Você pesquisou por y - Critical Care Science (CCS)
You searched for:"Letícia Sandre Vendrame"
We found (8) results for your search.Abstract
Rev Bras Ter Intensiva. 2009;21(1):104-108
DOI 10.1590/S0103-507X2009000100015
Treatment of pulmonary contusion when adequately established is very simple in most cases. Pathophysiological changes occur as a result of the effects produced by loss of chest wall integrity, accumulation of fluid in the pleural cavity, obstruction of the airways and lung dysfunction. The alveolar recruitment maneuver is the reopening of collapsed lung areas by increasing inspiratory pressure in the airway. The primary objective of this case report was to evaluate the effectiveness of the alveolar recruitment maneuver in a patient with pulmonary contusion. A 33 year old male patient, with a clinical condition of bilateral chest trauma and traumatic brain injury, evolved with reduction of the level of consciousness, acute respiratory failure, hypovolemic shock and hemoptysis. The patient underwent thoracentesis, bilateral thoracic drainage and was also submitted to invasive mechanical ventilation. After 48 hours of invasive mechanical ventilation, in accordance with protective strategy an alveolar recruitment maneuver mode, pressure-controlled ventilation, pressure controlled 10 cmH2O, respiratory rate 10 rpm, inspiratory time 3.0, positive end-expiratory pressure 30 cmH2O and FI0(2) 100%, for two minutes. After the alveolar recruitment maneuver, the patient presented clinical pulmonary improvement, but there was a variation of 185 to 322 of Pa0(2)/FiO2 (arterial partial pressure of oxygen/ fraction of inspired oxygen). He was discharged from the intensive care unit 22 days after admission. The alveolar recruitment maneuver in this patient showed significant results in the treatment of pulmonary contusion, improving blood oxygenation, preventing alveolar collapse and reversing atelectasis.
Abstract
Rev Bras Ter Intensiva. 2009;21(1):104-108
DOI 10.1590/S0103-507X2009000100015
Treatment of pulmonary contusion when adequately established is very simple in most cases. Pathophysiological changes occur as a result of the effects produced by loss of chest wall integrity, accumulation of fluid in the pleural cavity, obstruction of the airways and lung dysfunction. The alveolar recruitment maneuver is the reopening of collapsed lung areas by increasing inspiratory pressure in the airway. The primary objective of this case report was to evaluate the effectiveness of the alveolar recruitment maneuver in a patient with pulmonary contusion. A 33 year old male patient, with a clinical condition of bilateral chest trauma and traumatic brain injury, evolved with reduction of the level of consciousness, acute respiratory failure, hypovolemic shock and hemoptysis. The patient underwent thoracentesis, bilateral thoracic drainage and was also submitted to invasive mechanical ventilation. After 48 hours of invasive mechanical ventilation, in accordance with protective strategy an alveolar recruitment maneuver mode, pressure-controlled ventilation, pressure controlled 10 cmH2O, respiratory rate 10 rpm, inspiratory time 3.0, positive end-expiratory pressure 30 cmH2O and FI0(2) 100%, for two minutes. After the alveolar recruitment maneuver, the patient presented clinical pulmonary improvement, but there was a variation of 185 to 322 of Pa0(2)/FiO2 (arterial partial pressure of oxygen/ fraction of inspired oxygen). He was discharged from the intensive care unit 22 days after admission. The alveolar recruitment maneuver in this patient showed significant results in the treatment of pulmonary contusion, improving blood oxygenation, preventing alveolar collapse and reversing atelectasis.
Abstract
Rev Bras Ter Intensiva. 2006;18(1):104-108
DOI 10.1590/S0103-507X2006000100017
BACKGROUND AND OBJECTIVES: This study is a case report of a patient that was submitted to implant of enteric tube (ET) in the ICU, being evidenced false passage in proximal esophagus during endoscopic procedure, demonstrating tunnel for the submucosa. CASE REPORT: A 77 years old woman, transferred to ICU, where ET was installed (due to difficulty of being carried through both nostrils) being confirmed its position through thoraco-abdominal x-ray. The patient remained around 10 days with the ET, receiving diet, without any alteration. In the 10th day she was evolved with melena and reduction of the values of Hb/Ht, without hemodynamic repercussion. Submitted to the high digestive endoscopic that evidenced ulcer injury to bulbar, of about 2.5 cm, with signals of former bleeding. During the examination, a false passage of the ET in proximal esophagus was visualized: 2 cm below of the crico-faring, tunnel for the submucosa possibly for all above-mentioned segments, following its habitual passage until gastric chamber. CONCLUSIONS: Patients of high risk for esophagus perforation for ET installation can be identified and well-taken care of adjusted they can be used. If to occur perforation, this must be identified how much so early possible, for adequate treatment. The adequate treatment depends of each case and same the clinical therapy can be appropriate in selected cases.
