Maternal healthcare needs assessment survey at Rabia Balkhi Hospital in Kabul, Afghanistan

OBJECTIVE: Since the Department of Health and Human Services chose Rabia Balkhi Hospital (RBH) in Kabul, Afghanistan, as a site for intervention in 2002, the status of women's health there has been of interest. This study created a tool to assess accessibility and quality of care of women admitted from May to July, 2005. METHODS: A 39-item questionnaire was created in English and translated into Dari. Hospital staff administered the survey to 292 women admitted to RBH for obstetric and gynecological complaints. RESULTS: Approximately 40% of the women traveled between 1 and 5 hours to reach RBH. Only 54% (158/292) of women reported having their blood pressure monitored during their pregnancy. About one-third of women reported that they had never received an immunization. CONCLUSIONS: This survey tool ascertained that women who received care at RBH traveled great lengths to reach the facility. Preventative measures such as blood pressure checks and immunizations are areas that need improvement.     

Neutrophil stimulation with granulocyte colony-stimulating factor worsens ventilator-induced lung injury and mortality in rats

BACKGROUND: Based on the association between the neutrophil and ventilator-induced lung injury, the authors hypothesized that neutrophil inhibition with fucoidin would be beneficial and stimulation with granulocyte colony-stimulating factor (G-CSF) would be harmful in a rat model of lethal ventilator-induced lung injury. METHODS: Animals (n = 111) were randomly assigned to be pretreated with fucoidin, G-CSF, or placebo (control) before 4 h of low-tidal-volume (10 ml/kg) or high-tidal-volume (40 ml/kg) mechanical ventilation. RESULTS: All low-volume animals survived. With high volumes, compared with controls, fucoidin did not improve survival (3 of 20 control animals and 5 of 20 fucoidin animals died; P = 0.51) but G-CSF significantly worsened it (18 of 22 animals died; P < 0.001). Circulating neutrophils were increased early with G-CSF and late with fucoidin with low and high tidal volumes (P < 0.05 for each treatment and tidal volume). Fucoidin decreased lung neutrophils, but these were only significant with high tidal volumes, whereas G-CSF increased lung neutrophils but only significantly with low tidal volumes (P < or = 0.01 for each). Fucoidin did not alter any cardiopulmonary measure significantly. Compared with control, G-CSF increased airway pressures with high tidal volumes and worsened lung edema and arterial oxygen with both tidal volumes (P < 0.05 for each). CONCLUSIONS: In this model, neutrophil stimulation by G-CSF increased lung dysfunction and with high tidal volumes worsened survival rates. Extrapolated clinically, neutrophil stimulation either by agents such as G-CSF or conditions such as sepsis may aggravate ventilator-induced lung injury.     

Extravasation: a rare complication of central venous cannulation? Case report of an imminent erosion of the common carotid artery

Zusammenfassung Eine Extravasation—eine unbeabsichtigte Injektion oder Leckage von Substanzen in das perivaskuläre oder subkutane Gewebe—kann Gewebeschäden verursachen, die je nach Substanz, nach ausgetretener Menge und Konzentration bis hin zur ausgedehnten Weichteilnekrose reichen. Bedeutende Gewebeschäden werden neben Chemotherapeutika u. a. durch Elektrolytkonzentrate, Vasopressoren und hyperosmolare Lösungen verursacht. Um Extravasationen zu vermeiden ist eine Überwachung der Katheterlage, des Infusionsdrucks und der Weichteile um die Einstichstelle erforderlich. Sollte die Prävention versagt haben, muss die Infusion sofort unterbrochen werden. Innerhalb der ersten 24 h sollten die gewebetoxischen Substanzen mit Hilfe von Entlastungsinzisionen und Spülung mit Ringer-Laktat eliminiert werden. Eine später einsetzende Behandlung erfordert ein Débridement. Die Tiefenausdehnung einer möglichen Gewebenekrose wird häufig unterschätzt und sollte deshalb durch MRT beurteilt werden. Wir berichten über eine lebensbedrohliche Halsweichteilnekrose mit drohender Arrosion der A. carotis communis durch Extravasation von Kalium-Clorid-Lösung aus einem dislozierten Jugularis interna Mehrlumenkatheter. Die Pathophysiologie des Schädigungsmechanismus wird diskutiert und es wird ein Überblick über die Inzidenz, das medikamentenabhängige Komplikationsrisiko und die erforderlichen Sofortmaßnahmen bei Extravasationen zentraler und peripherer Venenkatheter gegeben.

