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Highlights • Intussusception is a rare disease in the adult population and difficult to identify and treat. • Mainstream treatment is for surgical resection however not always warranted in patients. • Present a unique case of highly active antiretroviral therapy (HAART) causing intussusception. • HAART can cause mitochondrial toxicity which produces lactic acidosis and can present as an acute surgical abdomen., Introduction Intussusception is a rare disease in adults and poses a challenge to identify and manage. In adults, surgical resection is the preferred treatment since half are due to malignancy. This case reveals an association between highly active antiretroviral therapy (HAART) and intussusception. Presentation of case A 44 year-old female with history of HIV on highly active antiretroviral therapy (HAART) presented with 3 month history of epigastric pain, nausea, emesis, weight loss, and lactic acidosis. CT of abdomen showed two small bowel intussusceptions and pericolic fat infiltration. A diagnosis of mitochondrial toxicity secondary to HAART medication was made. HAART medication was discontinued with resolution of symptoms. Further work-up to exclude a mechanical cause for her symptoms including colonoscopy, small bowel follow through, esophagogastroduodenoscopy, and repeat CT were performed. All established an absence of malignancy and intussusception. Discussion Mitochondrial toxicity (MT) is a well-known complication of HAART. A hallmark of MT is lactic acidosis which when untreated can be fatal. Although MT is known to cause gastrointestinal symptoms, intussusception has not been previously reported. In our patient with MT, prolonged usage of HAART medication resulted in severe gastrointestinal symptoms and intussusception mimicking a surgical abdomen. Laparotomy has been recommended on adult patients with intussusceptions because of the high likelihood of identifying a pathologic lesion. The doctrine of adult intussusception is to operate for concern of malignancy. Conclusion Surgeons, gastroenterologist and internist caring for patients on HAART therapy must be aware of the possibility of MT when evaluating HIV patients for possible surgical abdomen.

Background/Purpose: If the goal of partial liquid ventilation (PLV) with perfluorocarbons in the management of respiratory failure is to improve dynamic lung compliance (C dyn ) and pulmonary vascular resistance (PVR) while sustaing O 2 delivery, the optimal ventilatory management is unclear. The authors asked if volume-cycled or pressure-limited ventilation had different effects on PVR, cardiac index (CI), and C dyn in uninjured and injured neonatal piglet lungs. Methods: Anesthetized piglets (6 to 8 kg) were ventilated after tracheostomy. C dyn was measured by in-line Fleisch pneumotach/PC data acquisition terminal. Thermodilution instrumentation allowed determination of both Cl and PVR. Volume-control or pressure-limited ventilation was established in uninjured or injured (surfactant deficiency induced by saline lavage at 18 mL/kg) animals. After a stable 30-minute baseline, animals were assigned randomly to one of four groups: group I (n = 9), uninjured animals plus volume-cycled ventilation (intermittent mandatory ventilation [IMV], 10 bpm; tidal volume [TV], 15 mL/kg, positive end-expiratory pressure [PEEP], 5 cm H 2 O; Fio 2 , 1.0; and PLV for 150 minutes); group II (n = 9), uninjured animals plus pressure-limited ventilation (IMV, 10 bpm; peak inspiratory pressure (PIP), 25 cm H 2 O, PEEP, 5 cm H 2 O, Fio 2 , 1.0; and PLV for 150 minutes); group III (n = 7), injured animals plus volume-cycled ventilation (IMV, 10 bpm; TV, 15 mL/kg; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury for 30 minutes, followed by PLV rescue for 120 minutes); group IV (n = 7), injured animals plus pressure-limited ventilation (IMV, 10 bpm; PIP, 25 cm H 2 O; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury, and PLV rescue). Comparison within and between groups was accomplished by repeated measures analysis of variance (ANOVA) with Tukey correction. Results: There was no significant difference between volumecycled or pressure-limited ventilation in healthy lungs; however, in the setting of lung injury, dynamic compliance was 1.44 ± 0.15 after 180 minutes in the volume-cycled group and 0.91 ± 0.10 in the pressure-limited group after the same interval (mL/cm H 2 O · kg ± SEM). Similarly, PVR was 100 ± 6 in the volume-cycled group and 145 ± 12 in the pressurelimited group after 180 minutes of lung injury (mm Hg/L/kg · min ± SEM). Cardiac index declined significantly in all groups independent of ventilatory mode. Conclusions: These results suggest that in the setting of lung injury, C dyn and PVR improved significantly when volume-cycled, compared with pressure-limited ventilation was used. Although no difference existed between ventilatory modes in healthy lungs, pressure-limited ventilation, when combined with PLV in injured lungs, had adverse effects on lung compliance and pulmonary vascular resistance. Volume-cycled ventilation may optimize the ability of perfluorocarbon to recruit collapsed or atelectatic lung regions.

