Intensive therapy failure

A 23-year-old woman took 60 tablets of amlodipine intentionally and developed tachycardia and severe hypotension. She did not improve with intensive therapy and developed left ventricular failure and oliguria and underwent hemodiafiltration. Her condition slowly improved over 4 days. 

Patients requiring intensive therapy for advanced heart failure may present via several pathways. Patients with chronic progressive heart... 

In the Treat to New Targets (TNT) trial, more intensive therapy with atorvastatin, 80 mg/day, was compared with atorvastatin 10 mg/day in 10,001 patients with stable CHD [46] 15,464 patients were originally recruited with LDL-cholesterol 3.4-6.5 mmol/L. All patients received 8-week run-in therapy with atorvastatin 10 mg/day. If an LDL-cholesterol target <3.4 mmol/L was achieved, patients were rerandomised to take 10 or 80 mg/day. About 5461 patients were excluded because of failure to reach this target. Over a mean follow-up of 4.9 years, LDL-cholesterol in the intensively treated group was... 

If there is dear evidence of worsening prompt hospital admission for intensive therapy is necessary. As the availability of a suitable donor heart is not predictable, hemodynamic deterioration is first treated with intravenous inotropic support. When the low-cardiac-output syndrome continues to be refractory, patients are put on a mechanical circulatory device for temporary mechanical support. This bridge to transplantation concept enables patient stabilization, withdrawal of intravenous medication (inotropic agents, catecholamines, calcium sensitizers) and rehabilitation (Antretter et al. 2002a). During chronic mechanical circulatory support a low level of exercise is possible and the patients are able to walk around, to leave hospital and sometimes they are followed up by heart failure specialists in an outpatient clinic. Nearly 25% of the most recent cohort transplanted from 1 January, 2001 to 30 June, 2003 were on some type of mechanical circulatory support (Taylor et al. 2004). 

High-risk patients Hypertensive patients at risk of excessive hypotension include those with the following concurrent conditions or characteristics Heart failure, hyponatremia, high-dose diuretic therapy, recent intensive diureses or increase in diuretic dose, renal dialysis, or severe volume or salt depletion of any etiology. Single doses of enalaprilat as low as 0.2 mg have produced excessive hypotension in normotensive patients with these diagnoses. Because of the potential for an extreme hypotensive response in these patients, initiate therapy under very close medical supervision. The... 

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

Selection of the LSD dose is on the bases indicated earlier. In most cases, we have worked within the range of 200-400 fig. Some persons have reacted intensely to only too fig. We conceive of therapy as consisting of from one to five sessions at approximately weekly intervals. The patient should understand that his treatment will not last beyond a few sessions at the most, and possibly only one. Failure to achieve success within five sessions indicates a need for non-drug therapy. After six months to a year, and if the problem remains, an-... 

A patient developed atorvastatin-induced severe autoimmune hepatitis and a lupus-like syndrome. Although the drug was immediately withdrawn, the disease persisted and deteriorated to a fulminant form with acute hepatic failure. There was no response to conventional immunosuppression with glucocorticoids and azathioprine. Only the introduction of intense immunosuppressive therapy, as used in solid organ transplantation, led to a complete and sustained recovery. The patient had the HLA haplotypcs DR3 and DR4, which are well-known genetic factors associated with autoimmune diseases. 

Acute poisoning is treated with gastric aspiration and lavage combined with intensive supportive therapy, including thorough assessment of the patient plus measures to prevent respiratory failure. In cases of very severe poisoning, peritoneal dialysis or hemodialysis may be necessary. 

The water-soluble salt of vitamin K3 (menadione) should never be used in therapeutics. It is particularly ineffective in the treatment of warfarin overdosage. Vitamin K deficiency frequently occurs in hospitalized patients in intensive care units because of poor diet, parenteral nutrition, recent surgery, multiple antibiotic therapy, and uremia. Severe hepatic failure results in diminished protein synthesis and a hemorrhagic diathesis that is unresponsive to vitamin K. 

Acute pancreatitis is usually a self-limiting disease, which regresses spontaneously without further complications. However, in about 20% of cases it leads to organ failure and/or local complications and is associated with high morbidity and mortality rates (B15). Therefore, numerous attempts have been made to predict early the severe course of acute pancreatitis and to assess the possibility of complications. Objective identification of the risk of complications or death is essential for selection of those patients who should be hospitalized in the intensive care unit (ICU) and be subjected to more expensive and aggressive investigations. Moreover, it also permits interinstitutional comparison of data stratified for severity at admission and at the time of therapy. 

Acute renal failure secondary to ischemia-reperfusion or nephro-toxins represents a major cause of morbidity and mortality in hospitalized patients, particularly in the intensive care unit setting. The proximal tubule region of the nephron suffers the most damage in acute renal injury and is therefore the target site of therapeutic interventions. While several experimental therapies have been attempted to prevent or hasten recovery from acute renal injury,... 

Supportive therapy for acute opioid poisoning may be performed first by stomach wash, and then laxative and intensive supportive therapy to treat respiratory failure and shock. Further, naloxone may be given to treat severe respiratory depression and coma. However, intravenous infusions are preferred if the toxicity is the result of a long-acting opioid. The treatment of adverse effects itself may cause withdrawal symptoms.32... 

Four HIV-infected children undergoing intense antiretroviral combination therapy were switched to regimens including amprenavir and efavirenz after the failure of other drugs (9). Pharmacokinetic studies suggested that combinations of these drugs can result in suboptimal concentrations of amprenavir. This was evident in two of the children taking amprenavir and efavirenz, in combination with two NRTIs, who had undetectable concentrations of amprenavir within 4 hours of administration. The addition of ritonavir to the combination restored the blood concentrations of amprenavir to those normally recorded (median 3500 ng/ml). The most probable reason for this effect is enhanced metabolism of amprenavir due to induction by efavirenz. 

Doxazosin, and perhaps the whole class of alpha-blockers, should no longer be considered as first-line anti-hjrpertensive therapy. Doxazosin can still be used for sjmptom rehef in patients with nocturia secondary to prostatic hjrperplasia, although it should probably be avoided in patients with manifest or latent congestive heart failure (3). This issue has been intensely debated (4). 

Basic life-support measures should be instituted as necessary. Intensive support therapy may be required to correct respiratory failure and shock. Patients with mild to moderate toxicity may present with lethargy, miosis, decreased blood pressure, heart rate, temperature, and skeletal muscle tone. In patients experiencing severe toxicity, coma, respiratory depression, noncardiogenic pulmonary edema, apnea,... 

These questions of efficacy are especially important as new aerosol therapies are evaluated. Of special importance is the need for careful evaluation of aerosol treatments for acute lung injury, i.e., for patients in respiratory failure who are on a mechanical ventilator in an intensive care unit (ICU). Application of new therapies such as aerosol surfactant, various vasodilators, and others should not be adopted until clear proof of improved outcome is documented. 

Lack of muscle adenylate deaminase has been found in some muscle disorders in which other abnormalities could not be identified. Failure to produce ammonia during intense effort may be diagnostic. In the heart, AMP accumulation is typically due to ischemia, and the adenosine released as a result is a potent coronary vasodilator. Accordingly, myocardium has less adenylate deaminase than skeletal muscle. However, large losses of adenosine from myocardium are dangerous because they lead to a decrease in ATP concentration that does not respond to dilation, thrombolytic, or oxygen therapy. Lack of adenosine deaminase in lymphoid tissue causes a severe immunodeficiency (Chapter 27). 

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