Abstract
Rev Bras Ter Intensiva. 2006;18(1):104-108
DOI 10.1590/S0103-507X2006000100017
BACKGROUND AND OBJECTIVES: This study is a case report of a patient that was submitted to implant of enteric tube (ET) in the ICU, being evidenced false passage in proximal esophagus during endoscopic procedure, demonstrating tunnel for the submucosa. CASE REPORT: A 77 years old woman, transferred to ICU, where ET was installed (due to difficulty of being carried through both nostrils) being confirmed its position through thoraco-abdominal x-ray. The patient remained around 10 days with the ET, receiving diet, without any alteration. In the 10th day she was evolved with melena and reduction of the values of Hb/Ht, without hemodynamic repercussion. Submitted to the high digestive endoscopic that evidenced ulcer injury to bulbar, of about 2.5 cm, with signals of former bleeding. During the examination, a false passage of the ET in proximal esophagus was visualized: 2 cm below of the crico-faring, tunnel for the submucosa possibly for all above-mentioned segments, following its habitual passage until gastric chamber. CONCLUSIONS: Patients of high risk for esophagus perforation for ET installation can be identified and well-taken care of adjusted they can be used. If to occur perforation, this must be identified how much so early possible, for adequate treatment. The adequate treatment depends of each case and same the clinical therapy can be appropriate in selected cases.
Abstract
Rev Bras Ter Intensiva. 2007;19(2):205-209
DOI 10.1590/S0103-507X2007000200011
BACKGROUND AND OBJECTIVES: Obesity is an epidemic disease reaching more than 300 million people all over the world. Its prevalence has increased during the past few years and according to some studies its mortality in the critically ill patient seems to be much higher, especially among patients who were submitted to surgery. This study has as objective to discuss some particularities of managing obese patients in the intensive care unit after bariatric surgery. CONTENTS: The rate of obese patient in the ICU ranges from 9% to 26% and the increase in the number of bariatric surgeries has raised the number of obese patients in the ICU. It is important to know the physiopathology of obesity and to treat its particularities during the postoperative care. Such as pulmonary restriction, that causes an increase in pulmonary complications, coronary artery disease and thromboembolic events. CONCLUSIONS: The number of patients that undergo to bariatric surgery has increased; therefore, the number of obese patients in the ICU has also risen. Different physiological events and complications in obese patients are challenges to clinical practice. The knowledge of obese physiopathology helps in the managing routine procedures and complications after bariatric surgery.
Abstract
Rev Bras Ter Intensiva. 2007;19(2):205-209
DOI 10.1590/S0103-507X2007000200011
BACKGROUND AND OBJECTIVES: Obesity is an epidemic disease reaching more than 300 million people all over the world. Its prevalence has increased during the past few years and according to some studies its mortality in the critically ill patient seems to be much higher, especially among patients who were submitted to surgery. This study has as objective to discuss some particularities of managing obese patients in the intensive care unit after bariatric surgery. CONTENTS: The rate of obese patient in the ICU ranges from 9% to 26% and the increase in the number of bariatric surgeries has raised the number of obese patients in the ICU. It is important to know the physiopathology of obesity and to treat its particularities during the postoperative care. Such as pulmonary restriction, that causes an increase in pulmonary complications, coronary artery disease and thromboembolic events. CONCLUSIONS: The number of patients that undergo to bariatric surgery has increased; therefore, the number of obese patients in the ICU has also risen. Different physiological events and complications in obese patients are challenges to clinical practice. The knowledge of obese physiopathology helps in the managing routine procedures and complications after bariatric surgery.