Background/Purpose: Partial liquid ventilation (PLV) with perfluorocarbons decreases pulmonary vascular resistance (PVR) in injured piglet lungs without supplemental oxygen. These PVR changes may result either from direct mechanical effects or improved arterial oxygenation. In an uninjured hypoxic model of elevated PVR the authors asked the following questions: (1) Does prophylactic or therapeutic PLV ameliorate the PVR response to hypoxia? (2) Do prophylactic and therapeutic PLV have different PVR effects? (3) Does supplemental oxygen modify PVR response to PLV? Methods: Piglet (3 to 4 kg) lungs were isolated in situ without ischemia, hypoxia, or reperfusion injury. Pulmonary artery (PA) and left atrial (LA) cannulae were attached to a bloodprimed extracorporeal membrane oxygenation (ECMO) perfusion circuit with a flow (Q PA ) of 80 mL/kg/min. Pressure-limited, volume-cycled ventilation (PIP v = 15 mL/kg) was initiated. PLV with perfluorodecalin (15 mL/kg) was administered endotracheally. Continuously monitored blood gas parameters allowed airway and extracorporeal adjustment of Fio 2 to produce a Po 2 appropriate to the experimental phase. PVR was calculated as (PPA−PLAQPA). After a stable 30-minute normoxic baseline, animals were assigned randomly to three groups. In group I , control (n = 7), PVR was measured for 150 minutes in hypoxic lungs (Fio 2 = 0.07, P PA o 2 = 40 mm Hg, S PA o 2 = 70%). In group II , prophylactic (n = 8), PLV was administered, followed by 90 minutes of hypoxia, and 60 minutes of oxygen recovery (Fio 2 = 0.21 – 0.30, P PA o 2 > 100 mm Hg, S PA o 2 = 100%). In group III , therapeutic (n = 8), after 30 hypoxic minutes, PLV was administered and maintained for 90 minutes, followed by a 60-minute oxygen recovery phase. Results were expressed as mean ± SEM. Statistical analysis of groups was performed by repeated measures of analysis of variance (ANOVA) and Tukey correction. Results: In group I normoxic gas-ventilated PVR was 174 ± 12 mm Hg/L/kg/min. After 90 hypoxic minutes PVR was 318 ± 37 ( P v baseline). In group II baseline PVR was 183 ± 14. PVR after 30 normoxic minutes of PLV was 199 ± 14 ( P = ns v baseline). After 90 hypoxic minutes, PVR was 350 ± 31 ( P v baseline, and PLV alone) followed by a decrease to 192 ± 19 after 60 minutes of oxygen recovery ( P = ns v baseline or PLV alone). In group III baseline PVR was 160 ± 17 and 325 ± 29 after 30 hypoxic minutes. After 90 hypoxic minutes of PLV, PVR was 366 ± 22 ( P = ns v hypoxia control, P v normoxic baseline). PVR recovered to 189 ± 19 after 60 minutes of oxygen recovery ( P = ns v baseline). Conclusions: Prophylactic/therapeutic PLV had no effect on hypoxia-induced increases in PVR and did not differ from each other. Although PLV alone decreases PVR in the injured lung without supplemental oxygen, elevated PVR associated with hypoxia was ameliorated only by supplemental oxygen in the liquid ventilated lung.

