The first thing we need to know is that combustion of polyurethane at high temperature results in the release of cyanide (very intuitive, yes). Knowing this, and that we are dealing with cyanide poisoning, it is easier to answer the question. Among the basic initial treatment measures would be the administration of oxygen therapy with FiO2 1 (not 0.5 as stated in option 1), and an antidote, in this case hydroxycobalamin (this was asked similarly last year). Ventilation with hyperbaric chamber would only be indicated in case of coexistence of carbon monoxide (CO) poisoning. What is stated in option 4 about fluid therapy is not indicated; in case of associated shock, volume would be administered, but in any case not at that rate, but in rapid boluses.

The first thing we need to know is that combustion of polyurethane at high temperature results in the release of cyanide (very intuitive, yes). Knowing this, and that we are dealing with cyanide poisoning, it is easier to answer the question. Among the basic initial treatment measures would be the administration of oxygen therapy with FiO2 1 (not 0.5 as stated in [HIDDEN]), and an antidote, in this case hydroxycobalamin (this was asked similarly last year). Ventilation with hyperbaric chamber would only be indicated in case of coexistence of carbon monoxide (CO) poisoning. What is stated in [HIDDEN] about fluid therapy is not indicated; in case of associated shock, volume would be administered, but in any case not at that rate, but in rapid boluses.

A patient is brought to the ED from a fire occurring inside an enclosed building where polyurethane foams were present. He is conscious, but presents with increasing mental dullness, headache, and severe dyspnea. Oxygen saturation by pulse oximetry is 92% and capillary lactic acid is 8 mEq/l. What specific treatment do you consider most appropriate?

Administration of oxygen by means of a 50% Venturi type mask.

Administration of intravenous hydroxycobalamin.

Fluid therapy with infusion of physiological saline solution at 21 ml/h.

Decompression illness

First aid First aid is common for both DCS and AGE: Monitor the patient for responsiveness, airway, breathing and circulation, resuscitate if necessary. Treat for shock. Lay the patient on their back, or for drowsy, unconscious, or nauseated victims, on their side. Administer 100% oxygen as soon as possible. Seek immediate medical assistance, locate a hospital with hyperbaric facilities and plan for possible transport. Allow the patient to drink water or isotonic fluids only if responsive, stable, and not suffering from nausea or stomach pain. Administration of intravenous saline solution is preferable. Record details of recent dives and responses to first aid treatment and provide to the treating medical specialist. The diving details should include depth and time profiles, breathing gases used and surface intervals. Prognosis

Demand valve oxygen therapy

When used in diving recompression chambers and multi-place medical hyperbaric chambers, a built-in breathing system venting to the exterior is generally used to avoid buildup of oxygen partial pressure in the chamber to dangerous levels which would otherwise require more frequent venting. Procedure Contraindications Hazards and precautions High oxygen concentrations in the surroundings constitute a fire hazard. Oxygen therapy should be accompanied by good ventilation and avoidance of ignition sources, and where reasonably practicable, removal of combustible materials. Oxygen firebreaks are a requirement in some countries for patients using oxygen therapy. See also Oxygen for cluster headaches - Information for cluster headache patients, carers, and clinicians References Diving medicine Medical treatments Oxygen Respiratory therapy

InternalMed_Harrison

Use of low-flow oxygen if available Treatment with acetazolamide (250 mg q12h) and/or dexamethasone (4 mg q6h)c Administration of oxygen (2–4 L/min) Treatment with dexamethasone (8 mg PO/IM/IV; then 4 mg q6h) Hyperbaric therapy if descent is not possible Minimization of exertion while patient is kept warm Administration of oxygen (4–6 L/min) to bring O2 saturation to >90% Adjunctive therapy with nifedipinee (30 mg, extended-release, q12h)

Chokes -- Treatment / Management

At the emergency department (ED), the patient must be given high-flow oxygen at 100% or the maximum possible concentration, which addresses hypoxemia and accelerates the reabsorption of extra-alveolar gas. Intravenous cannulation must be started for fluid resuscitation and medication administration. If the patient deteriorates, the medical team must be ready to administer basic (BLS) and advanced cardiac (ACLS) life support. Once stable, the patient must be immediately evacuated to a hyperbaric chamber and placed in the care of the hyperbaric team. If the patient was initially taken to a hospital without a hyperbaric chamber, they must be transferred to an appropriately equipped facility with staff capable of treating patients with pulmonary DCS.