Abstract
Rev Bras Ter Intensiva. 2006;18(3):292-297
DOI 10.1590/S0103-507X2006000300012
BACKGROUND AND OBJECTIVES: The Stevens Johnson Syndrome (SJS) and Toxical Epidermal Necrolisys (TEN) are important skin and mucosal lesions that need intensive care treatment. The aim of this article is to show a literature review about SJS and TEN. CONTENTS: This article reviews the concepts, diagnostic topics, clinical presentation and the principle of basic treatment in Intensive Care Unit for SJS and TEN. CONCLUSIONS: These illnesses are characterized as dermatological emergencies and its adequate management and cares must be part of the routine knowledge of the intensive care doctors.
Abstract
Rev Bras Ter Intensiva. 2006;18(3):292-297
DOI 10.1590/S0103-507X2006000300012
BACKGROUND AND OBJECTIVES: The Stevens Johnson Syndrome (SJS) and Toxical Epidermal Necrolisys (TEN) are important skin and mucosal lesions that need intensive care treatment. The aim of this article is to show a literature review about SJS and TEN. CONTENTS: This article reviews the concepts, diagnostic topics, clinical presentation and the principle of basic treatment in Intensive Care Unit for SJS and TEN. CONCLUSIONS: These illnesses are characterized as dermatological emergencies and its adequate management and cares must be part of the routine knowledge of the intensive care doctors.
Abstract
Rev Bras Ter Intensiva. 2006;18(3):307-310
DOI 10.1590/S0103-507X2006000300014
BACKGROUND AND OBJECTIVES: The diffuse axonal polyneuropathy, more commonly known as Critical Illness Polyneuropathy (CIP), has been discussed by authors by decades; however, it has only been deeply studied over the last thirty years, becoming more important as an important cause of long term dependence on mechanical ventilation by seriously ill patients in intensive care medicine. CONTENTS: A significant reason for such interest is due to the importance of the CIP as complication of the septic shock and in patients with multiple organ failure, as much as responsible for the prolonging hospitalization in the Intensive Care Unit, as for the gradual reduction of the chance of survival. It has been suggested that the polyneuropathy is related with cytokines and other mediators which would increase the permeability of the vases, resulting in endoneural edema and causing the axonal injury. It is difficult to do the initial diagnostic, which, in general, are only possibly recognized when the sepsis complications or the multiple organs failure have been satisfactorily controlled. The diagnosis is made through the eletroneuromiography exam, and although there is still no effective drug treatment other than the control of the basic illness, it is consensus among multidisciplinary team that the development of the CIP does not have to be understood as a way to reduce the intensity of treatment. CONCLUSIONS: Spit of your prevalence, it is still unknown the mainly factors which are physiopathology associated as soon as your correct therapy.
Abstract
Rev Bras Ter Intensiva. 2006;18(3):307-310
DOI 10.1590/S0103-507X2006000300014
BACKGROUND AND OBJECTIVES: The diffuse axonal polyneuropathy, more commonly known as Critical Illness Polyneuropathy (CIP), has been discussed by authors by decades; however, it has only been deeply studied over the last thirty years, becoming more important as an important cause of long term dependence on mechanical ventilation by seriously ill patients in intensive care medicine. CONTENTS: A significant reason for such interest is due to the importance of the CIP as complication of the septic shock and in patients with multiple organ failure, as much as responsible for the prolonging hospitalization in the Intensive Care Unit, as for the gradual reduction of the chance of survival. It has been suggested that the polyneuropathy is related with cytokines and other mediators which would increase the permeability of the vases, resulting in endoneural edema and causing the axonal injury. It is difficult to do the initial diagnostic, which, in general, are only possibly recognized when the sepsis complications or the multiple organs failure have been satisfactorily controlled. The diagnosis is made through the eletroneuromiography exam, and although there is still no effective drug treatment other than the control of the basic illness, it is consensus among multidisciplinary team that the development of the CIP does not have to be understood as a way to reduce the intensity of treatment. CONCLUSIONS: Spit of your prevalence, it is still unknown the mainly factors which are physiopathology associated as soon as your correct therapy.
