Brugada-like electrocardiographic patterns induced by hyperkalemia.

Brugada syndrome was described in 1992 as a new clinical and electrocardiographic syndrome involving susceptibility to ventricular arrhythmias and sudden cardiac death in patients with no obvious structural heart disease. Brugada syndrome is characterized by a hereditary anomaly in the sodium ion channel (mutation of the SCN5A gene) identified by a wide QRS associated with the ST-segment elevation and the T­wave inversion in the right precordial leads. The Brugada-like electrocardiographic pattern can be caused by sodium channel-blocking drugs and electrolyte disorders. Hyperkalemia may produce multiple ECG abnormalities, including the ST-segment elevation and pseudomyocardial infarction with a resolution of these abnormalities after the correction of hyperkalemia. This article describes 8 cases of pseudoanteroseptal myocardial infarction in acute renal insufficiency with hyperkalemia. The ST-segment elevation related to hyperkalemia is resolved by the reduced serum potassium level. Clinicians should recognize that hyperkalemia is one of the etiologies of the Brugada-like electrocardiographic pattern.

[Muscle crush injury and crush syndrome]. / Raumenu sutraiskymas ir sutraiskymo sindromas.

Crush injury is defined as compression of extremities or other parts of the body that causes muscle breakdown (traumatic rhabdomyolysis). Systemic consequences of crush injuries are as follows: rhabdomyolysis, electrolyte and acid-base abnormalities, hypovolemia, and acute renal failure. Crush injuries are important injuries in disaster situations: earthquakes, hurricanes, mining and road traffic accidents, war, collapse of buildings, etc. In this review article, there are discussed about epidemiology of crush syndrome, risk factors, pathophysiology (mechanisms of muscle cell injury, release of substances from injured muscles, other consequences of reperfusion), clinical features, differential diagnosis, investigations, complications (acute renal failure, hypovolemic shock, hyperkalemia, infection, compartment syndrome), approach to treatment (adequate rehydration, a forced mannitol-alkaline diuresis, intravenous fluids, management of hyperkalemia, wound care, hyperbaric oxygen, etc.), prognosis, the mortality rate and prevention (timely support may reduce morbidity and mortality).

[Use of recombinant activated factor VII]. / Rekombinantinio aktyvinto VII kresejimo faktoriaus vartojimas.

Recombinant activated factor VII (rFVIIa) has been used in the treatment of various congenital and acquired hemostatic disorders for more than 10 years. Hemostasis is initiated by the FVIIa bound to tissue factor (TF), which constitutes only approximately 1% of total amount of the FVII protein existing in the blood. rFVII becomes activated only after the binding to the TF, released at the site of tissue injury. The efficiency of rFVIIa in the treatment of such life-threatening hemorrhagic states like hemophilia reaches up to 76-84%. rFVIIa is successfully used in the treatment of congenital deficiency of factor VII. It normalizes prothrombin time in the patients with the liver diseases and in cases of overdose of indirect anticoagulants. It is also useful for patients suffering from thrombocytopenia, thrombocyte function disorders, hemophilia A and B with development of inhibitors. rFVIIa allows overcoming uncontrollable hemorrhages, etc. It is supposed that rFVIIa is becoming a universal hemostatic drug.

[Methadone treatment and its dangers]. / Metadonas ir gydymo juo pavojai.

Methadone is a long-acting synthetic opioid with high affinity for various opioid receptors, especially for m-opioid receptors. Methadone has been used as a successful pharmacologic intervention for the treatment of heroin dependence and acute and chronic pain. This treatment is effective for opiate addiction, reducing morbidity and mortality associated with heroin use. However, overdosing with methadone has become a growing phenomenon because of the increased availability of this drug. Patients enrolled in a methadone maintenance treatment program may become physically dependent and may experience methadone withdrawal symptoms. In this review article, there are discussed about pharmacokinetic and pharmacodynamic properties of methadone, clinical symptoms of its overdose, dosage problems, detection of methadone in biological samples, treatment, and causes of methadone overdose-related deaths.

[Epileptic seizures in critically ill patients]. / Epilepsiniai priepuoliai, istinkantys kritiniu bukliu ligonius.

