B H Saggi

Virginia Commonwealth University, Richmond, VA, United States

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Publications (17)37.76 Total impact

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    ABSTRACT: Acute abdominal compartment syndrome (ACS) is a clinical entity that develops from a progressive, acute increase in pressure within the confined space of the abdominal cavity from a multitude of etiologies. This increase in intra-abdominal pressure (IAP) impacts multiple organ systems in a graded fashion due to differential susceptibilities. While the classic renal, pulmonary, and cardiovascular signs are seen with marked elevations in IAP, we now know that the gut is most sensitive to increases in IAP and develops evidence of end-organ damage earlier in the development of ACS. Furthermore, intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and ultimately death. The scenarios of multiple trauma, hemorrhage with massive volume resuscitation, and/or protracted operation are where ACS is most frequently encountered. However, knowledge of ACS is also essential for the management of critically ill pediatric patients and intensive care patients with acute medical illnesses. The role of intra-abdominal hypertension (IAH) in the etiology of necrotizing enterocolitis, central obesity comorbidities, and preeclampsia/eclampsia remains to be fully elucidated. This article reviews the experimental background, organ system pathophysiology, diagnosis, and treatment of ACS with emphasis on the latest concepts in the literature as they apply to critically ill patients.
    Journal of Intensive Care Medicine 06/2008; 14(5):207 - 219.
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    ABSTRACT: This study evaluates the utility of quantitative polymerase chain reaction (QPCR) to determine duration of treatment of transplant patients with human cytomegalovirus (HCMV) disease. Eighteen patients with HCMV disease were prospectively evaluated and followed for recurrence using a QPCR assay. We used plasma samples from which nucleic acid was extracted. Quantification was determined by using an internal standard that contained the same primer sequences as for HCMV. During treatment, weekly QPCR assays were performed. Patients were treated with HCMV immunoglobulin-G for a finite period, but intravenous ganciclovir was continued until less than 100 viral copies (vc) per mL was detectable. After cessation of therapy, patients were followed for 6 months with monthly clinical assessment and QPCR. No patient developed recurrence of HCMV at a mean follow-up of 16 months. This preliminary study suggests that the use of QPCR to assess viral load is useful in deciding the length of HCMV treatment with ganciclovir but requires further randomized validation.
    Transplantation 09/2002; 74(4):573-6. · 3.78 Impact Factor
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    ABSTRACT: To study the effects of an externally applied negative abdominal pressure device designed to lower the effects of intra-abdominal pressure (IAP) on headaches and pulsatile tinnitus in severely obese women with pseudotumor cerebri (PTC). Short-term clinical intervention trial in the Clinical Research Center. Days 1 and 3 were 'control' days; on days 2 and 4-6 patients were in the device from 8:00 am to noon and from 1:00 to 5:00 pm, and on nights 7-11 they were in the device from 10:00 pm to 8:00 am. The last four patients were treated in a device with a counter-traction mechanism. Seven centrally obese women with PTC. Headache and pulsatile tinnitus severity were graded by the patient using visual analog scale (1-10) and averaged for the time that the device was in use or not in use. IAP was estimated from urinary bladder pressure (UBP) before and during device use. The internal jugular vein (IJV) elliptical cross-sectional area was measured with B-mode ultrasonography; the timed average velocity was measured by Doppler. There was a decrease in both headache (6.8+/-0.8 to 4.2+/-0.8, P<0.05) and pulsatile tinnitus (4.2+/-0.5 to 1.8+/-0.5, P<0.02) within 5 min, and in headache (to 2.2+/-0.8, P<0.01) and tinnitus (to 1.7+/-0.5, P<0.01) within 1 h of device activation. UBP decreased (P<0.001) from 19.1+/-3 to 12.5+/-2.8 cmH2O. Headache remained improved throughout time that the device was used. During the second week, five of seven patients slept in the device without difficulty and four awoke without headache. There was a progressive decrease (P<0.01) in headache during the day after sleeping in the device at night as compared with days 1 and 3 when it was not used (6.5+/-0.5, day 1; 4.1+/-0.7, day 3; 3.1+/-0.8, day 8; 2.3+/-0.8, day 10). Headaches returned late in the afternoon in two patients; the device was reactivated and headache again improved. Five patients underwent IJV sonography; the IJV area decreased (129+/-53 to 100+/-44 mm2, P=0.06) without a change in IJV flow (1004+/-802 to 1000+/-589 ml/min) with the device. When activated, the device was pulled into the patient, creating discomfort that was alleviated with the counter-traction mechanism in the last four patients. One patient developed a 5 cm area of blisters that resolved when the device was worn over a hospital gown. Decreasing IAP relieved headaches and pulsatile tinnitus in PTC. When patients slept in the device, they awoke without headache or tinnitus, which remained markedly improved throughout most of the following day. This study supports the hypothesis that PTC in obese women is secondary to an increased IAP.