Abstract
Rev Bras Ter Intensiva. 2007;19(4):490-493
DOI 10.1590/S0103-507X2007000400015
BACKGROUND AND OBJECTIVES: Hepatic infarction is characterized by parenchyma ischemic necrosis involving at least two acinis. It is extremely uncommon due to the arterial and portal venous blood supply. We report a case of a patient not know to have diabetes who developed massive areas of ischemic infarcts of the liver after episode of acutely diabetes decompensated. CASE REPORT: A 67 year-old hypertensive female who has been presenting, for the last 10 days, polydipsia, high urinary volume, visual and gait impairment, nausea and vomiting was admitted to the emergency room (ER). During the physical examination it was observed dehydration, skin discoloration, peripheral cyanosis, hypothermia, tachycardia, hypotension and mild diffuse abdominal pain. Admissional laboratory exams demonstrated total leukocytes: 16.800, Cr: 3.7, Ur: 167, Na: 133, K: 6.9, glucose: 561; arterial gasometry (O2 catheter: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, B.E.: -28.8, HCO3: 2.4, Sat 91.3%, lactato: 79; urinalysis: pH: 6; leukocytes: 13; density: 1015; erythrocytes: 19; protein: ++; glucose: +++; bilirubin: negative; ketonic bodies: + denote ketonemia. EKG: sharp T wave, right branch block. Patient was treated with intravenous insulin, hydration, sodium bicarbonate and ceftriaxone. After initial treatment, the laboratory exams showed Cr: 2.2, Ur: 122, Na: 162, K: 4.3, Ca: 6.4, glucose: 504, pH: 7.01, HCO3: 7.1, B.E.: -22. One day after admission the patient presented with important abdominal pain and peritoneal irritation, followed by difficulty for talking and somnolence; routine laboratory exams showed arterial gasometry: pH: 7.4, pCO2: 31, pO2: 68, BE: -4.4, HCO3: 19, SatO2: 93.5%; Ur: 95,Cr: 1.4, albumin: 2.4, Ca: 0.95, Na: 166, K:4, bilirubin: 0.5, bilirubin D/I: 0.2/0.3, Amylase: 1157, Gamma-GT: 56, AST 7.210, ALT: 2.470, SR (sedimentation rate): 15, Lipase: 84. Abdominal ultrasound was unremarkable. Patient respiratory function and conscience level worsened, requiring intubation. Despite all resuscitation efforts, she died. Necropsy showed multiple ischemic infarcts of the liver with vascular thrombosis, splenic infarcts, generalized visceral congestion and atherosclerosis of aorta and its branches. Pancreas was normal. CONCLUSIONS: The mechanisms of hepatic and splenic infarctions in this case were unclear. The following factors may have contributed to necrosis: vomiting and fever should be considered to induce dehydration and hypotension, which further decreased portal and hepatic arterial inflows; elevated level of catecholamine in hyperglycemic states might induce vasoconstriction effects; widespread atherosclerosis is commonly seen in diabetic and hypertensive patients. This case underlies the importance of searching for hepatic necrosis or infarction in any diabetic patient with elevated liver enzymes. Anticoagulation therapy should be instituted promptly upon recognition of vascular thromboses.
