What are the possible causes of acute respiratory failure after surgery?
Aug 07, 2018 · As an example , the STICH trial (surgical treatment for ischemic heart failure) that studied the effectiveness of coronary bypass surgery in patients with heart failure took place ultimately in 26 countries, in 127 study sites, and involved 2135 patients. Originally, the study was designed to cover 32 study sites in the USA and Canada, but low ...
What is the preoperative identification of risk factors for postoperative acute respiratory failure?
After rotator cuff repair, few patients require revision surgery, and failure to heal does not always translate into clinical failure, although healing is associated with better outcomes. Failure of rotator cuff repair is perceived differently by the patient, by the surgeon, and in terms of social and occupational abilities.
What is a failure to provide a diagnosis?
Mar 05, 2021 · Seven factors were found to be independently predictive of the development of PPCs: low preoperative arterial oxygen saturations when breathing room air and lying supine, acute respiratory infection associated with a fever and the need for antibiotic therapy during the preceding month, age, preoperative anemia, upper abdominal or intrathoracic surgery, a …
How many surgical errors occur each year?
Extensive tumor involvement with poor response to preoperative chemotherapy or pathologic fractures could contribute to surgical failure of rotationplasty because of alternation of blood supply or drainage, although to the best of our knowledge, there is no literature that specifically focuses on surgical failure and preoperative conditions.
What is acute respiratory failure?
Acute respiratory failure occurs when the lungs fail to oxygenate arterial blood adequately and it is one of the commonest postoperative complications. The preoperative identification of risk factors for postoperative acute respiratory failure allows identification of those patients who may benefit from preoperative optimization ...
What happens if you leave a PPC untreated?
It is the most common PPC, with radiographic evidence in up to 70% of patients undergoing a thoracotomy or a celiotomy.17If left untreated, it can result in pulmonary gas exchange alterations leading to severe hypoxemia and acute respiratory failure.
What is the role of bronchoscopy?
The role of bronchoscopy is limited to the retrieval of large particulate matter. The acidic aspirate is neutralized by pulmonary secretions within minutes of aspiration, therefore bronchoscopy and saline lavage are not required for the aspiration of nonparticulate matter.
What is the second stage of aspiration?
In the second stage, chemical injury occurs in response to the acidity of the aspirate. The pattern of injury includes mucosal edema, bronchorrhea, and bronchoconstriction, all resulting in an increased risk of bacterial infection. The third stage in the pathophysiology of aspiration is the inflammatory response.
Is atelectasis asymptomatic or asymptomatic?
Clinically, atelectasis ranges from asymptomatic to severe hypoxemia and acute respiratory failure. The variability in presentation depends on the rapidity of onset, the degree of lung involvement, and the presence of an underlying pulmonary infection.
Is atelectasis passive or absorptive?
In this case, atelectasis is either passive or absorptive. Passive atelectasis is secondary to external or internal compression of a lung segment (e.g., pneumothorax, hemothorax, abdominal distention). Absorptive atelectasis occurs when the inhaled gas is rich in oxygen and poor in nitrogen.
What is rotationplasty? What are its uses?
Rotationplasty is one treatment option for femoral bone sarcomas in skeletally immature patients and can be used in adults with large tumors or failed limb salvage procedures. This procedure enables patients to avoid phantom pain because the sciatic nerve or its branches are not divided as they are in amputation. It also avoids issues of limb length discrepancy or loosening of an endoprosthesis, and good functional outcome has been reported; however, rotationplasty is only rarely indicated and surgical complications or risk factors for failure of the procedure have not been well reported [ 7, 13 ]. We reviewed 25 patients with rotationplasty focusing on risk factors for failure and postoperative complications. We observed that rotationplasty is a relatively successful procedure with a low amputation rate and that those patients whose rotationplasties result in amputation have risk factors such as pathologic fractures, poor response to chemotherapy, or vascular anastomosis.
What is rotationplasty for femoral osteosarcoma?
Rotationplasty is one treatment option for femoral osteosarcoma and other sarcomas in skeletally immature patients. Rotationplasty is an alternative to amputation and has the advantages of avoiding phantom pain, limb length discrepancy, and loosening of an endoprosthesis. The reported functional outcomes are good [ 7, 13 ]. This procedure can also be used to save failed limb salvage procedures [ 3, 17, 20 ]. Rotationplasty is particularly favored in patients with extensive soft tissue mass, intraarticular extension of tumor, or pathologic fractures [ 8 ]. The femoral or tibial sarcoma can be resected en bloc with surrounding soft tissue without opening the knee joint. The major arteries and veins can be resected and anastomosed if soft tissue involvement by the tumor so requires. Rotationplasty only requires the ability to retain an intact sciatic nerve so this procedure can be used for patients with large femoral sarcomas who are not candidates for endoprosthesis or osteoarticular allograft reconstruction, and wide margins can be obtained.