    International Journal of Obesity 04/2001; 25(4):486-90. · 5.22 Impact Factor
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    ABSTRACT: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). The cause of acute renal failure in AACS is thought to be multifactorial, including increased renal venous pressure, renal parenchymal pressure (RPP), and decreased cardiac output. Previous studies have established the role of renal venous pressure as an important mediator of this renal derangement. In this study, we evaluate the role of renal parenchymal compression on renal function. Two groups of swine (20-26 kg) were studied after left nephrectomy and placement of a renal artery flow probe and ureteral cannula. Two hours were allowed for equilibration, and an inulin infusion was begun to calculate inulin clearance as a measurement of glomerular filtration. In group 1 animals (n = 6), RPP was elevated by 30 mm Hg for 2 hours with renal parenchymal compression. RPP then returned to baseline for 1 hour. In group 2 (n = 6), the RPP was not elevated. The cardiac index, preload, and mean arterial pressure remained stable. Blood samples for plasma renin activity and plasma aldosterone were taken at baseline and at hourly intervals. Elevation of RPP in the experimental group showed no significant decrease in renal blood flow index or glomerular filtration when compared with control animals. There were no significant elevations of plasma aldosterone or plasma renin activity in the experimental animals when compared with control. Elevated renal compression alone did not create the pathophysiologic derangements seen in AACS. However, prior data from this laboratory found that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma aldosterone, and urinary protein leak. These changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS. These data strengthen the proposal that renal vein compression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.
    The Journal of trauma 06/2000; 48(5):874-7. · 2.35 Impact Factor
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    ABSTRACT: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). Although the cause of acute renal failure in AACS may be multifactorial, renal vein compression alone has not been investigated. This study evaluated the effects of elevated renal vein pressure (RVP) on renal function. Two groups of swine (18-22 kg) were studied after left nephrectomy and placement of a renal artery flow probe to measure renal artery blood flow, renal vein catheter, and ureteral cannula. Two hours were allowed for equilibration and an inulin infusion was begun to calculate inulin clearance for measurement of glomerular filtration rate. Group 1 animals (n = 4) had RVP elevated by 30 mm Hg for 2 hours with renal vein constriction. RVP was then returned to baseline for 1 hour. In group 2 (n = 4), the RVP was not elevated. The cardiac index (2.9 +/- 0.5 L/min/m2) and mean arterial pressure (101 +/- 9 mm Hg) remained stable. Plasma renin activity and serum aldosterone were measured every 60 minutes. Elevation of RVP (0-30 mm Hg above baseline) in the experimental group showed a significant decrease in renal artery blood flow index (2.7 to 1.5 mL/min per g) and glomerular filtration rate (26 to 8 mL/min) compared with control. In addition, there was significant elevation of plasma serum aldosterone (14 to 25 microng/dL) and plasma renin activity (2.6 to 9.5 microng/mL per h) as well as urinary protein leak in the experimental animals compared with control. These changes were partially or completely reversible as RVP returned toward baseline. Elevated RVP alone leads to decreased renal artery blood flow and glomerular filtration rate and increased plasma renin activity, serum aldosterone, and urinary protein leak. These changes are consistent with the renal pathophysiology seen in AACS, morbid obesity, and preeclampsia. The changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS.