Saline (medicine)

Hypertonic saline may be used in perioperative fluid management protocols to reduce excessive intravenous fluid infusions and lessen pulmonary complications. Hypertonic saline is used in treating hyponatremia and cerebral edema. Rapid correction of hyponatremia via hypertonic saline, or via any saline infusion > 40 mmol/L (Na+ having a valence of 1, 40 mmol/L = 40 mEq/L) greatly increases risk of central pontine myelinolysis (CPM), and so requires constant monitoring of the person's response. Water privation combined with diuretic block does not produce as much risk of CPM as saline administration does; however, it does not correct hyponatremia as rapidly as administration of hypertonic saline does. Due to hypertonicity, administration may result in phlebitis and tissue necrosis. As such, concentrations greater than 3% NaCl should normally be administered via a central venous catheter, also known as a 'central line'. Such hypertonic saline is normally available in two strengths, the

InternalMed_Harrison

Management of HPS during the first few hours after presentation is critical. The goal is to prevent severe hypoxemia by oxygen therapy, with intubation and intensive respiratory management if needed. During this period, hypotension and shock with increasing hematocrit invite aggressive fluid administration, but this intervention should be undertaken with great caution. Because of low cardiac output with myocardial depression and increased pulmonary vascular permeability, shock should be managed expectantly with pressors and modest infusion of fluid guided by pulmonary capillary wedge pressure. Mild cases can be managed by frequent monitoring and oxygen administration without intubation. Many patients require intubation to manage hypoxemia and developing shock. Extracorporeal membrane oxygenation is instituted in severe cases, ideally before the onset of shock. The procedure is indicated in patients who have a cardiac index of 2.3 L/min/m2 or an arterial oxygen tension/fractional

Volume expander

Normal saline Normal saline (NS) is the commonly used term for a solution of 0.9% w/v of NaCl, about 300 mOsm/L. Less commonly, this solution is referred to as physiological saline or isotonic saline, neither of which is technically accurate. NS is used frequently in intravenous drips (IVs) for patients who cannot take fluids orally and have developed or are in danger of developing dehydration or hypovolemia. NS is typically the first fluid used when hypovolemia is severe enough to threaten the adequacy of blood circulation, and has long been believed to be the safest fluid to give quickly in large volumes. However, it is now known that rapid infusion of NS can cause metabolic acidosis. Ringer's solution Lactated Ringer's solution contains 28 mmol/L lactate, 4 mmol/L K+ and 1.5 mmol/L Ca2+. It is very similar – though not identical – to Hartmann's Solution, the ionic concentrations of which differ slightly.

Diving chamber

A hyperbaric oxygen therapy chamber is used to treat patients, including divers, whose condition might improve through hyperbaric oxygen treatment. Some illnesses and injuries occur, and may linger, at the cellular or tissue level. In cases such as circulatory problems, non-healing wounds, and strokes, adequate oxygen cannot reach the damaged area and the body's healing process is unable to function properly. Hyperbaric oxygen therapy increases oxygen transport via dissolved oxygen in serum, and is most efficacious where the haemoglobin is compromised (e.g. carbon monoxide poisoning) or where the extra oxygen in solution can diffuse through tissues past embolisms that are blocking the blood supply as in decompression illness. Hyperbaric chambers capable of admitting more than one patient (multiplace) and an inside attendant have advantages for the treatment of decompression sickness (DCS) if the patient requires other treatment for serious complications or injury while in the chamber,

[Base excess. Parameter with exceptional clinical significance].

The base excess of blood (BE) plays an important role in the description of the acid-base status of a patient and is gaining in clinical interest. Apart from the Quick test, the age, the injury severity score and the Glasgow coma scale, the BE is becoming more and more important to identify, e. g. the risk of mortality for patients with multiple injuries. According to Zander the BE is calculated using the pH, pCO(2), haemoglobin concentration and the oxygen saturation of haemoglobin (sO(2)). The use of sO(2 )allows the blood gas analyser to determine only one value of BE, independent of the type of blood sample analyzed: arterial, mixed venous or venous. The BE and measurement of the lactate concentration (cLac) play an important role in diagnosing critically ill patients. In general, the change in BE corresponds to the change in cLac. If DeltaBE is smaller than DeltacLac the reason could be therapy with HCO(3)(-) but also with infusion solutions containing lactate. Physician are very familiar with the term BE, therefore, knowledge about an alkalizing or acidifying effect of an infusion solution would be very helpful in the treatment of patients, especially critically ill patients. Unfortunately, at present the description of an infusion solution with respect to BE has not yet been accepted by the manufacturers.

