The Postoperative Airway Compromise Score-First Steps to Developing a Postoperative Tool for the Assessment of Upper Airway-Related Complications Following Anterior Cervical Spine Surgery.

BACKGROUND: Acute upper airway compromise is a rare but catastrophic complication after anterior cervical discectomy and fusion. This study aims to develop a score to identify patients at risk of acute postoperative airway compromise (PAC). METHODS: Potential risk factors for acute PAC were selected by a modified Delphi process. Ten patients with acute PAC were identified of 1466 patients who underwent elective anterior cervical discectomy and fusion between July 2014 and May 2019. A comparison group was created by a randomized selection process (non-PAC group). Factors associated with PAC and a P value of < 0.10 were entered into a logistic regression model and coefficients contributed to each risk factor's overall score. Calibration of the model was evaluated using the Hosmer-Lemeshow goodness-of-fit test. Quantitative discrimination was calculated, and the final model was internally validated with bootstrap sampling. RESULTS: We identified 18 potential risk factors from our Delphi process, of which 6 factors demonstrated a significant association with airway compromise: age >65 years, current smoking status, American Society of Anesthesiologists class >2, history of a bleeding disorder, surgery of upper subaxial cervical spine (above C4), and duration of surgery >179 minutes. The final prediction model included 5 predictors with very strong performance characteristics. These 5 factors formed the PAC score, with a range from 0 to 100. A score of 20 yielded the greatest balance of sensitivity (80%) and specificity (88%). CONCLUSIONS: The acute PAC score demonstrates strong performance characteristics. The PAC score might help identify patients at risk of upper airway compromise caused by surgical site abnormalities.

Hemodynamic Management in the Prevention and Treatment of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.

One of the most serious complications after subarachnoid hemorrhage (SAH) is delayed cerebral ischemia, the cause of which is multifactorial. Delayed cerebral ischemia considerably worsens neurological outcome and increases the risk of death. The targets of hemodynamic management of SAH have widely changed over the past 30 years. Hypovolemia and hypotension were favored prior to the era of early aneurysmal surgery but were subsequently replaced by the use of hypervolemia and hypertension. More recently, the concept of goal-directed therapy targeting euvolemia, with or without hypertension, is gaining preference. Despite the evolving concepts and the vast literature, fundamental questions related to hemodynamic optimization and its effects on cerebral perfusion and patient outcomes remain unanswered. In this review, we explain the rationale underlying the approaches to hemodynamic management and provide guidance on contemporary strategies related to fluid administration and blood pressure and cardiac output manipulation in the management of SAH.

Intraoperative adherence to a low tidal volume ventilation strategy in critically ill patients with preexisting acute lung injury.

PURPOSE: Low tidal volume (LTV) ventilation reduces mortality in patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). This study investigates adherence of intraoperative LTV and whether patient outcomes were different with or without continued intraoperative LTV ventilation in patients with previously established ALI or ARDS. MATERIALS AND METHODS: A retrospective analysis was performed of adults with ALI/ARDS over a 2-year period who underwent surgery between 24 hours and 14 days after the diagnosis of ALI/ARDS. The main outcome was intraoperative LTV use. Secondary outcomes included perioperative respiratory and clinical outcomes. RESULTS: Of the 249 patients who underwent surgery between 24 hours and 14 days after ALI/ARDS diagnosis, 101 (41%) received preoperative LTV ventilation. Fifty-four (53%) received intraoperative LTV ventilation, whereas 47 (47%) did not. Use of preoperative LTV ventilation was associated with use of intraoperative LTV ventilation (P < .01). No differences in respiratory or clinical outcomes between patients with or without intraoperative LTV ventilation were observed. CONCLUSIONS: Adherence to intraoperative LTV in surgical patients was low. Adherence of LTV intraoperatively was not associated with improved oxygenation, reductions in hospital length of stay, or in-hospital mortality. The importance of adhering to an intraoperative LTV strategy remains unclear.

Intensive insulin therapy and mortality in critically ill patients.

