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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-six of 403 deaths after tracheotomy were direct complications of that procedure. Arterial hemorrhage caused three deaths, venous bleeding, seven. Airway obstruction resulted in six fatalities. Tracheoesophageal fistula caused five deaths. Eight deaths were due to infection and sepsis. Tension pneumothorax developed in one patient and the remaining six deaths were due to cardiopulmonary collapse. Many of the complications of tracheotomy can be avoided with accurate knowledge of anatomic variations, ideal operating conditions, proper technic, careful arterial and venous hemostasis, routine postoperative chest x-ray films, sterile suction technic, proper use of soft cuffed tracheotomy tubes, adequate humidification, and careful postoperative blood gas monitoring.
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PMID:Fatal complications of tracheotomy. 76 82

All hospitalized patients except infants (a total of 1,647 patients) who received central venous TPN solutions at UCDMC from 1981 through 1985 were studied to determine the incidence of complications from the use of TPN. A complication was considered to have occurred if the patient experienced obvious morbidity, mortality, or both; an event known to be deleterious, despite a lack of demonstrable morbidity; or premature loss of the central venous catheter. Complications related to catheter placement occurred in 5.7 percent of patients, sepsis in 6.5 percent, mechanical complications in 9 percent, and metabolic complications in 7.7 percent. The incidence of induction of sepsis increased during 1984 to 1985 due to the introduction of multilumen central venous catheters. The most frequent catheter placement complications were hemorrhage and pneumothorax. Major venous thrombosis and nursing mishaps were the most common mechanical complications. Metabolic complications were infrequent and were generally not severe after adjustment of the protocol in late 1981. Four patients (0.2 percent) died from TPN-associated complications: a child on home TPN who underwent a catheter change and in whom hyperosmolar hyperglycemic coma developed, a patient with end-stage chronic obstructive pulmonary disease in whom tension pneumothorax occurred, a patient who died from complications of subclavian artery laceration, and a patient who died from Candida septicemia. Complications of TPN are frequent and may be severe. Quality assurance mechanisms for identification of these complications are necessary and should form the basis for the establishment of appropriate protocols.
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PMID:Complications of parenteral nutrition. 308 44

Extracorporeal membrane oxygenation (ECMO) has been successful (greater than 80% survival) in 35 centers in greater than 900 newborns with severe respiratory failure having an estimated mortality of greater than 80% on conventional management. During the last 3 years we have treated 79 newborns with 74 survivors (94%). Their diagnoses included meconium aspiration, persistent fetal circulation, respiratory distress syndrome, congenital diaphragmatic hernia, and sepsis. Seven patients (9%) had life-threatening intrathoracic complications requiring emergent intervention while on ECMO: tension hemothorax (3), tension pneumothorax (2), and pericardial tamponade (2). Pericardial tamponade and tension hemothorax and pneumothorax show a similar pathophysiology of increasing intrapericardial pressure and decreasing venous return. Perfusion is initially maintained by the nonpulsatile flow of the ECMO circuit before further decrease in venous return results in decreasing ECMO flow and progressive hemodynamic deterioration. Each of the seven patients demonstrated a clinical triad that includes increasing PaO2 and decreasing peripheral perfusion (as evidenced by decreasing pulse pressure and decreasing SvO2) followed by decreasing ECMO flow with progressive deterioration. The diagnoses were confirmed by transillumination, chest x-ray, or cardiac echocardiogram. Initial emergent placement of a percutaneous drainage catheter was temporizing in all seven cases. However, four patients required emergent thoracotomy for definitive treatment while still on ECMO. All seven patients were weaned from ECMO and are short-term survivors (6 months to 3.5 years). As use of ECMO for newborn severe respiratory failure increases, responsible physicians must be familiar with life-threatening intrathoracic complications and appropriate treatment strategies.
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PMID:Life-threatening intrathoracic complications during treatment with extracorporeal membrane oxygenation. 320 57