Description and evaluation of a delivery system for aerosolized prostacyclin.

Inhaled vasodilators such as nitric oxide and aerosolized prostacyclin (PGI(2)) are used to treat severe hypoxemia in acute respiratory distress syndrome. Preferential distribution of nitric oxide and PGI(2) to ventilated areas of the lung causes selective pulmonary vasodilation, improved ventilation/perfusion matching, and decreased hypoxemia. Because of the technical limitations of previously described methods, we developed a PGI(2) delivery technique that allows the aerosolized drug dose to be easily calculated, set, and adjusted. A 50 mL solution of PGI(2) (3.0x10(4) ng/mL) and a 500 mL normal saline solution were infused by a dual-channel volumetric infusion pump into a MiniHEART jet nebulizer that has a manufacturer-specified output of 8 mL/h at a set flow of 2 L/min. By adjusting the pump infusion rate to achieve a total output of 8 mL/h, the PGI(2) concentration was altered to deliver a calculated aerosolized dose of 10-50 ng/kg/min. The effectiveness of the delivery system was retrospectively evaluated by way of the responses of 11 severely hypoxemic acute respiratory distress syndrome patients who received PGI(2) via the system we describe. The MiniHEART nebulizer output, particle size, and dose delivery were evaluated in a laboratory bench study, using a set flow of 2 L/min. Aerosolized PGI(2) therapy (mean dose 28 +/- 17 ng/kg/min, range 10-50 ng/kg/min) significantly increased the ratio of P(aO)(2) to fraction of inspired oxygen (P(aO)(2)/F(IO)(2)) (60 +/- 11 mm Hg vs 80 +/- 17 mm Hg, p = 0.003) and arterial oxygen saturation measured via pulse oximetry (86 +/- 8% vs 94 +/- 3%, p = 0.005) (differences evaluated with the Wilcoxon signed rank test). There was no difference in positive end-expiratory pressure, mean airway pressure, or F(IO)(2), before and after aerosolized PGI(2) (p > 0.05). Nebulizer output was 6.8 +/- 0.9 mL/h, range 6.0-7.8 mL/h. The inhaled aerosol particles had a mass median diameter of 3.1 micro m. Emitted dose was 67 +/- 13% (range 57-81%) of the calculated dose. Our system is effective in delivering aerosolized PGI(2) to the alveolar-capillary interface, as indicated by significant oxygenation improvements soon after therapy commenced. The performance of the MiniHEART nebulizer varies from the manufacturer's specifications, which may alter the delivered dose.

[What's new in cardiopulmonary resuscitation? American Heart Association].

A strong consensus was reached for several changes in the guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC) in the 1992 conference on CPR and ECC held by the Emergency Cardiac Care Committee of the American Heart Association. These new recommendations, together with differing recommendations of the European Resuscitation Council, are described. An unresponsive person with spontaneous respirations should be placed in the recovery position if no cervical trauma is suspected. Compared with endotracheal intubation, other airway-protecting devices such as combination esophageal-tracheal tubes are of minor acceptance. During ventilation, the time for filling the lungs is increased to 1.5-2 s to decrease the likelihood of gastric insufflation. Delivery of i.v. drugs can be enhanced by an i.v. flush of sodium chloride. In endotracheal drug administration, higher doses and drug dilution are recommended. In infants and children up to 6 years of age, the value of intraosseous drug administration is emphasized. For pulseless adult victims, the initial dosage of epinephrine of 1 mg i.v. remains unchanged. For repeat doses, high-dose epinephrine up to 0.1 mg/kg is classified as of uncertain but possible efficacy. For lidocaine, the recommended i.v. dosage is 1.5 mg/kg. Sodium bicarbonate and calcium are not routinely recommended for resuscitation. For atropine, the maximum dose is 0.04 mg/kg. If hypomagnesaemia is present in recurrent and refractory ventricular fibrillation, it should be corrected by administration of 1 to 2 g magnesium sulfate i.v. Thrombolytic agents are classified as useful and effective in acute myocardial infarction and should be administered as early as possible. Glucose-containing fluids are discouraged for resuscitative efforts.