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Granulocyte colony-stimulating factor has differing effects comparing intravascular versus extravascular models of sepsis

BACKGROUND: Previously, neutrophil stimulation with granulocyte colony-stimulating factor (G-CSF) pretreatment increased survival rates in canines challenged with intraperitoneal or intrabronchial Escherichia coli and in rats challenged with intrabronchial Staphylococcus aureus. We investigated whether G-CSF pretreatment would be beneficial with intravascular challenge in these models. METHODS: Animals were randomized to G-CSF or placebo pretreatment followed by intravenous E. coli challenge in canines (n = 24) or intravenous or intrabronchial S. aureus challenge in rats (n = 273). All animals were treated with antibiotics. RESULTS: In canines, G-CSF before intravenous E. coli did not decrease mortality rates (7 of 12 [58%] G-CSF vs. 5 of 12 [42%] controls), which contrasted with prior reductions during extravascular infection (10 of 35 [29%] G-CSF vs. 37 of 65 [57%] controls). Consistent with the present and previously published studies in canines, in rats, G-CSF decreased mortality rates with intrabronchial S. aureus (22 of 90 [24%] G-CSF vs. 26 of 51 [51%] controls, p = 0.009) but did not decrease them with intravenous infection (34 of 67 [50%] G-CSF vs. 27 of 65 [42%] controls, p = 0.2) in patterns that were very different (p = 0.005 for the effects of G-CSF with intravascular vs. intrabronchial S. aureus). CONCLUSION: In contrast to extravascular infection, sepsis with intravascular E. coli in canines and S. aureus in rats may not provide a compartmentalized nidus of bacteria on which G-CSF-stimulated neutrophils can exert a beneficial antimicrobial effect. Extrapolated clinically, a proinflammatory agent like G-CSF may be most beneficial with sepsis related primarily to a compartmentalized extravascular site of infection.     

Protection with Antibody to Tumor Necrosis Factor Differs with Similarly Lethal Escherichia coli versus Staphylococcus aureus Pneumonia in Rats

Background: Differing factors may alter the effects of antibody to tumor necrosis factor (TNF) in infection and sepsis. The authors tested whether bacteria type or treatment route alters antibody to TNF in a rat model of bacterial pneumonia.

Methods: Rats (n = 231) received similarly lethal doses of either intratracheal Escherichia coli or Staphylococcus aureus followed by treatment with either intratracheal or intraperitoneal antibody to TNF or control serum. Animals received antibiotics (cefotiam daily dose, 100 mg/kg) starting 4 h after inoculation and were studied for up to 96 h.

Results: Compared with S. aureus, E. coli increased serum TNF and interleukin-6 concentrations, lung lavage TNF concentrations, neutrophil counts, and alveolar-to-arterial oxygen gradients and decreased circulating neutrophils and lymphocytes (P >= 0.05 for all). Compared with controls, with both bacteria, except for lung lavage TNF concentrations (which decreased with intratracheal but not with intraperitoneal antibody to TNF), treatment route did not alter the effects of antibody to TNF on any parameter (P = not significant for all). Antibody to TNF reduced mortality rates (relative risk of death +/- SEM) with both E. coli (-1.6 +/- 0.6;P = 0.006) and S. aureus (-0.5 +/- 0.04;P = 0.185), but these reductions were greater with E. coli than with S. aureus in a trend approaching statistical significance (P = 0.09). Compared with controls, similarly (P = not significant) with both bacteria, antibody to TNF decreased lung lavage and tissue bacteria concentrations (both P < 0.05) and serum TNF concentration (P < 0.09) and increased circulating neutrophils and lymphocytes (both P <= 0.01). Compared with S. aureus, with E. coli antibody to TNF decreased alveolar-to-arterial oxygen gradients (P = 0.04) and increased serum interleukin-6 concentrations (P = 0.003).     

The effects of increasing concentrations of isoflurane and desflurane on pulmonary perfusion and systemic oxygenation during one-lung ventilation in pigs.

During one-lung ventilation (OLV), hypoxic pulmonary vasoconstriction (HPV) reduces venous admixture and attenuates the decrease in arterial oxygen tension by diverting blood from the nonventilated lung to the ventilated lung. In vitro, desflurane and isoflurane depress HPV in a dose-dependent manner. Accordingly, we studied the effects of increasing concentrations of desflurane and isoflurane on pulmonary perfusion, shunt fraction, and PaO(2) during OLV in vivo. Fourteen pigs (30-42 kg) were anesthetized, tracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a left-sided double-lumen tube (DLT) was placed via tracheotomy. After DLT placement, FIO(2) was adjusted at 0.8 and anesthesia was continued in random order with 3 concentrations (0.5, 1.0, and 1.5 minimal alveolar concentrations) of either desflurane or isoflurane. Differential lung perfusion was measured with colored microspheres. All measurements were made after stabilization at each concentration. Whereas mixed venous PO(2), mean arterial pressure, cardiac output, nonventilated lung perfusion, and shunt fraction decreased in a dose-dependent manner, PaO(2) remained unchanged with increasing concentrations of desflurane and isoflurane during OLV. In conclusion, increasing concentration of desflurane and isoflurane did not impair oxygenation during OLV in pigs. IMPLICATIONS: In an animal model of one-lung ventilation, increasing concentrations of desflurane and isoflurane dose-dependently decreased shunt fraction and perfusion of the nonventilated lung and did not impair oxygenation. The decreases in shunt fraction are likely the result of anesthetic-induced marked decreases in cardiac output and mixed venous saturation.