    The Journal of trauma 12/1999; 47(6):1000-3. · 2.35 Impact Factor
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    ABSTRACT: To determine the ability of an externally applied continuous negative abdominal pressure device (CNAP) to reverse the effects of elevated intra-abdominal pressure on the central nervous and cardiovascular systems. Anesthetized, ventilated swine had catheters placed for measurement of intra-abdominal (IAP), intracranial (ICP), central venous, pulmonary artery, pulmonary artery occlusion, mean arterial, peak inspiratory, inferior vena cava, and femoral vein pressures. After the animals stabilized, baseline measurements were obtained. IAP was increased by incrementally instilling an isosmotic polyethylene glycol solution into the peritoneal cavity until it was 25 mm Hg above baseline. IAP was maintained at 25 mm Hg above baseline for 2 hours. CNAP was then applied for 2 hours. All parameters were remeasured 30 minutes after each increase in IAP, at 2 hours after attaining maximum IAP, and lastly at 2 hours after abdominal decompression. Cardiac index was maintained near baseline by volume expansion. Elevation of IAP to 25 mm Hg above baseline for 2 hours caused increases (p<0.05) in central venous pressure (10.3+/-0.9 to 15.2+/-1.7), inferior vena cava pressure (13.0+/-1.0 to 29.5+/-1.5), femoral vein pressure (13.5+/-0.5 to 33.3+/-1.3), ICP (10.6+/-1.5 to 21.0+/-1.5), and peak inspiratory pressure (18.3+/-0.3 to 34.2+/-1.0). The mean arterial pressure (106.3+/-3.5 to 125.8+/-3.4), pulmonary artery pressure (24.3+/-2.3 to 31.3+/-1.7), and pulmonary artery occlusion pressure rose (12.3+/-0.9 to 17.5+/-3.5), but not significantly. Cardiac index (3.3+/-0.5 to 3.4+/-0.4) remained essentially unchanged. CNAP significantly (p<0.05) decreased IAP (30.7+/-1.3 to 18.2+/-1.3), central venous pressure (15.2+/-1.7 to 12.4+/-2.1), inferior vena cava (29.5+/-1.5 to 19.2+/-1.3), and ICP (21.0+/-1.5 to 16.2+/-1.3). Pulmonary artery occlusion pressure (17.5+/-3.5 to 15.0+/-3.1) and peak inspiratory pressure (34.2+/-1.0 to 29.7+/-1.1) decreased, but not significantly. Acutely elevated IAP causes a significant increase in ICP and impaired cardiovascular and pulmonary function. Abdominal decompression remains the standard of care for abdominal compartment syndrome. However, in patients in whom an increased IAP does not require surgical decompression, the results of this study suggest that externally applied CNAP may be of value.
    The Journal of trauma 06/1999; 46(6):1009-14; discussion 1014-6. · 2.35 Impact Factor
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    ABSTRACT: Elevated intra-abdominal pressure (IAP) increases intracranial pressure (ICP) and reduces cerebral perfusion pressure (CPP). We evaluated a nonsurgical means of reducing IAP to reverse this process. Swine with a baseline ICP of 25 mm Hg produced by an intracranial balloon catheter were studied. In group 1 (n = 5), IAP was increased by 25 mm Hg. Continuous negative abdominal pressure (CNAP) was then applied. Group 2 (n = 4) had neither IAP elevation nor CNAP. Group 3 (n = 4) had CNAP without IAP elevation. Elevation of IAP by 25 mm Hg above baseline led to deleterious changes in ICP (25.8+/-0.8 to 39.0+/-2.8; p < 0.05) and CPP (85.2+/-2.0 to 64.8+/-2.6; p < 0.05). CNAP led to a reduction in IAP (30.2+/-1.2 to 20.4+/-1.3; p < 0.05) and improvements in cerebral perfusion (ICP, 33+/-2.7; CPP, 74.4+/-1.2; both p < 0.05). Group 2 had stable ICP (25.8+/-0.25 to 28.7+/-1.7; p > 0.05) and CPP (80.8+/-1.4 to 80.5+/-1.8; p > 0.05). In group 3, CNAP decreased cardiac index (2.9+/-0.2 to 1.1+/-0.4; p < 0.05), mean arterial pressure (105.2+/-4.0 to 38.2+/-12.0; p < 0.05), and CPP (74.2+/-4.7 to 14.5+/-12.2; p < 0.05). Elevations in IAP led to increased ICP and decreased CPP. CNAP ameliorated these intracranial disturbances. With normal IAP, CNAP impaired cerebral perfusion.