THE AIM OF THIS ARTICLE: To review the causes, clinical signs, pathophysiology, consequences, and treatment of seizures and status epilepticus in critically ill patients. Only 25% of people, who have seizures and status epilepticus, have epilepsy as well. In the intensive care settings, seizures and status epilepticus are a common neurologic complication, which is attributable to primary neurologic pathology (stroke, hemorrhage, tumor, central nervous system infection, head trauma) or secondary to critical illness (anoxic brain damage, intoxications, metabolic abnormalities) and clinical management. There are three main subtypes of status epilepticus in intensive care units: generalized convulsive status epilepticus, focal motor status epilepticus, and nonconvulsive status epilepticus. A seizure is a consequence of electrical neurological derangement because of sudden imbalance between the inhibitory and excitatory forces within the network of cortical neurons. The main inhibiting neurotransmitter in the brain is gamma-aminobutyric acid (GABA), which binds to GABA-A and GABA-B receptors. The main excitatory neurotransmitter is glutamate, which binds to N-methyl-D-aspartate receptors. Different ions (Cl(-), K(+), Na(+), Ca(2+)) also play a role in the pathophysiology of seizures. Prolonged status epilepticus may lead to different systemic and neurologic consequences. Generalized convulsive status epilepticus is one of the most common emergencies encountered in clinical practice, which requires immediate treatment. The first-line drugs are benzodiazepines (lorazepam, diazepam), the second-line ones - phenytoin and fosphenytoin. For the treatment of refractory status epilepticus, barbiturates (phenobarbital, pentobarbital, thiopental), valproate, midazolam, propofol, and isoflurane are used. The dosage of drugs and parameters to monitor are referred in the article. The mortality from generalized convulsive status epilepticus is 15-50%; the main factors, influencing prognosis, are the cause and the duration of status epilepticus and age of a patient.

[Heparin-induced thrombocytopenia]. / Heparino sukelta trombocitopenija.

SUMMARY: In clinical use for over 50 years, heparin is an important and widely used anticoagulant for the prophylaxis or treatment of thromboembolic disease as well as other numerous clinical situations. Ordinarily, heparin prevents clotting and does not affect the platelets, components of the blood that help to form blood clots. However, heparin can also cause heparin-induced thrombocytopenia. Two distinct types of heparin-induced thrombocytopenia can occur: nonimmune and immune mediated. Nonimmune heparin-induced thrombocytopenia, which occurs most frequently, is characterized by a mild decrease in the platelet count and is not harmful. The second type, immune-mediated heparin-induced thrombocytopenia, occurs much less frequently but is dangerous. Immune-mediated heparin-induced thrombocytopenia causes much lower platelet count. Paradoxically, despite a very low platelet count, patients who suffer from heparin-induced thrombocytopenia are at risk for arterial or venous thrombosis. In this review article, there are discussed about pathogenesis of heparin-induced thrombocytopenia, other causes of thrombocytopenia, clinical features, laboratory confirmation of diagnosis, and management of patients (direct thrombin inhibitors, other therapies, duration of therapy, and use of oral anticoagulants). Prognosis and prophylaxis of this life-threatening disorder, which can develop from the use of unfractionated or (less commonly) low-molecular-weight heparin, are also discussed.

[Acute right ventricular failure]. / Uminis desiniojo skilvelio nepakankamumas.

Acute right ventricular failure is a syndrome, which is related to pulmonary and right heart dysfunction. It may occur with or without cardiopulmonary pathologies. It is often life threatening and requires early recognition and urgent treatment. In this review article, precipitating factors for right ventricular failure and its pathophysiological mechanisms, clinical picture and hemodynamic manifestations, the principles of the management of acute right ventricular failure (optimization of preload, increase in cardiac output, specific pulmonary vascular vasodilators, problems of mechanical ventilations, etc.) are discussed.

[Pulmonary arterial hypertension]. / Plauciu arterine hipertenzija.