INTRODUCTION: Intensive insulin therapy (IIT) with tight glycemic control may reduce mortality and morbidity in critically ill patients and has been widely adopted in practice throughout the world. However, there is only one randomized controlled trial showing unequivocal benefit to this approach and that study population was dominated by post-cardiac surgery patients. We aimed to determine the association between IIT and mortality in a mixed population of critically ill patients. METHODS: We conducted a cohort study comparing three consecutive time periods before and after IIT protocol implementation in a Level 1 trauma center: period I (no protocol); period II, target glucose 80 to 130 mg/dL; and period III, target glucose 80 to 110 mg/dL. Subjects were 10,456 patients admitted to intensive care units (ICUs) between 1 March 2001 and 28 February 2005. The main study endpoints were ICU and hospital mortality, Sequential Organ Failure Assessment score, and occurrence of hypoglycemia. Multivariable regression analysis was used to evaluate mortality and organ dysfunction during periods II and III relative to period I. RESULTS: Insulin administration increased over time (9% period I, 25% period II, and 42% period III). Nonetheless, patients in period III had a tendency toward higher adjusted hospital mortality (odds ratio [OR] 1.15, 95% confidence interval [CI] 0.98, 1.35) than patients in period I. Excess hospital mortality in period III was present primarily in patients with an ICU length of stay of 3 days or less (OR 1.47, 95% CI 1.11, 1.93 There was an approximately fourfold increase in the incidence of hypoglycemia from periods I to III. CONCLUSION: A policy of IIT in a group of ICUs from a single institution was not associated with a decrease in hospital mortality. These results, combined with the findings from several recent randomized trials, suggest that further study is needed prior to widespread implementation of IIT in critically ill patients.

Red blood cells prevent inhibition of hypoxic pulmonary vasoconstriction by nitrite in isolated, perfused rat lungs.

Nitrite reduction to nitric oxide (NO) may be potentiated by a nitrite reductase activity of deoxyHb and contribute to systemic hypoxic vasodilation. The effect of nitrite on the pulmonary circulation has not been well characterized. We explored the effect of nitrite on hypoxic pulmonary vasoconstriction (HPV) and the role of the red blood cell (RBC) in nitrite reduction and nitrite-mediated vasodilation. As to method, isolated rat lungs were perfused with buffer, or buffer with RBCs, and subjected to repeated hypoxic challenges, with or without nitrite. As a result, in buffer-perfused lungs, HPV was reduced at nitrite concentrations of 7 muM and above. Nitrite inhibition of HPV was prevented by excess free Hb and RBCs, suggesting that vasodilation was mediated by free NO. Nitrite-inhibition of HPV was not potentiated by mild acidosis (pH = 7.2) or xanthine oxidase activity. RBCs at 15% but not 1% hematocrit prevented inhibition of HPV by nitrite (maximum nitrite concentration of approximately 35 muM) independent of perfusate Po(2). Degradation of nitrite was accelerated by hypoxia in the presence of RBCs but not during buffer perfusion. In conclusion, low micromolar concentrations of nitrite inhibit HPV in buffer-perfused lungs and when RBC concentration is subphysiological. This effect is lost when RBC concentration approaches physiological levels, despite enhanced nitrite degradation in the presence of RBCs. These data suggest that, although deoxyHb may generate NO from nitrite, insufficient NO escapes the RBC to cause vasodilation in the pulmonary circulation under the dynamic conditions of blood flow through the lungs and that RBCs are net scavengers of NO.

Red blood cells and hemoglobin in hypoxic pulmonary vasoconstriction.

Nitric oxide (NO) plays an important role in the modulation of hypoxic pulmonary vasoconstriction; in turn, red blood cells (RBCs) augment HPV by hemoglobin-mediated oxidation and inactivation of NO. In addition, scavenging of reactive oxygen species by RBCs may play a role in augmentation of HPV. NO delivery and/or production by RBCs does not appear to be important in the control of pulmonary vasomotor tone. This review will discuss regulation of HPV by RBCs with an emphasis on hemoglobin-NO interactions. In addition, the review will discuss how biologic (S-nitrosation) or pharmacologic (cross-linking) modification of hemoglobin may affect pulmonary circulatory-hemoglobin interactions.

The effects of apparatus dead space on P(aCO2) in patients receiving lung-protective ventilation.