Abstract
Rev Bras Ter Intensiva. 2007;19(4):490-493
DOI 10.1590/S0103-507X2007000400015
BACKGROUND AND OBJECTIVES: Hepatic infarction is characterized by parenchyma ischemic necrosis involving at least two acinis. It is extremely uncommon due to the arterial and portal venous blood supply. We report a case of a patient not know to have diabetes who developed massive areas of ischemic infarcts of the liver after episode of acutely diabetes decompensated. CASE REPORT: A 67 year-old hypertensive female who has been presenting, for the last 10 days, polydipsia, high urinary volume, visual and gait impairment, nausea and vomiting was admitted to the emergency room (ER). During the physical examination it was observed dehydration, skin discoloration, peripheral cyanosis, hypothermia, tachycardia, hypotension and mild diffuse abdominal pain. Admissional laboratory exams demonstrated total leukocytes: 16.800, Cr: 3.7, Ur: 167, Na: 133, K: 6.9, glucose: 561; arterial gasometry (O2 catheter: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, B.E.: -28.8, HCO3: 2.4, Sat 91.3%, lactato: 79; urinalysis: pH: 6; leukocytes: 13; density: 1015; erythrocytes: 19; protein: ++; glucose: +++; bilirubin: negative; ketonic bodies: + denote ketonemia. EKG: sharp T wave, right branch block. Patient was treated with intravenous insulin, hydration, sodium bicarbonate and ceftriaxone. After initial treatment, the laboratory exams showed Cr: 2.2, Ur: 122, Na: 162, K: 4.3, Ca: 6.4, glucose: 504, pH: 7.01, HCO3: 7.1, B.E.: -22. One day after admission the patient presented with important abdominal pain and peritoneal irritation, followed by difficulty for talking and somnolence; routine laboratory exams showed arterial gasometry: pH: 7.4, pCO2: 31, pO2: 68, BE: -4.4, HCO3: 19, SatO2: 93.5%; Ur: 95,Cr: 1.4, albumin: 2.4, Ca: 0.95, Na: 166, K:4, bilirubin: 0.5, bilirubin D/I: 0.2/0.3, Amylase: 1157, Gamma-GT: 56, AST 7.210, ALT: 2.470, SR (sedimentation rate): 15, Lipase: 84. Abdominal ultrasound was unremarkable. Patient respiratory function and conscience level worsened, requiring intubation. Despite all resuscitation efforts, she died. Necropsy showed multiple ischemic infarcts of the liver with vascular thrombosis, splenic infarcts, generalized visceral congestion and atherosclerosis of aorta and its branches. Pancreas was normal. CONCLUSIONS: The mechanisms of hepatic and splenic infarctions in this case were unclear. The following factors may have contributed to necrosis: vomiting and fever should be considered to induce dehydration and hypotension, which further decreased portal and hepatic arterial inflows; elevated level of catecholamine in hyperglycemic states might induce vasoconstriction effects; widespread atherosclerosis is commonly seen in diabetic and hypertensive patients. This case underlies the importance of searching for hepatic necrosis or infarction in any diabetic patient with elevated liver enzymes. Anticoagulation therapy should be instituted promptly upon recognition of vascular thromboses.
Abstract
Rev Bras Ter Intensiva. 2006;18(1):95-98
DOI 10.1590/S0103-507X2006000100015
BACKGROUND AND OBJECTIVES: Iatrogenic conditions was due of the medical, correctly intervention or not, justified or not, which harmful consequences to the patient. The cares in Intensive Care Medicine present substantial challenges with relation to the security of the patient. The objective of this article is to make one brief revision of literature on the iatrogenic in its concepts and basic terms and its taxes prevalence in Intensive Care Medicine. CONTENTS: Intensive Care Medicine supplies subsidies that improve the morbidity and mortality, but that also the significant risks of adverse events and serious errors associate. The Iatrogenic can be minimized with the adequate monitorization or can be friction as waited aggravation, idiopathic and if to perpetuate in the anonymity. CONCLUSIONS: It is basic to recognize the necessity of the constant learning and recycling and conscience of the susceptibilities to the error; in this context, the respect for the human being must guide the professional behavior.
Abstract
Rev Bras Ter Intensiva. 2006;18(1):95-98
DOI 10.1590/S0103-507X2006000100015
BACKGROUND AND OBJECTIVES: Iatrogenic conditions was due of the medical, correctly intervention or not, justified or not, which harmful consequences to the patient. The cares in Intensive Care Medicine present substantial challenges with relation to the security of the patient. The objective of this article is to make one brief revision of literature on the iatrogenic in its concepts and basic terms and its taxes prevalence in Intensive Care Medicine. CONTENTS: Intensive Care Medicine supplies subsidies that improve the morbidity and mortality, but that also the significant risks of adverse events and serious errors associate. The Iatrogenic can be minimized with the adequate monitorization or can be friction as waited aggravation, idiopathic and if to perpetuate in the anonymity. CONCLUSIONS: It is basic to recognize the necessity of the constant learning and recycling and conscience of the susceptibilities to the error; in this context, the respect for the human being must guide the professional behavior.