Hypovolemic shock

Hypothermia increases the mortality rate of patients suffering hypovolemic shock. It is advised to keep the patient warm for the sake of maintaining the temperatures of all kinds of fluids inside the patient. Monitoring parameters Oxygen saturation by pulse oximetry (SpO2). Respiratory rate. Pulse rate. Arterial blood pressure. Pulse pressure. Central venous pressure. Urine output. Base deficit and/or lactic acid. Temperature. Mental state. Changes in the electrocardiogram. Prognosis If the vital organs are deprived of perfusion for more than just a short time, the prognosis is generally not good. Shock is still a medical emergency characterized by a high mortality rate. Early identification of patients who are likely to succumb to their illness is of utmost importance. Epidemiology Blood loss

[Can modern infusion solutions cause serious disruption of inner environment of an organism?].

The article brings a description of a patient case when an application of mineral balanced infusion solutions led to a disruption of inner environment, beginning of a combined failure of the acid-base balance with a serious metabolic acidosis. Patient J. was artificially respirated after a CPR. During the therapy the patient was given basically without any changes a combination of mineral solution Plasma-Lyte 148, amino-acid and 20% glucose. During 8 days a serious metabolic alkalosis had developed (caused by a lack of chlorides, phosphates and other reasons), combined with respirational acidosis. Hydrogencarbonate level was increased to 47.2 mmo/l (at norm of 24 mmol/l), base excess level to 21.4 mmol/l (at norm of 0 mmol/l). Metabolic acidosis led to reduction of sensibility of the respiratory centers and therefore it was not possible to restore spontaneous respiration. After the therapy change and reduction of metabolic acidosis the state of the patient got better. Application of acidifying solutions, supplementation of phosphate and potassium levels and replenishment of actual losses of phosphates led to regulation of the inner environment. Together with the application of sufficient amount of basic nutrients was the improvement of acid-base balance the key factor which enabled the restoration of spontaneous respiration and disconnection of the patient from the ventilator. In short summary you can see reasons which cause different effect of identical infusions to acid-base balance of the inmates in different situations. The article points to a necessity of controlling groovy medical procedures according to actual patient's needs.

Hyperbaric medicine

In the larger multiplace chambers, patients inside the chamber breathe from either "oxygen hoods" – flexible, transparent soft plastic hoods with a seal around the neck similar to a space suit helmet – or tightly fitting oxygen masks, which supply pure oxygen and may be designed to directly exhaust the exhaled gas from the chamber. During treatment patients breathe 100% oxygen most of the time to maximise the effectiveness of their treatment, but have periodic "air breaks" during which they breathe chamber air (21% oxygen) to reduce the risk of oxygen toxicity. The exhaled treatment gas must be removed from the chamber to prevent the buildup of oxygen, which could present a fire risk. Attendants may also breathe oxygen some of the time to reduce their risk of decompression sickness when they leave the chamber. The pressure inside the chamber is increased by opening valves allowing high-pressure air to enter from storage cylinders, which are filled by an air compressor. Chamber air

[Iso- and hypervolemic hemodilution with hydroxyethyl starch (HES 200/.05 10%) in patients with II b peripheral arterial occlusive disease].

The basic therapy in stage IIb of peripheral arterial occlusive disease (PAOD) according to Fontaine is exercise. The aim of this study was to test whether (given initial physiological hematocrit values of 43 to 46%) a mild hypervolemic to isovolemic to hematocrit values of 40% with HES 200/0.5 10% or Ringer lactate in combination with exercise is even more favorable. In order to answer this question, 3 groups of 25 patients each were formed. One group exercised three times weekly and the second group, in addition to exercise, underwent a mild, hypervolemic to isovolemic 6-week dilution therapy with HES. In the final group the hematocrit value was reduced to the same extent by means of venesection and volume substitution with Ringer lactate. The walking distance increased in the HES group from 216 to 311 m (44%), in the Ringer lactate group from 214 to 258 m (20%), and in the exercise group from 213 to 242 m (14%). In comparison of the groups, the increase in pain-free walking distances in the HES group is found to differ significantly from those in the other groups. It was clearly demonstrated that hemodilution with HES in combination with exercise brings about a clinical effect of an order three times of that achieved by exercise alone. Venesection with subsequent administration of Ringer lactate and exercise is superior to exercise alone, but is markedly inferior to the combination therapy with HES.

