırsak tıkanıklığı ve septik şokta sıvı resüsitasyonu çocukluk çağında karıniçi basınç artışına neden olabilen yüksek riskli hastalıklardan bazılarıdır. İzlem ve tedavileri sırasında gelişebi-len İAB artışı çoklu organ yetersizliğine yol açabilmektedir. Bu hastalıkların tedavisi İVB ölçümü kontrolü altında daha etkin ve güvenilir bir şekilde yapılabilir mi?

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Effects of Increased Renal Parenchymal Pressure on Renal Function

Cited by 138 publications

References 14 publications

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Acute kidney injury adjusted to volume status in critically ill patients: recognition of delayed diagnosis, restaging, and associated outcomes

Can high risk diseases for increasing intraabdominal pressure be treated more efficiently under intravesical pressure measurement?

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