Cases reported "Multiple Organ Failure"

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1/22. The abdominal compartment syndrome: a report of 3 cases including instance of endocrine induction.

    Three patients with the abdominal compartment syndrome are presented and discussed. In one of the patients the condition was induced in an endocrine fashion, since trauma was sustained exclusively by the middle third of the left leg. The development of the syndrome as a remote effect of local trauma has never been reported previously. In all three instances only insignificant amounts of intraperitoneal fluid was found and the increase in abdominal pressure was due to severe edema of the mesentery and retroperitoneum. Since the condition is highly lethal, early diagnosis is imperative, and this starts by carrying a high index of suspicion. Measurement of the intraperitoneal pressure easily confirms this diagnosis. It is emphasized that measurements at various sites, like bladder and stomach, in each patient is essential to confirm the diagnosis, since one of the sites may be rendered unreliable due to intraperitoneal processes impinging on the affected site and affecting its distensibility.
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2/22. Acute pancreatic damage associated with convulsive status epilepticus: a report of three cases.

    Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures.
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3/22. Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion.

    The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's glasgow coma scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.
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4/22. Japanese spotted fever associated with multiorgan failure.

    A 49-year-old man was admitted to our hospital, with a diagnosis of multiple organ failure, on June 10, 2000. physical examination revealed high fever, generalized maculopapular erythema, and an eschar on his lower leg. Laboratory findings revealed severe renal and liver dysfunction, disseminated intravascular coagulation (DIC), and markedly elevated soluble interleukin 2-receptor (sIL2-R) level (>10 000 U/ml). Administration of minocycline was started immediately, with a diagnosis of rickettsial infection. Simultaneously, anti-thrombin III and heparin were started to treat the DIC, and hemodialysis was also initiated. However, the day after admission, his consciousness level lapsed, to the level of coma, and blood pressure was less than 60 mmHg, indicating shock. Therefore, 500 mg of methylprednisolone was administered once; as a result, rapid pyretolysis and improvement of consciousness disturbance were achieved. Laboratory data indicative of inflammation gradually improved after a few days. Hemodialysis was required ten times. During the recovery period, the level of specific IgM antibody against rickettsia japonica increased to x2560, and he was diagnosed as having Japanese spotted fever. On July 11, he was discharged without sequelae. The course in our patient was very severe, and treatment with minocycline alone may have resulted in a fatal outcome. The level of sIL2-R, which is produced by activated lymphocytes, was markedly increased. Therefore, markedly elevated lymphocyte activation and hypercytokinemia may have been present on admission. The short-term steroid therapy may have been effective in inhibiting the excessive activation of lymphocytes in the critical stage. In the severe form of Japanese spotted fever with organ failure, combination therapy with minocycline and short-term steroids may be very useful.
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5/22. Hypercapnic respiratory failure and partial upper airway obstruction during high frequency oscillatory ventilation in an adult burn patient.

    PURPOSE: To present a case of severe hypercapnic respiratory failure in an adult burn patient and to describe our clinical problem solving approach during support with an unconventional mode of mechanical ventilation. CLINICAL FEATURES: A 19-yr-old male with smoke inhalation and flame burns to 50% total body surface area was admitted to the Ross Tilley Burn Centre. High frequency oscillatory ventilation (HFOV) was initiated on day three for treatment of severe hypoxemia. By day four, the patient met consensus criteria for acute respiratory distress syndrome. On day nine, alveolar ventilation was severely compromised and was characterized by hypercapnea (PaCO(2) 136 mmHg) and acidosis (pH 7.10). Attempts to improve CO(2) elimination by a decrease in the HFOV oscillatory frequency and an increase in the amplitude pressure failed. An intentional orotracheal tube cuff leak was also ineffective. A 6.0-mm nasotracheal tube was inserted into the supraglottic hypopharynx to palliate presumed expiratory upper airway obstruction. After nasotracheal tube placement, an intentional cuff leak of the orotracheal tube improved ventilation (PaCO(2) 81 mmHg) and relieved the acidosis (pH 7.30). The improvement in ventilation (with normal oxygen saturation) was sustained until the patient's death from multiple organ dysfunction four days later. CONCLUSION: During HFOV in burn patients, postresuscitation edema of the supraglottic upper airway may cause expiratory upper airway obstruction. The insertion of a nasotracheal tube, combined with an intentional orotracheal cuff leak may improve alveolar ventilation during HFOV in such patients.
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6/22. Cardiac failure and multiple organ dysfunction syndrome in a patient with endocrine adenomatosis.