Crush syndrome

Intravenous hydration of up to 1.5 L/h should continue to prevent hypotension. A urinary output of at least 300 mL/h should be maintained with IV fluids and mannitol, and hemodialysis considered if an increase in urine is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys. To prevent hyperkalemia/hypocalcemia, consider the following adult doses: calcium gluconate 10% 10 mL or calcium chloride 10% 5 mL IV over 2 minutes sodium bicarbonate 1 meq/kg IV slow push regular insulin 5–10 U 50% glucose 1–2 ampules IV bolus kayexalate 25–50 g with sorbitol 20% 100 mL by mouth or rectum. Even so, abnormal heart rhythms may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly. References External links Life or Limb: What happens when your leg gets trapped under a building? Injuries Early complications of trauma Nephrology Syndromes

[Basis for the clinical management of fire smoke poisoning "Docohumo Madrid 2010"].

Poisoning by smoke is the main cause of morbidity and mortality in fires. Smoke is a mixture of carbonaceous particles suspended in hot air and toxic gases. Of these, carbon monoxide (CO) and primarily hydrocyanic acid (CNH), are those that provoke tissue anoxia. The clinical manifestations of smoke poisoning are variables. Some of the potential manifestations could be: eye irritation, sore throat, laryngeal stridor, dysphagia, carbonaceous sputum, cough, dyspnea, laryngospasm, bronchospasm, coronary syndrome, coma, hypoxemia, lactic acidosis, cyanosis and death. In the assessment of these patients the presence of soot in the nose, mouth or sputum suggests serious poisoning. Lactate levels higher than 10mmol/L indicates levels of cyanide major than 40micromole/L. The pulse co-oximetry has assumed an important step forward for the diagnosis, appraisal and monitoring of these patients. In the treatment it will be essential to assess the need of an early intubation. The administration of oxygen to the 100% will be essential. As an antidote to the cyanide, the first-choice is the hydroxocobalamin. Its administration has to be early. Its administration criteria are: patient who has inhaled smoke (remnants of soot in the mouth, pharynx or sputum) and has neurological disorder (confusion, coma, agitation, seizures) and also presents one of the following circumstances: bradypnea, respiratory arrest, cardiorespiratory arrest, shock, hypotension, lactate ≥8mmol/L or lactic acidosis. Logically, the rest of the management will be conventional depending on symptoms or complications.

[Hypertonic solutions in the intensive care unit].

The use of small volumes of hypertonic saline (HTS) 7.2-7.5% (small volume resuscitation) in combination with colloidal solutions has been proved to be of value in stabilizing oxygen transport in hemorrhagic shock. The specific effects of HTS lead to an improvement in tissue oxygenation by increasing the cardiac preload, decreasing the afterload and endothelial and interstitial edema within the microcirculation. This study investigates whether the use of HTS combined with hydroxyethylstarch (HAES) leads to a significant increase in the O2 delivery (DO2) and O2 consumption (VO2) in hyperdynamic critically ill patients. A total of 41 patients, 20 septic patients and 21 patients without sepsis were investigated. When a hyperdynamic circulation (DO2 > 700 ml/min/m2) was attained, 2-4 ml/kg 7.5% HTS in 6% HAES were infused over 15 minutes. In the septic patients this leads to a significant increase in the DO2 of 14% (p < 0.001). The VO2 (calculated from the cardiovascular Fick) increased by 7% (p < 0.05). The VO2 calculated from the respiratory gases increased by 4% (n.s.). This < 10% increase in VO2 does not seem to be due to a relevant tissue oxygen debt. This is supported by the fact that in the non septic group the DO2 and VO2 increased by the same extent, there was no significant difference between the two groups. Further there was an equal increase in the O2 extraction ratio of 10% (septic patients) and 9.5% (non septic patients). In both groups the mean plasma lactate levels before and 90 min after the HTS/HAES infusion were within normal range so that a wash-out phenomenon was not discernible.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen therapy