What does each author certify?
Each author certifies that he or she has no commercial associations (eg, consultancies, stock ownership, equity interest, patent/licensing arrangements, etc) that might pose a conflict of interest in connection with the submitted article.
What is urine biochemistry?
Urine biochemistry is frequently used to diagnose prerenal azotemia and guide fluid administration in the perioperative setting and in ICU patients , suggesting that the given parameters are indicators of renal tissue integrity and preserved tubular function. Recent evidence has suggested that urine chemistry is not a reliable tool for predicting the rapid reversibility of AKI. Preserved renal tubular sodium or urea handling does not necessarily indicate an absence of renal injury. Recently, Nejat et al. 13 found that patients with suspected prerenal azotemia showed evidence of structural injury, with increased biomarkers of renal injury. However, increased sodium excretion does not indicate tubular necrosis. Inflammation mediators have been shown to induce tubular cell dysfunction with conformational changes of the tubule Na+/H+ exchanger, urea, or chloride channels, which influence urine composition independent of any structural damage. 13, 40 Biomarkers of renal injury ( i.e., neutrophil gelatinase-associated lipocalin, kidney injury molecule-1) are expected to be used in diagnosis of tubular damage. 41 Many uncertainties remain regarding their validity at the bedside. The most promising biomarkers for renal injury appear to be the neutrophil gelatinase-associated lipocalin and kidney injury molecule-1. As an example, mild renal structure damage can lead to the profound loss of glomerular and/or tubular function in a patient with underlying structural alteration ( e.g., chronic hypertension, diabetes); however, the same injury will not alter the function of an intact kidney ( fig. 3 ). A combination of biomarkers of structural injury may therefore provide a more accurate picture of renal injury compared with a single-biomarker approach.
What is AKI in renal disease?
AKI is defined under the Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE), the acute kidney injury network (AKIN), or the kidney disesase improving global outcome (KDIGO) classification 9 as an increase in serum creatinine level and decrease in urine output. The use of GFR estimation by Cockcroft–Gault or the Modification of Diet in Renal Disease formulae should be restrained to preoperative evaluation of GFR when renal function is stable because these formulae yield substantial disagreements regarding creatinine in patients with AKI. However, anesthesiologists must be aware of two important factors while interpreting serum creatinine levels. First, it takes time for serum creatinine to reach a steady state after a fall in GFR because of its large volume of distribution (~60% of total body weight). It is therefore difficult to predict the course of AKI when serum creatinine increases (in other words, when the plateau of GFR is reached). Second, fluid loading and hemodilution may underestimate the increase in serum creatinine levels. Macedo et al. 10 described a simple formula to correct serum creatinine for fluid balance and overcome this limitation (adjusted creatinine = serum creatinine × correction factor with correction factor= (hospital admission weight [kg]) × 0.6 + Σ (daily cumulative fluid balance [l])/hospital admission weight × 0.6). In the present case scenario, the correction of serum creatinine with respect to fluid overload allows reclassification as stage 1 AKI according to the AKIN classification in the immediate postoperative period, with earlier diagnoses. The baseline serum creatinine was 69 μ m and increased postoperatively to 77 μ m. This value became 94 µ m after adjustment on cumulative fluid balance, which corresponds with stage 1 AKI.
What is the highest risk for AKI?