Introduction : Partial liquid ventilation (PLV) with perfluorocarbons can be advantageous in treating lung injury. We studied this phenomenon in isolated piglet lungs devoid of systemic detractors by studying the changes in pulmonary vascular resistance (PVR) after lung injury with and without PLV. The following questions were asked. (1) Does PLV alone affect PVR in the uninjured lung? (2) Does PLV prevent the increase in PVR associated with oleic acid-induced lung injury? (3) Does PLV modify the increase in PVR associated with oleic acid lung injury? (4) Are the prophylactic and therapeutic effects of PLV on the increased PVR associated with oleic acid-induced lung injury different? Methods : Neonatal piglet (3 to 4 kg) lungs were prepared without pulmonary ischemia, hypoxia, or reperfusion injury for in situ study. Before pulmonary vascular isolation (eg, aortic and ductus arteriosus ligation) the pulmonary artery (PA) and left atrium (LA) were cannulated and attached to a blood-primed perfusion circuit (flow, 80 mL/kg/min). Pressure-limited volume-cycled ventilation (FIO 2 , 0.21; TV, 15 mL/kg; PIP, 25 cm H 2 O) was accomplished via occlusive tracheostomy. Blood gas parameters were monitored continuously and maintained within normal range (SpaO 2 , 75%; pH, 7.35 to 7.45; pCO 2 , 35 to 45 torr). Pulmonary artery pressure (P pa ), left atrial pressure (P ia ) and pulmonary blood flow (Q pa ) were recorded and PVR calculated (PVR = Ppa − PiaQpa). After achieving a stable baseline with gas ventilation only, the animal preparations were assigned to one of the following four groups. In group 1 (n = 7) PLV was given alone, using endotracheally administered perfluorodecalin (15 mL/kg). In group 2 (Prophylactic, n=7) PLV was given prophylactically 60 minutes before lung injury induced by injecting oleic acid (OA) at 0.08 mL/kg into the pulmonary artery. In group 3 (Therapeutic, n=8) PLV was given 60 minutes after OA-induced lung injury. P PA , P LA , and Q PA were measured and PVR was calculated. In group 4 (n = 7) OA was given alone. Significance of differences between groups was obtained by repeated measures analysis of variance (ANOVA). Results were expressed as mean ± SEM (mm Hg/L/Kg). Results : Group I showed baseline PVR of the normoxic gas ventilated animals was 127 ± 19 mm Hg/L/kg. PVR 180 minutes after PLV administration was 160 ± 15 mm Hg/L/kg ( P = ns v baseline). In group 2 after OA infusion, PVR increased from 109 ± 13 to 281 ± 26 mm Hg/L/kg ( P v baseline), and 60 minutes later, PVR decreased to 193 ± 22 mm Hg/L/kg ( P v OA). In group 3 PVR on gas ventilation, before lung injury, was 137 ± 28 mm Hg/L/kg. Sixty minutes after OA infusion, PVR increased to 314 ± 23 mm Hg/L/kg ( P v baseline). After 60 additional minutes of PLV, PVR decreased to 201 ± 31 mm Hg/L/kg, ( P v maximum). In group 4 baseline PVR was 96 ± 16 mm Hg/L/kg. After 120 minutes of OA injection, PVR increased to 414 ± 20 mm Hg/L/kg ( P v baseline). Endpoint analysis of PVR at the conclusion of the recording interval showed no difference between group 2 and group 3 (P = not significant [ns]). Conclusions : (1) PLV does not significantly alter PVR in the uninjured lung when given for 2 hours; (2) prophylactic administration of PLV prevents the sustained increase in PVR known to be induced by OA injury; (3) PLV abates OA-induced elevation in PVR when given therapeutically after injury; and (4) Prophylactic and therapeutic PLV have similar effects on PVR in the OA-injured lung.