    The Journal of trauma 04/1999; 46(4):646-51. · 2.35 Impact Factor
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    ABSTRACT: The Th-1/Th-2 paradigm proposes clonal expansion of Th-2 lymphocytes as the basis of tolerance towards allografts. Intragraft cytokine expression was evaluated in a highly stringent model of renal transplantation. ACI and Lewis rats were used as donors and recipients, respectively, for heterotopic renal transplantation. Group A (n = 8) received a single dose of rapamycin and cyclosporin 12 h prior to engraftment, followed by 7 d of cyclosporin post-operatively. Isografts (Group B, n = 5) and control allografts (Group C, n = 4) received no immunosuppression. Sacrifice was performed after 120 d. Intragraft expression of IL-10, IL-4, and IFN-gamma was determined using qualitative reverse transcriptase-polymerase chain reaction (RT-PCR). All groups had functionally normal grafts at sacrifice, with 50% histological tolerance among Group A animals. No isografts showed evidence of cellular infiltrate, and all control allografts showed severe rejection. IL-10 was only detected in the tolerant animals (p < 0.001). Similarly, IL-4 was detected predominantly in the tolerant allografts (p < 0.05). IFN-gamma was only isolated in rejected allografts, whether treated or untreated (p < 0.001). We conclude that the expansion of Th-2 cells is associated with tolerance, while the expansion of Th-1 cell is associated with acute cellular rejection.
    Clinical Transplantation 02/1999; 13(1 Pt 2):90-7. · 1.63 Impact Factor
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    ABSTRACT: Intragraft cytokine expression was evaluated in a model of renal transplantation. ACI and Lewis rats were used as donors and recipients, respectively, for heterotopic renal transplantation. Treated allograft rats (n=10) received a preoperative dose of rapamycin and cyclosporine, followed by 7 days of cyclosporine postoperatively. Isograft rats (n=5) and control allograft rats (n=4) received no immunosuppression. Sacrifice was performed after 120 days. Expression of interleukin (IL)-4, IL-10, and interferon-gamma (IFN-gamma) transcripts was determined with semiquantitative reverse transcriptase-polymerase chain reaction. All treated allograft rats had normal function with 50% histologic rejection. All isografts had normal function. IL-4 and IL-10 were in greater density in allografts with normal histology, whereas IFN-gamma was only seen in allografts with cellular rejection. No IL-10 was seen in isografts, but IL-4 was detected in 3/5 isografts. We conclude that the lymphocyte population's elaboration of IL-4 and IL-10 is associated with tolerance, whereas the production of IFN-gamma and absence of IL-4 is associated with histology suggestive of acute cellular rejection.
    Transplantation 02/1999; 67(2):206-10. · 3.78 Impact Factor
  • The Journal of Trauma Injury Infection and Critical Care 01/1999; 47(1).
  • Journal of Intensive Care Medicine - J INTENSIVE CARE MED. 01/1999; 14(5):207-219.