Cardiovascular surgery is by far the highest risk procedure associated with postoperative AKI, with up to 30% of patients experiencing AKI. In comparison, the prevalence of AKI after major noncardiac surgery procedures 1 such as in the presented case, is approximately 1%. The preoperative estimation of the risk of postoperative AKI by an anesthesiologist relies on checking the risk factors of AKI. Most of the risk factors are nonmodifiable because they are procedure-related (urgent surgery, need for surgical reexploration, and cardiopulmonary bypass duration) or patient-related (age >70 yr, diabetes, atrial fibrillation, left ventricular dysfunction, preoperative intraaortic balloon pump, or chronic renal insufficiency). Preoperative evaluation ( e.g., with echocardiography) of left and right ventricular functions is recommended in patients with a dyspnea of unknown origin or worsening dyspnea with a known cardiomyopathy. 3 In addition, Karkouti et al. 4 identified a per-cardiopulmonary bypass hematocrit of less than 20% and erythrocyte transfusion as potential modifiable risk factors for postoperative AKI. These findings are in line with experimental data showing the impact of normovolemic hemodilution promoting renal hypoxia. 5 However, perioperative erythrocyte transfusion was associated with an increased risk of AKI. The negative impact of erythrocyte transfusion supports the poor tolerance of multiple morphological and functional changes induced by erythrocyte storage (less deformability, depletion of 2, 3-diphosphoglycerate, inflammation, and decrease of bioavailability of nitric oxide with the liberation of free hemoglobin). These storage-induced modifications may induce a poor restoration of microcirculatory oxygenation associated with inflammation and changes in immune status. These observations emphasize the need for strategies that limit perioperative anemia and transfusion. 6
What is AKI in medical terms?
Acute kidney injury (AKI) is associated with poor outcome both in critically ill patients and after major surgery. 1 The occurrence of AKI has been associated with poor short-term and long-term outcome, increased risk of chronic renal failure, and increased risk of death. 2 Several risk factors of postoperative AKI have been identified, and may help identifying patients with the highest risk of AKI. However, recognizing contributors to AKI ( e.g., systemic inflammation, systemic hemodynamics alterations, nephrotoxic agents, and others) remains a challenge for anesthesiologists and intensivists because these factors are often associated and AKI multifactorial.
What is septic AKI?
For instance, an episode of septic AKI is mainly related to the systemic and regional inflammatory response to infection causing microvascular disorders, apoptosis, necrosis. However, a superimposed nephrotoxic agent or severe hypoperfusion can lead to further damage and/or impaired recovery.
Does hemodynamics increase renal perfusion?
The optimization of systemic hemodynamics is believed to increase renal perfusion. However, the true contribution of renal hypoperfusion to the development of AKI, especially in severe sepsis and septic shock, remains a matter of debate. Intrarenal microcirculatory defects, regional and systemic inflammatory cell infiltration, and apoptosis are believed to be central in the development of AKI. Although a correlation between cardiac output and renal blood flow has been described in patients with AKI, the relationship among cardiac output, renal blood flow, renal injury, and renal function remains poorly explored. Although the development of new biomarkers of renal injury may allow the assessment of renal structure damage, tools to reliably assess renal perfusion and rapid changes in renal perfusion in patients at the bedside remain lacking. Renal Doppler of renal interlobar arteries can provide information on renal vascular resistance; however, this method does not measure renal blood flow per se. Therefore, developing tools to measure renal perfusion ( i.e., renal blood flow and distribution of renal microvascular blood flow within the renal parenchyma) will allow a better understanding of the role of renal perfusion in renal damage.
Does hydroxyethyl starch cause AKI?
The fluid resuscitation of brain-dead organ donors, based on hydroxyethyl starches (HES), is associated with an increased risk of AKI in kidney transplantations. In another randomized controlled trial, Schortgen et al. 36 found that septic patients treated with HES 200/0.6 showed a higher incidence of AKI compared with patients treated with gelatins. The Efficacy of Volume Substitution and Insulin Therapy in Severe Sepsis study showed a higher incidence of AKI in septic patients treated with HES 200/0.5 compared with those treated by crystalloids. Developed HES with lower molecular weight (130 kd) have been proposed because of the expected better risk/benefit ratio. The recently published 6S and Crystalloid versus Hydroxyethyl Starch trials did not confirm these expectations because the risk of AKI persisted with smaller molecular weight HES (HES 130/0.4), which induced a higher rate of mortality and/or dialysis. 37, 38 Together, these trial data indicate an increased risk of AKI when HES are used. Precautions can be extended to other conditions, especially with the presence of acute inflammation ( e.g., burns, cardiopulmonary bypass, postcardiac arrest syndrome). The safety profile of HES remains matter of debate during surgery. 39 Gelatins appear to have a safer profile, but there is little evidence for the potential risk of AKI. Finally, extra physiologic plasma oncotic pressure after the administration of a large amount of hyperoncotic solutions can decrease the GFR.
What are the two types of errors in medical terminology?
A lack of standardized nomenclature and overlapping definitions of medical errors has hindered data analysis, synthesis, and evaluation. There are two major types of errors: Errors of omission occur as a result of actions not taken.
Why are medical errors important?