Abstract
Rev Bras Ter Intensiva. 2008;20(1):99-102
DOI 10.1590/S0103-507X2008000100016
BACKGROUND AND OBJECTIVES: Hyperleukocytosis (> 100 x 10(9)/L) is an uncommon presentation of chronic leukemias and it can present clinical symptoms of hyperviscosity syndrome. Hearing loss and blindness rarely occurs in patients with leukemia; however, it can be strong association with hyper-viscosity syndrome. The purpose of this paper is to report a case of acute hearing loss as the initial manifestation of acute leukemia and hyper-viscosity syndrome and also mainly aspects of the intensive care treatment. CASE REPORT: A 41 year-old, male patient, who has been complaining about dizziness for six months with no response to symptomatic medications, was admitted to the emergency department with acute hearing loss. The physical examination was normal except for a bilateral hearing loss without an apparent cause. Laboratory exams showed total leukocyte: 645.000 with 66.4% blasts, hemoglobin: 7.0, hematocrit: 20.5, urea: 94, creatinine: 1.59, K: 5.6, Na: 138, INR: 1.38, TTPa: 0.89, troponin lower than 0.2, CK: 218, CKMB: 50, uric acid: 11.1. After a first hypothesis of leukemia with a high risk of hyper-viscosity complications, the patient was admitted to the Intensive Care Unit for monitoring and treatment. A bone marrow biopsy was performed and than started hidratation, hydroxyurea, allopurinol, dexamethasone. According to hematologists the patient had a chronic myeloid leukemia. Leukopheresis was performed one week after admission when total blood leukocytes were around 488.000. Ten days after the procedure the patient had no improvement of the hearing loss but total leukocytes were 10.100. He was discharge to the ward and 2 weeks later went home to continue ambulatory treatment. CONCLUSIONS: The frequency of sensitive manifestations in patients with leukemia include not only visual and hearing loss but also many others manifestations such as conductive vertigo, facial palsy and infections. Hyperviscosity syndrome due to hyperleukocytosis is also a possible cause of sensorial loss, but the syndrome is often dependent on leukocyte counts greater than (>100 x 10(9)/L).This case is a representative of rare cases in which acute sensorineural hearing loss occurred as the initial manifestation of hyper-viscosity syndrome due to leukemia.
Abstract
Rev Bras Ter Intensiva. 2008;20(1):99-102
DOI 10.1590/S0103-507X2008000100016
BACKGROUND AND OBJECTIVES: Hyperleukocytosis (> 100 x 10(9)/L) is an uncommon presentation of chronic leukemias and it can present clinical symptoms of hyperviscosity syndrome. Hearing loss and blindness rarely occurs in patients with leukemia; however, it can be strong association with hyper-viscosity syndrome. The purpose of this paper is to report a case of acute hearing loss as the initial manifestation of acute leukemia and hyper-viscosity syndrome and also mainly aspects of the intensive care treatment. CASE REPORT: A 41 year-old, male patient, who has been complaining about dizziness for six months with no response to symptomatic medications, was admitted to the emergency department with acute hearing loss. The physical examination was normal except for a bilateral hearing loss without an apparent cause. Laboratory exams showed total leukocyte: 645.000 with 66.4% blasts, hemoglobin: 7.0, hematocrit: 20.5, urea: 94, creatinine: 1.59, K: 5.6, Na: 138, INR: 1.38, TTPa: 0.89, troponin lower than 0.2, CK: 218, CKMB: 50, uric acid: 11.1. After a first hypothesis of leukemia with a high risk of hyper-viscosity complications, the patient was admitted to the Intensive Care Unit for monitoring and treatment. A bone marrow biopsy was performed and than started hidratation, hydroxyurea, allopurinol, dexamethasone. According to hematologists the patient had a chronic myeloid leukemia. Leukopheresis was performed one week after admission when total blood leukocytes were around 488.000. Ten days after the procedure the patient had no improvement of the hearing loss but total leukocytes were 10.100. He was discharge to the ward and 2 weeks later went home to continue ambulatory treatment. CONCLUSIONS: The frequency of sensitive manifestations in patients with leukemia include not only visual and hearing loss but also many others manifestations such as conductive vertigo, facial palsy and infections. Hyperviscosity syndrome due to hyperleukocytosis is also a possible cause of sensorial loss, but the syndrome is often dependent on leukocyte counts greater than (>100 x 10(9)/L).This case is a representative of rare cases in which acute sensorineural hearing loss occurred as the initial manifestation of hyper-viscosity syndrome due to leukemia.