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    ABSTRACT: The ACS is a clinical entity that develops from progressive, acute increases in IAP and affects multiple organ systems in a graded fashion because of differential susceptibilities. The gut is the organ most sensitive to IAH, and it develops evidence of end-organ damage before the development of the classic renal, pulmonary, and cardiovascular signs. Intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and, ultimately, death. Multiple trauma, massive hemorrhage, or protracted operation with massive volume resuscitation are the situations in which the ACS is most frequently encountered. Knowledge of the ACS, however, is also essential for the management of critically ill pediatric patients (especially those with AWD) and in understanding the limitations of laparoscopy. The role of IAH in the pathogenesis of NEC, central obesity co-morbidities, and pre-eclampsia/eclampsia remains to be fully studied.
    The Journal of trauma 10/1998; 45(3):597-609. · 2.35 Impact Factor
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    ABSTRACT: One of the proposed mechanisms of tolerance induction is the Th-1/Th-2 paradigm. The Th-1 cell is proinflammatory, secreting IFN-gamma and IL-2. Conversely, the Th-2 cell is anti-inflammatory, secreting IL-4 and IL-10. In our earlier studies a shift toward Th-2 dominance was required for tolerance induction in this model. ACI and Lewis rats were used as donors and recipients, respectively. Twelve hours prior to engraftment, rapamycin 1.5 mg/kg po and cyclosporin 10 mg/kg sc were given, followed by 5 mg/kg sc postop (days 1-7). Lewis rats were used as isografts. Functional allograft tolerance was induced consistently in 100% of the recipients with 50% of the allografts exhibiting normal histology beyond 120 days. Qualitative RT-PCR was performed on the grafts to determine IFN-gamma expression with beta-actin housekeeping gene as control. IFN-gamma was expressed in all untreated allografts (5/5) and all treated, yet rejecting, allografts (4/4). None of the isografts (0/5) or histologically tolerant allografts (0/4) expressed IFN-gamma. This distribution was statistically significant (P < 0.001, Fischer's exact test). Our findings support a shift from Th-2 to Th-1 predominance as the corollary mechanism responsible for preventing histologic tolerance.
    Journal of Surgical Research 08/1998; 78(2):103-7. · 2.02 Impact Factor
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    ABSTRACT: Chimerism, produced by the two-way migration of cells between graft and host, is a proposed mechanism by which tolerance occurs. The appearance of donor/recipient chimeras in tolerant ACI to Lewis rat heterotopic renal transplants was assessed in peripheral blood leukocytes using flow cytometry after staining with monoclonal antibodies. ACI and Lewis rats were used as donor and recipient, respectively, after Rapamycin and Cyclosporin immunosuppression with or without donor blood or bone marrow transfusion. ACI and Lewis animals were also used for isograft and single-kidney controls. Animals were sacrificed at various time points after initial operation. Flow cytometry was performed on isolated peripheral blood leukocytes at sacrifice. Histologic and functional data were also obtained. The monoclonal antibody panel included RT1(a) (ACI, MHC I) combined with CD2, CD4, CD8, CD16, and CD25 or RT1(a,c) (bone marrow chimeras). RT1(a)+, CD8+ cells were transiently present in the peripheral blood leukocytes of Lewis recipients with the exception of allogeneic bone marrow recipients. No significant number of RT1(a)+, CD16+ ("dendritic" cell-line) chimeras was seen. Veto cells (RT1(a,c)+) were transiently present in the bone marrow recipients, but they did not lead to improved outcome. Furthermore, no correlation was made between histologic tolerance and any of these donor-derived cells. Donor/recipient chimerism, and the veto cell phenomenon are not operational tolerance mechanisms in this stringent model of ACI to Lewis rat renal transplantation.
    Journal of Surgical Research 08/1998; 77(2):179-86. · 2.02 Impact Factor
  • Transplantation 06/1998; 65(12):S45. · 3.78 Impact Factor
  • Transplantation 01/1998; 66(8). · 3.78 Impact Factor
  • The Journal of Trauma: Injury, Infection, and Critical Care. 01/1998; 45:597.