It is challenging to uncover a consistent cause of errors and, even if found, to provide a consistent viable solution that minimizes the chances of a recurrent event. By recognizing untoward events occur , learning from them, and working toward preventing them, patient safety can be improved. [1]
How much do medical errors cost?
Depending on the study, medical errors account for over $4 billion per year. Medical errors cost approximately $20 billion a year. Medical errors in hospitals and clinics result in approximately 100,000 people dying each year.
What is a never event?
Never events are errors that should not ever have happened. A classic example of a never event is the development of pressure ulcers or wrong-site surgery. The National Quality Forum has identified the following as Serious Reportable Events:
What is an active error?
Active errors are those taking place between a person and an aspect of a larger system at the point of contact. Active errors are made by people on the front line such as clinicians and nurses. For example, operating on the wrong eye or amputating the wrong leg are classic examples of an active error.
How does failure mode effect analysis work?
Failure mode effect analysis fosters safety and the prevention of accidents through a proactive process of identifying potential or real failures, causes, and effects. Failure mode effect analysis concludes errors will occur even if healthcare professionals are careful. Failure mode effect analysis engages in a continual process of quality improvement to assess and correct areas where an error has occurred or is likely to occur. The strategy with failure mode effect analysis is to build redundancies to serve as safety nets that trap errors. [11]
How to decrease infection transfer?
Appropriate hand-washing is one of the single most effective methods to decrease infection transfer. High-risk procedures such as indwelling Foley catheter and vascular catheter infection rates can be decreased by adhering to the use of sepsis bundles.
What is open access?
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What is a disconnected pancreatic duct?
Disconnected main pancreatic duct (DPD) is defined as a discontinuity of the main pancreatic duct (MPD) and is a feature of severe necrotizing pancreatitis with central pancreatic necrosis first described in 1993 [ 64 ]. An external pancreatic fistula will therefore be usually expected using MARPN/VARD/percutaneous drainage for severe necrotizing pancreatitis. It can be managed as an outpatient procedure by gradual shortening of external drain then downsizing using a smaller French diameter nasogastric tube cut to size and aggressive endoscopic or surgical interventions are not usually necessary [ 65 ]. Late recurrence leading to a drain tract pseudocyst can occasionally occur due to a distal structure in the neck or head of the pancreas and is then best managed by Roux-en-Y pseudocyst-enterostomy [ 65 ].
What causes AP in the pancreas?
The commonest causes for AP are gallstones (40–65%) and alcohol (25–40%), and the remainder (10–30%) are due to a variety of causes including autoimmune and genetic risk factors (Table 1) [ 1, 2 ]. Irrespective of etiology, the trigger factors cause supraphysiological intracellular signaling resulting in trypsin activation within the zymogen granules [ 3, 4, 5 ]. The resultant acinar cell death causes a localized and systemic inflammatory response. Initially, the most prominent features are distant organ dysfunction notably the lungs and kidneys, which in most cases is of short duration (< 48 h) [ 6, 7 ].
What is AP in medical terms?
Acute pancreatitis (AP) is defined as an acute inflammatory attack of the pancreas of sudden onset. Around 25% of patients have either moderately severe or severe disease with a mortality rate of 15–20%.
Is AP a life threatening condition?
Severe AP still is a life-threatening condition requiring a multidisciplinary approach. An accurate diagnosis should be made a soon as possible, and initiating resuscitation with large volume intravenous fluids and oxygen by mask. If there is any doubt of the diagnosis, then an urgent contrast-enhanced CT scan should be undertaken. If severe disease is predicted using clinical assessment and serum CRP > 150 mg/L, the patient will require intensive monitoring. Most deaths within the first week or so are due to multi-organ failure so severe cases will require management on the intensive therapy unit. During the second phase of the disease, death is due to local complications arising from the pancreatic inflammation. Accurate identification of these local complications is required to determine the correct form of treatment. Acute peripancreatic fluid collections are common, not requiring any treatment. Most pancreatic pseudocysts also largely resolve on conservative management, not needing intervention. Necrotizing pancreatitis causing acute necrotic collections and later walled-off necrosis will require treatment if symptomatic or infected. Initial endoscopic transgastric or percutaneous drainage will resolve less serious collections but necrosectomy using minimally invasive approaches will be needed for more serious collections and usually require a combination of techniques for larger extensive collections. To prevent recurrent attacks of AP, then causative factors need to be removed where possible. Future progress needs to be focused on better management of multi-organ failure in the first phase and more effective minimally invasive techniques for removal of necrosis.