BACKGROUND: Lung-protective ventilation using tidal volume (V(T)) of 4-6 mL/kg (predicted body weight) reduces mortality (compared with traditional V(T)) in patients with acute respiratory distress syndrome and acute lung injury. Standardized use of lower V(T) can result in respiratory acidosis and has raised new concerns about the appropriate configuration of the ventilator circuit, especially in regard to the dead space (V(D)) of the apparatus. We hypothesized that, with a patient receiving lung-protective ventilation, the removal of all apparatus dead space from the circuit would reduce P(aCO2) and allow a reduction in minute ventilation. METHODS: All the studied patients met the American-European consensus-conference criteria for acute respiratory distress syndrome/acute lung injury, were receiving a lung-protective ventilation strategy, were > 18 years of age, and were hemodynamically stable. We prospectively tested 3 different ventilator-circuit configurations, in random sequence, for 15 min each: (1) standard hygroscopic heat-and-moisture exchanger (HME) with 15-cm flexible tubing, (2) 15-cm flexible tubing only, (3) no HME or flexible tubing. V(T), respiratory rate, positive end-expiratory pressure, and fraction of inspired oxygen were maintained constant throughout the study, and exhaled CO2 was measured continuously. Physiologic dead space (V(D)/V(T)) was calculated using the Enghoff modification of the Bohr equation. RESULTS: Seven patients were studied. Removal of the HME from the circuit significantly decreased V(D)/V(T) (by approximately 6%) and P(aCO2) (by approximately 5 mm Hg). Removal of both the HME and flexible tubing from the circuit reduced V(D)/V(T) by an additional 5%, and P(aCO2) by an additional 6 mm Hg. With both circuit-configuration changes, minute ventilation fell from a mean of 11.51 L/min to 10.35 L/min, and pH increased from 7.30 to 7.38. Carbon-dioxide production did not change significantly. CONCLUSION: In patients receiving lower-V(T) ventilation, removing all the apparatus V(D) from the ventilator circuit reduces P(aCO2) and increases pH, at a lower minute ventilation. This information will help guide ventilator-circuit configuration for patients receiving lung-protective ventilation.

Contributions of nitric oxide synthase isozymes to exhaled nitric oxide and hypoxic pulmonary vasoconstriction in rabbit lungs.

We investigated the source(s) for exhaled nitric oxide (NO) in isolated, perfused rabbits lungs by using isozyme-specific nitric oxide synthase (NOS) inhibitors and antibodies. Each inhibitor was studied under normoxia and hypoxia. Only nitro-L-arginine methyl ester (L-NAME, a nonselective NOS inhibitor) reduced exhaled NO and increased hypoxic pulmonary vasoconstriction (HPV), in contrast to 1400W, an inhibitor of inducible NOS (iNOS), and 7-nitroindazole, an inhibitor of neuronal NOS (nNOS). Acetylcholine-mediated stimulation of vascular endothelial NOS (eNOS) increased exhaled NO and could only be inhibited by L-NAME. Selective inhibition of airway and alveolar epithelial NO production by nebulized L-NAME decreased exhaled NO and increased hypoxic pulmonary artery pressure. Immunohistochemistry demonstrated extensive staining for eNOS in the epithelia, vasculature, and lymphatic tissue. There was no staining for iNOS but moderate staining for nNOS in the ciliated cells of the epithelia, lymphoid tissue, and cartilage cells. Our findings show virtually all exhaled NO in the rabbit lung is produced by eNOS, which is present throughout the airways, alveoli, and vessels. Both vascular and epithelial-derived NO modulate HPV.

Effects of S-nitrosation and cross-linking of hemoglobin on hypoxic pulmonary vasoconstriction in isolated rat lungs.

Free hemoglobin (Hb) and red blood cells augment hypoxic pulmonary vasoconstriction (HPV) by scavenging nitric oxide (NO). S-nitrosation of Hb (SNO-Hb) may confer vasodilatory properties by allowing release of NO during deoxygenation and/or by interaction with small-molecular weight thiols. Likewise, cross-linking of free Hb may limit its vasoconstrictive effect by preventing abluminal movement of the molecule. We compared the effects of free SNO-Hb and Hb intramolecularly cross-linked at the beta-cysteine 93 residue [Bis(maleidophenyl)-polyethylene glycol2000HbA (Bis-Mal-PEGHb)] to those of free oxyHb on pulmonary artery pressure (PAP), HPV, and exhaled NO (eNO) in isolated, perfused rat lungs. Ventilation of lungs with anoxic gas for 5 minutes reduced perfusate PO2 to 11+/-1.0 Torr. Addition of SNO-Hb or Bis-Mal-PEGHb (100 micromol/L) to buffer perfusate increased normoxic PAP and augmented HPV in similar magnitude as free oxyHb, but had no effect on eNO. Addition of the allosteric modulator inositol hexaphosphate to increase Hb P50 and the thiol glutathione (GSH) to allow removal of NO from Hb via transnitrosation to the perfusate did not reduce augmentation of HPV by SNO-Hb or increase eNO. GSH resulted in an approximately 50% reduction in perfusate [S-nitrosothiol], in association with an increase in perfusate [metHb]. Free SNO-Hb is a net NO scavenger and pulmonary vasoconstrictor in this model, although thiol-mediated release of NO from SNO-Hb does occur. However, release of NO from SNO-Hb was not influenced by deoxygenation-mediated allosteric changes in Hb across a broad range of oxyHb saturation. Cross-linking of Hb does not limit its pulmonary vasoconstrictor effects.