Pulmonary arterial hypertension is a life-threatening, progressive disorder of pulmonary blood vessels leading to an increase in pressure in pulmonary artery. Diagnosis is based on a mean pulmonary artery pressure of more than 25 mmHg at rest or more than 30 mmHg during exercise. No cure exists for it yet. However, specialized treatment can lower pulmonary pressure, reduce symptoms, increase the capacity to be active, and prolong lifespan. In this review article, we attempt to summarize the current knowledge regarding clinical classification, risk factors and associated conditions, pathology and pathogenesis of this disease, diagnostic tests and detection of it, clinical course, current therapeutic strategies for the treatment of pulmonary arterial hypertension (calcium channel blockers, prostacyclin analogues, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, etc.). Interventional procedures, combination therapy, and new strategies (selective serotonin reuptake inhibitors, antivascular endothelial growth factor agents, potassium channel openers, etc.) for the management of pulmonary arterial hypertension and prognosis of this rare disease are also discussed.

[Beta-adrenergic receptor blocker poisoning]. / Apsinuodijimas beta adrenerginiu receptoriu blokatoriais.

Beta-adrenergic receptor blocking drugs are used in the treatment of hypertension, angina, myocardial infarction, cardiac dysrhythmia, cardiomyopathy, migraine headache, thyrotoxicosis, and glaucoma. beta-adrenergic receptor blocking agents are competitive antagonist at beta(1), beta(2), or both types of adrenergic receptors. Overdoses of beta-adrenergic receptor blockers are uncommon, but are associated with significant morbidity and mortality. This review article discusses the properties of beta-adrenergic receptor blockers, presents the doses of these drugs causing toxicity and doses, after ingestion of which, referral to an emergency department is recommended. Clinical presentation of overdose (the cardiovascular, neurologic manifestations, pulmonary and other complications), diagnosis, and treatment (gastrointestinal decontamination; the usage of atropine, phosphodiesterase inhibitors, glucagon, insulin; indications for cardiac pacing, extracorporeal procedures of drug removal, etc.) are analyzed. In addition, this article focuses on clinical course and prognosis of beta-blocker overdose.

[QTc-prolonging drugs and the risk of sudden death]. / Vaistai, ilginantys QTc. Staigios mirties rizika.

Various drugs can be associated with QT prolongation. A prolonged QT interval leads to an increased risk for the development of ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia (torsades de pointes). Polymorphic arrhythmia may rapidly develop into ventricular fibrillation and cause sudden death. Torsades de pointes is classically associated with early depolarization. This review article discusses the mechanisms of QTc prolongation and triggering factors for proarrhythmia, drugs that prolong QT interval (class III antiarrhythmic agents, antimicrobial agents - fluoroquinolone and macrolide antibiotics, antipsychotic and antidepressant drugs, agents used in general anesthesia, antimycotics, and several other drugs), nonpharmacological and pharmacological risk factors for arrhythmias (due to pharmacokinetic-pharmacodynamic interactions), the treatment and recommendations to prevent arrhythmia related to QT prolongation.

[The consequence of epinephrine (adrenaline) overdose]. / Epinefrino (adrenalino) perdozavimo pasekmes.

Epinephrine is an adrenergic agonist used to treat bronchospasm, anaphylactic reactions, bradycardia, cardiac arrest, and hypotension. Its toxicity is usually caused by iatrogenic errors. In overdose there is a typical rapid onset of agitation, hypertension, tachycardia, and dysrhythmias. This review article focuses on the causes of overdose, signs and symptoms, treatment and expected course, and prognosis of this iatrogenic pathology.

[Ecstasy toxicity]. / Ekstazio toksiskumas.

The substance, 3,4-methylenedioxymethamphetamine (MDMA) or ecstasy, is an amphetamine derivate. A mistaken belief that it is a safe drug of low toxicity and a long duration of action has led to its widespread popularity among teenagers and young adults in recent years. Unfortunately, ecstasy use has increased to epidemic proportions. In this review article pharmacokinetics and pathophysiology of MDMA, general medical adverse effects, cardiovascular effects, serotonin syndrome, hyponatremia, neurologic effects, hepatotoxicity, and long-term neuropsychiatric effects, clinical features of toxicity, prehospital and emergency department care problems, and mortality/morbidity, prophylactic advices are discussed.

[Acute salicylate poisoning]. / Apsinuodijimas salicilatais.