Many factors may contribute to producing a shock state within the surgical environment. The classic causes of shock--hypovolemia, cardiac failure, and sepsis--occur commonly in the operating room. Additionally, concurrent surgery and anesthesia may contribute to produce clinical shock. Surgery may produce hypovolemia from "third space" loss and/or from blood loss. Some anesthetic drugs, by inhibiting the autonomic nervous system, impair the body's ability to compensate for hypovolemia, cardiac failure, or sepsis. Other entities such as tension pneumothorax, drug allergy, or mechanical factors produced by surgical exposure may contribute to hemodynamic compromise of the patient. Shock that occurs outside the surgical suite may also be produced by a variety of insults. One or more factors may contribute to inadequate tissue perfusion, thus making diagnosis of the cause(s) of shock a clinical challenge. Presented in this review is an anesthesiologist's approach to shock on a macrocirculatory level. Two important concepts are vital to this approach. First, one must act immediately to restore adequate perfusion to the brain and heart when confronted with a patient in shock. This is possible without knowing the specific cause(s) of the poor perfusion. Second, a rapid, accurate diagnosis of the cause(s) must be made if the patient is slow to respond to the initial therapy. Through the use of pulmonary artery catheterization, the factors producing any given shock state may be identified, and appropriate therapy may be instituted and monitored.
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PMID:Shock in the operating room. 651 89

Literature dealing with the management of undilatable oesophageal strictures in Africa is either scanty or non-existent. This report reviews 73 cases of adult undilatable corrosive strictures treated by oesophageal replacement at the University of Nigeria Teaching Hospital (UNTH) Enugu over a 5-year period (March 1986 to February 1991). Almost all the cases were suicidal or parasuicidal. All the patients had colon transplants; the right colon was used in 68 patients while the left colon was used in five patients. The age range was 13 to 48 years with a mean of 26 years. There were 65 males and 8 females. Four patients died in the postoperative period, earlier on in our surgical experience, a mortality of 5%. Of the 69 survivors, 62 patients (90%) experienced no dysphagia after 6-9 months of follow-up. Four patients (6%) swallowed with some difficulty while three patients who could not swallow at all 6 months after surgery underwent further surgery, the strictured upper part of the transplants being replaced with myocutaneous tube grafts after which two patients were able to swallow. Major postoperative complications were proximal anastomotic leak 49% (34 patients) of survivors, wound sepsis 25% (17 patients), tension pneumothorax 7% (five patients), colon graft necrosis 4% (three patients), and Ascaris upper intestinal obstruction 4% (three patients). The short and medium term results after colon transplant for oesophageal corrosive strictures are good. Our experience emphasizes the fact that these patients are from the very low social class, usually ignorant and most default at the follow-up clinics, once they start swallowing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oesophageal replacement in adult Nigerians with corrosive oesophageal strictures. 827 37

A 54 year old man with a staphylococcal sepsis developed staphylococcal pneumonia complicated by multiple pneumatoceles and bilateral tension pneumothoraces caused by bronchopleural fistulae. Excessive enlargement of the right sided pneumatoceles and a tension pneumothorax not improved by drainage led to mediastinal shift and compression of the right lung. Reversal of the mediastinal shift and closure of the bronchopleural fistulae was achieved by assisted independent lung ventilation.
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PMID:Pneumatoceles and pneumothoraces complicating staphylococcal pneumonia: treatment by synchronous independent lung ventilation. 832 53

The incidence of chest trauma has increased significantly since the turn of the century especially in developed countries where rapid means of transportation has become part of daily life. Although gunshot wounds (GSWs) were the commonest causes of chest trauma in wartime, road traffic accidents (RTAs) have become the scourge of peacetime and modern civilization. Chest trauma is more common in males during the 2nd to the 5th decades of life with an average age of 40 years reducing their life expectancy by another 40 years at the most productive and active period of their lives. Despite improvement in ambulance service and rapid mobilization of victims from the scene of accident, about 10% of chest injured patients will die on the spot and another 5% die within an hour of reaching the hospital. Of the remaining 85%, five percent will require emergency thoracotomy for various reasons while 80% will respond to resuscitative measures and tube thoracostomy drainage alone. The primary aims in the management of chest trauma are prompt restoration of normal cardiorespiratory functions, control of haemorrhage, treatment of associated injuries and prevention of sepsis. Although the overall survival rate of trauma has improved in recent years, deaths are often due to airway obstruction, exsanguinating haemorrhage, flail chest, tension pneumothorax, cardiac tamponade and associated intracranial, intraabdominal and skeletal injuries.
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PMID:Management of chest trauma: a review. 839 32