Medical uses Oxygen is widely used by hospitals, EMS, and first-aid providers in a variety of conditions and settings. A few indications frequently requiring high-flow oxygen include resuscitation, major trauma, anaphylaxis, major bleeding, shock, active convulsions, and hypothermia. Acute conditions In context of acute hypoxemia, oxygen therapy should be titrated to a target level based on pulse oximetry (94–96% in most patients, or 88–92% in people with COPD). This can be performed by increasing oxygen delivery, described as FIO2(fraction of inspired oxygen). In 2018, the British Medical Journal recommended that oxygen therapy be stopped for saturations greater than 96% and not started for saturations above 90 to 93%. This may be due to an association between excessive oxygenation in the acutely ill and increased mortality. Exceptions to these recommendations include carbon monoxide poisoning, cluster headaches, sickle cell crisis, and pneumothorax.

Using blood gases for the v.i.p..

We have tried to expand the routine analysis of blood gases to include some fine-tuning aspects of critical care. Test your understanding by answering the following question: A 70-year-old smoker falls into Lake Dillon (outside Denver) suffering a near-drowning episode. The pulse oximeter shows 93% on 6L nasal oxygen. His pulse and blood pressure are normal. Because you've read this article, you know that the patient's smoking habit and the city's elevation can affect the pulse oximeter's accuracy, leading one to underestimate the severity of the problem. So, you draw labs and note that his hemoglobin is 12, with blood gases showing PaO2 of 90, PaCO2 of 30 and a pH of 7.36. The lab forgot to calculate the base excess for you and his temperature is 89 degrees F rectally. A diagnosis of life-threatening inadequate oxygenation is supported by which of the following astute observations: a) An abnormal base deficit is proven by the borderline acidic pH and the low PaCO2. b) His anemia reduces both his buffer base and his oxygen carrying capacity. c) His hypothermia overstates his PO2 because the blood was heated up before measurement. d) His smoking makes a CO level likely, worsening his anemia and ignored by the pulse oximeter. e) The high level of supplemental oxygen has minimal effect on his arterial oxygen tension, showing severe pulmonary gas transfer problems (shunting). f) The measurement of his PaO2 is artificially high because he is at altitude. All of the following except (f). Measuring his oxygen tension at altitude actually works in his favor, since the barometric effect will be to reduce the PaO2 at a given level of sea level pathology. Now you are ready to give your patients the V.I.P. treatment!

Hyperbaric nursing

Hyperbaric nurses are responsible for administering hyperbaric oxygen therapy to patients and supervising them throughout the treatment. These nurses must work under a supervising physician trained in hyperbarics who is available during the treatment in case of emergency. Hyperbaric nurses either join the patient inside the multiplace hyperbaric oxygen chamber or operate the machine from outside of the monoplace hyperbaric oxygen chamber, monitoring for adverse reactions to the treatment. Patients can experience adverse reactions to the hyperbaric oxygen therapy such as oxygen toxicity, hypoglycemia, anxiety, otic barotrauma, or pneumothorax. The nurse must know how to handle each adverse event appropriately. The most common adverse effect is otic barotrauma, trauma to the inner ear due to pressure not being released on descent. Since hyperbaric oxygen therapy is usually administered daily for a set number of treatments, adverse effects must be prevented in order for the patient to

[Acute dyspnea--what should I not forget?].

Acute dyspnea represents a diagnostic challenge even for the experienced physician. There are no prospectively evaluated diagnostic algorithms dealing with this frequent clinical problem. First of all, the emergency has to be assessed and life supporting measures have to be considered. In addition to a thorough medical history and clinical examination, chest X-ray, spirometry, ECG, hemoglobin measurement, BNP and D-dimer testing represent valuable diagnostic tools and are available to GP's. Most commonly, acute dyspnoea is pulmonary or cardiac in origin. Up to one third of all cases will have several causes. Functional dyspnea is difficult to diagnose but should be taken into consideration after excluding any somatic cause. Hyperventilation is found in both, organic and non organic diseases, and is therefore an inappropriate criterion to differentiate between the two. The mainstay in the management of any symptom is to primarily treat the underlying disease. A significant hypoxemia (SO2 < 90%, pO2 < 60 mmHg) ought to be corrected by supplemental oxygen. It is inappropriate to withhold oxygen from patients with COPD and severe hypoxemia just to avoid hypercapnia. Besides oxygen, opiates efficiently relief dyspnoea but harbour the risk of respiratory depression, altered mental status or aspiration.