Although aspirin (acetylsalicylic acid) has become widely available without prescription, cases of self-poisoning due to overdose of salicylates are quite uncommon, with a low reported mortality. However, severe poisoning with these preparations is life threatening. Besides the aspirin, there are other sources of salicylate poisoning, such as an excessive application of topical agents, ingestion of salicylate containing ointments, use of keratolytic agents or agents containing methyl salicylate (e.g. oil of wintergreen). Most of these preparations are liquid, highly concentrated and lipid soluble, and, therefore, they are able to provoke a severe, rapid salicylate poisoning. On the basis of clinical and metabolic features or salicylate concentration in plasma it is very important to diagnose severe poisoning with salicylates in time and prescribe an adequate treatment. In the present review article various aspects of salicylate poisoning and its treatment are discussed: epidemiology, pharmacokinetics and pharmacodynamics of salicylates, clinical manifestations of their toxicity, management, enhanced elimination and prognosis.

[The novelty in the treatment of heart failure]. / Sirdies nepakankamumo gydymo naujove.

Heart failure is a very common clinical pathology. The treatment of heart failure is expensive; therefore, it is a large burden on the health care system in the world. Despite many recent advances in heart failure therapy, the prognosis remains poor. Levosimendan is a novel inotropic vasodilator agent. This drug induces enhanced contractility mainly via its calcium sensitizing actions. Levosimendan does not increase myocardial oxygen demand and also reduces significantly systemic vascular resistance, pulmonary artery pressure, and pulmonary vascular resistance. It causes venous, arterial, and coronary vasodilation. The drug is not proarrhythmic, has anti-ischemic and anti-stunning effects. It is well-tolerated drug for the treatment of cardiac failure. This review article discusses mechanism of action of levosimendan, its pharmacokinetics and metabolism, hemodynamic studies with this drug, effects on morbidity and mortality, therapeutic indication for its use, contraindications, special warnings and precautions for use, interactions with others medical products, undesirable effects of levosimendan.

[Hypertensive emergencies and urgencies]. / Hipertenzines bukles, kurioms gydyti reikalinga neatideliotina arba skubi medicinine pagalba.

Hypertension is one of the most common medical problems affecting approximately 1 billion individuals worldwide. Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis. Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies. Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction. Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury. Blood pressure can be lowered less rapidly in this condition. In this review article it is discussed about clinical assessment of patients under these conditions, evaluating neurological, cardiovascular, renal end-organ damage; how much blood pressure should be lowered, which medication should be used to lower blood pressure, treating hypertensive emergencies and urgencies; and management of specific conditions (acute intracranial events, acute left ventricular dysfunction etc).

[Hydroxyethyl starch solutions]. / Hidroksietilkrakmolo tirpalai.

Hypovolemia is common among surgical, trauma, and intensive care unit patients. It can occur in the absence of obvious fluid loss secondary to vasodilatation or during generalized alterations of the endothelial barrier resulting in increased capillary permeability. Hydroxyethyl starch solutions are increasingly used for the volume replacement therapy. Hydroxyethyl starch solutions are synthetic colloids with the pharmacological properties that are the closest to natural colloids. Important characteristics for these products are molecular weight, their concentration, the degree of molar substitution, and the substitution pattern. In this review article a large variety of hydroxyethyl starch solutions, their physical and chemical characteristics, pharmacokinetics and metabolism, the main route of elimination, mechanism of action, effect on blood plasma volume, safety, tolerability and side effects (the risk of adverse effects on hemostasis, platelet function, frequency of pruritus, anaphylactoid reaction, incidence of rise in serum amylase) are presented.

[Hallucinogenic mushrooms]. / Haliucinogeniniai grybai.