A multicenter, double-blind, placebo-controlled trial randomized 28 patients with primary (acute) human immunodeficiency virus (HIV)-1 infection (PHI) to receive zidovudine, 1000 mg daily, or placebo for 24 weeks. At week 48, compared with placebo patients, zidovudine-treated patients had significantly higher CD4 cell counts (zidovudine, 666 cells/mm3; placebo, 362; P = .004) and lower peripheral blood mononuclear cell (PBMC) culture titers (zidovudine, 0.58 log infectious units per million cells; placebo, 1.68; P = .02) but no difference in plasma RNA (zidovudine, 3.93 log copies/mL; placebo, 4.00; P = .83). Serious adverse events and minor clinical events were infrequent and comparable in both arms. There were two deaths: 1 patient died of sepsis and renal disease (zidovudine arm), and 1 patient died of sepsis and tension pneumothorax (placebo arm). Six months of high-dose zidovudine initiated during PHI results in higher CD4 cell counts and lower PBMC culture titers but no difference in plasma HIV-1 RNA. Further studies with more potent antiretroviral combination therapies are warranted.
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PMID:Zidovudine treatment in patients with primary (acute) human immunodeficiency virus type 1 infection: a randomized, double-blind, placebo-controlled trial. DATRI 002 Study Group. Division of AIDS Treatment Research Initiative. 965 26

Shock in childhood is most commonly related to injury and blood loss, but hemodynamic compromise is occasionally caused by severe head or spinal injury, tension pneumothorax, myocardial injury, arrhythmias, and sepsis. Regardless of the cause, the initial management of the hypertensive child is establishment of a secure airway, maintenance of ventilation, and initiation of volume replacement via an adequate intravenous catheter. At the present time, crystalloid resuscitation with lactated Ringer's solution and buffering of acidosis with sodium bicarbonate is the standard approach, although in the future hypertonic saline solution may play a role. Hemorrhage may be classified according to the percentage of blood volume lost; losses in excess of 30% of blood volume (class III and IV hemorrhage) usually require administration of packed red blood cells and/or albumin as well. With appropriate management, the typical clinical signs of shock will be reversed and the child will demonstrate improved vital signs, peripheral circulation and sensorium, normalization of body temperature, reversal of metabolic acidosis, and resumption of normal urine output. The more aggressive the approach to resuscitation, the more prompt the patient's response and the more likely morbidity and mortality will be minimized.
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PMID:Hemorrhagic and obstructive shock in pediatric patients. 965 22

Hypotension and shock can be classified as hypotension caused by reduced or maintained left ventricular (LV) ejection. Reduced left ventricular ejection can result from intrinsic left ventricular, aortic valve or mitral valve failure, which includes dilated or ischemic cardiomyopathy, left main trunk disease, acute myocarditis, etc. Acute and subacute severe aortic regurgitation can also cause shock. Echocardiography allows noninvasive diagnosis of infective endocarditis and Takayasu's arteritis to cause severe arotic regurgitation and can also be used to diagnose obstruction of the left ventricular outflow tract. Reduced left ventricular preload can be caused by pericardial effusion and right ventricular ejection failure, and can result from pulmonary embolism, tricuspid regurgitation, right ventricular infarction, tension pneumothorax, hypovolemia and others characterized by a small left ventricle with good ejection fraction. Normal left ventricular ejection may be associated with hypotension. Sepsis, anaphylactic shock and neural disorder are associated with hypotension and normal cardiac output. Pseudohypotension may result from aortic dissection, Takayasu's arteritis, arteriosclerosis obliterans and aortic coarctation. A right parasternal approach enables better visualization of the ascending aorta. Fundamental echochocardiographic scanning allows approximate yet useful diagnosis of hypotension and shock.
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PMID:[Easy echo diagnosis for hypotension and shock]. 1908 1


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