    In this case report, we present the successful therapy of severe cardiac failure in pituitary adrenal insufficiency. A previously healthy 56-year-old-man in pituitary coma due to an atypical variant of multiple endocrine adenomatosis (pituitary adenoma and pheochromocytoma) suffered from cardiac failure resistant to catecholamine and standard hydrocortisone therapy. After two bolus injections of dexamethasone (2 x 24 mg) mean arterial pressure and cardiac function dramatically improved, probably due to restoration of permissive effects on catecholamine action and reversal of pathophysiological mechanisms of cardiac failure. We conclude that in patients with severe cardiovascular failure in pituitary coma the administration of potent glucocorticoids may be more effective in reversing cardiovascular failure than standard dosages of hydrocortisone.
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7/22. multiple organ failure with the adult respiratory distress syndrome in homicidal arsenic poisoning.

    A 30-year-old man and a 39-year-old woman, who was 28 weeks pregnant, were simultaneously poisoned by eating chocolate containing arsenic trioxide. They developed a picture of multiple organ failure peaking around the 8th to 10th day after ingestion, with the development of life-threatening adult respiratory distress syndrome (ARDS) in both patients. This rarely reported complication of arsenic poisoning was managed successfully by intubation and mechanical ventilation with positive end expiratory pressure in both patients. Hemodynamic and laboratory data are presented supporting the clinical course. Arsenic toxicity further resulted in intrauterine fetal death. The effects of severe arsenic poisoning leading to early multiple organ failure with ARDS as well as to protracted, debilitating polyneuropathy are discussed.
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8/22. Agnogenic myeloid metaplasia with pleural extramedullary leukemic transformation.

    Agnogenic myeloid metaplasia (AMM) is one of the myeloproliferative disorders, and is usually accompanied by extramedullary hematopoiesis (EMH) in various organs, mainly in the liver, spleen and lymph nodes. Extramedullary hematopoiesis and/or leukemic transformation of EMH in the pleura is a rare occurrence and is usually asymptomatic. Pleural involvement is usually diagnosed on postmortem examination. Herein we describe a 71-year-old man with newly diagnosed agnogenic myeloid metaplasia who was evaluated for progressively worsening dyspnea, pulmonary hypertension and bilateral pleural effusions. EMH involving the lungs and pleura was suspected. A sulfur colloid technetium 99m bone marrow scan performed to detect extramedullary hematopoiesis was negative. The diagnostic thoracentesis yielded bloody fluid that contained a large population of myeloblasts, indicating pleural leukemic transformation. The patient received 100 cGy to the whole lung for treatment of pulmonary hypertension due to EMH. This was followed by 1500 cGy total dose of radiation to the left lung for pleural extramedullary leukemic transformation. Pleural effusions resolved and repeat echocardiography showed reduction of the pulmonary artery pressure. Three months later he had leukemic transformation involving the skin and lymph nodes. Four months after radiation therapy, he had full-blown acute myeloid leukemia. He received 2 cycles of Gemtuzumab ozogamicin (Mylotarg), allopurinol and hydroxyurea. Three months after initiation of chemotherapy, he deteriorated and received salvage chemotherapy of prednisone, VP-16 and imatinib mesylate (Gleevec). He was hospitalized for neutropenic fever and was diagnosed to have pulmonary aspergillosis. He died of multisystem failure 8 1/2 months after being diagnosed with AMM.
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9/22. Employing vasopressin as an adjunct vasopressor in uncontrolled traumatic hemorrhagic shock. Three cases and a brief analysis of the literature.

    Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.
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10/22. multiple organ failure caused by end-stage liver disease successfully treated with living donor liver transplantation using perioperative percutaneous cardiopulmonary support: a case report.

    A 54-year-old female diagnosed with primary biliary cirrhosis (PBC) 10 years earlier was referred for a living donor liver transplant (LDLT). During her workup, she developed pulmonary edema and respiratory failure due to aspiration pneumonia, which required artificial ventilation. The PaO2/FiO2 (P/F) ratio at that time was 60. Although continuous hemodiafiltration (CHDF) and plasma exchange (PE) were initiated, improvement in the P/F ratio was limited to 133. As transplantation was the only approach to save this patient, we performed LDLT using a right lobe graft aided by percutaneous cardiopulmonary support (PCPS). The graft weight was 650 g and the graft weight/recipient weight ratio was 1.6%. During LDLT, the patient's cardiopulmonary function was stable with PCPS, and the surgical procedure was completed without complications. Following the surgery, she continued to have high-end inspiratory pressure and progressed to the chronic phase of adult respiratory distress syndrome (ARDS). We treated her with low-dose steroid therapy and she improved gradually. The patient was weaned off mechanical ventilation and was discharged approximately 25 weeks after LDLT. In the condition of cardiac or respiratory failure, cadaveric liver transplantation using plasmapheresis is contraindicated because of the associated high mortality rate. Our case suggests that if infections are controlled, a patient with multiple organ failure (MOF) due to end-stage liver disease might be successfully treated with LDLT aided by plasmapheresis and PCPS.
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