The group of hallucinogenic mushrooms (species of the genera Conocybe, Gymnopilus, Panaeolus, Pluteus, Psilocybe, and Stropharia) is psilocybin-containing mushrooms. These "magic", psychoactive fungi have the serotonergic hallucinogen psilocybin. Toxicity of these mushrooms is substantial because of the popularity of hallucinogens. Psilocybin and its active metabolite psilocin are similar to lysergic acid diethylamide. These hallucinogens affect the central nervous system rapidly (within 0.5-1 hour after ingestion), producing ataxia, hyperkinesis, and hallucinations. In this review article there are discussed about history of use of hallucinogenic mushrooms and epidemiology; pharmacology, pharmacodynamics, somatic effects and pharmacokinetics of psilocybin, the clinical effects of psilocybin and psilocin, signs and symptoms of ingestion of hallucinogenic mushrooms, treatment and prognosis.

[Intravenous catheters and nosocomial infection]. / Intraveniniai kateteriai ir nozokomine infekcija.

Peripheral, especially central venous catheters, are used with increasing frequency in the intensive care unit and in general medical wards to administer intravenous fluids and blood products, drugs, parenteral nutrition, and to monitor hemodynamic status. Catheter infection is associated with increased morbidity, mortality, and duration of hospital stay. Risk factors in the development of catheter colonization and bloodstream infections include patient factors (increased risk associated with malignancy, neutropenia, and shock) and treatment-related factors (increased risk associated with total parenteral nutrition, intensive care unit admission for any reason, and endotracheal intubation). In this review article terms and definitions of catheter-related infections, pathophysiology and epidemiology of "catheter sepsis", factors determining risk of infection, catheter types and materials, insertion procedure, choice of insertion site, indwelling time, dressing and care of the insertion site, various preventive strategies and future developments, special situations and procedures, and treatment are discussed. Reducing catheter infections rates requires a multiple-strategy approach. Therefore, intensive care units and other locations where catheters are used should implement strict guidelines and protocols for catheter insertion, care, and maintenance.

[Procalcitonin as a marker of the systemic inflammatory response to infection]. / Prokalcitoninas--sistemines uzdegimines reakcijos i infekcija zymuo.

Despite advances in the diagnosis and treatment of infections diseases, sepsis and ensuing multiorgan failure are the major causes of morbidity and mortality in the intensive care units. Such manifestations of systemic inflammation as fever, leukocytosis, tachycardia, etc. may be noninfectious in origin and are neither specific nor sensitive for sepsis. Procalcitonin is a new potential marker for detection of bacterial, fungal and protozoal infections. Procalcitonin, a propeptide of calcitonin, is normally produced in the C-cells of the thyroid gland. Procalcitonin is a polypeptide consisting of 116 amino acids and with a molecular weight of about 13 kDa. During severe systemic infections it is produced by extrathyroidal tissues. Procalcitonin can be put to immediate use in both diagnostic and therapeutic decision-making. This review article discusses biology of procalcitonin, its laboratory determination, usage as an indicator for severe infection and sepsis, and comparison with circulating cytokines in severe infection. It also reviews value of procalcitonin in differentiation of infectious vs non-infectious inflammatory host response, possible elevation of procalcitonin in the absence of infection, its use for differentiation of viral and non-viral infections and as marker for prognosis and evaluation of therapy. Specific indications for determination of procalcitonin are also discussed.

[Diagnosis of acute respiratory failure and nosocomial pneumonia]. / Uminio kvepavimo nepakankamumo ir nozokomines pneumonijos diagnozavimas.

The aim of this study was to determine diagnosis and factors influencing acute respiratory failure and nosocomial pneumonia according to literature and clinical findings in critically ill patients. The term "respiratory failure" implies the inability to maintain either normal delivery of oxygen to tissues or normal removal of carbon dioxide from the tissues. There are many patients suffering from acute respiratory failure caused by nosocomial pneumonia, septic syndrome, aspiration, interstitial or alveolar lung edema, thromboembolism of a. pulmonalis, polytrauma and contusion of the lungs, acute respiratory distress syndrome, acute lung injury, status asthmaticus, rather massive transfusions of blood products, and lipid embolism in the intensive care unit. There are actually three processes involved: transfer of oxygen across the alveolus, transport to the tissues (by cardiac output), and removal of carbon dioxide from the blood into the alveolus with subsequent exhalation into the environment. Failure of any step in this process can lead to respiratory failure. Long-term hypoxia causes ischemic changes and dysfunction of brain, heart, kidney, lungs and can worsen the outcome of disease or can cause higher mortality.