Ringer's lactate solution

Ringer's lactate solution is used because the byproducts of lactate metabolism in the liver counteract acidosis, which is a chemical imbalance that occurs with acute fluid loss or kidney failure. The IV dose of Ringer's lactate solution is usually calculated by estimated fluid loss and presumed fluid deficit. For fluid resuscitation the usual rate of administration is 20 to 30 mL/kg body weight/hour. RL is not suitable for maintenance therapy (i.e., maintenance fluids) because the sodium content (130 mEq/L) is considered too low, particularly for children, and the potassium content (4 mEq/L) is too low, in view of electrolyte daily requirement. Moreover, since the lactate is converted into bicarbonate, long-term use will cause patients to become alkalotic. Ringer's lactate and other crystalloids are also used as vehicles for the IV delivery of medications. In a large-volume resuscitation over several hours, LRS maintains a more stable blood pH than normal saline.

[Treatment of 522 patients with sudden deafness performed oxygenation at high pressure].

Oxygenation at high pressure (OHP) is thought to be useful, even though regional blood flow is decreased, because increasing dissolved oxygen prevents the death of nerve tissue. In this report, we retrospectively investigated the effect of OHP on sudden deafness. We reviewed 522 patients treated with OHP at Kagawa Rosai Hospital over a ten-year period (January 1989 to December 1998). We discussed some prognostic factors: comparison between cases which had been treated with OHP previously and those which had not, number of days between onset and beginning of the treatment which included OHP, age, initial averaged five-frequency hearing level, vertigo, tinnitus, complications of OHP, cases of relapse and the time of the onset, which is about season, month and week. OHP was administered at a pressure of 2.5 atmospheres for 80 minutes a day from 10 to 15 times. All patients also received a course of intravenous administration of steroid, vitamin B12, Prostaglandin E1, ATP, and low-molecular dextran. Overall, complete recovery occurred in 19.7% of the patients, definite improvement in 34.9% (complete recovery included), and slight improvement in 58.1% (definite improvement included). Most of the patients (78.0%) were referred by other hospitals, because our hospital was the only one in the Sikoku area which had a big equipment of OHP. All 161 patients had already been treated in other hospitals over 8 days, but they had shown little improvement after the initial therapy. Of this group, complete recovery after the second course of treatment occurred in 13.0% of the patients, definite improvement in 19.3%, and slight improvement in 39.1%. OHP was thus effective for about 40% of patients who had been unresponsive to the initial therapy. Delay in treatment usually produces poor hearing recovery. There was a significant difference between those patients treated within 14 days and those treated 15 days or more after onset. The improvement rate also decreased with age. The prognosis of patients with vertigo was worse than those without vertigo. Tinnitus had no influence on the prognosis. There were no severe complications during the course of OHP, but otitis media with effusion occurred in 90 patients, and paracentesis was performed for 53 patients. The treatment of sudden deafness with OHP has been discussed in this report. Important prognostic factors were time between onset and beginning of the treatment which included OHP, age, vertigo, and the initial averaged five-frequency hearing level. We conclude that OHP should be performed within 14 days from onset, and that OHP was able to achieve hearing improvement in many cases unresponsive to the initial therapy if it was performed very early.

Hemodynamic and metabolic responses to repeated hemorrhage and resuscitation with hypertonic saline dextran in conscious swine.

Previous work in our laboratory has demonstrated that HSD is an effective small-volume resuscitation fluid for the treatment of hemorrhagic hypotension, but limitations to its usefulness in severe hemorrhage have not been explored. In the present study, animals (N = 12) were bled from an arterial line at a rate of 1 mL/kg/min until continuously monitored aortic blood flow was reduced to one-half its baseline value, and then they were immediately resuscitated with 7.5% NaCl/6% dextran 70 (hypertonic saline dextran, 4 mL/kg) administered intravenously over 3 min. After recording the maximum improvement in blood pressure, blood samples were obtained and the hemorrhage-resuscitation sequence was repeated until no further measurable increase in cardiac index or blood pressure could be elicited by resuscitation. In the majority of the animals, cardiac index and right and left ventricular stroke work could be improved at least through two bleedings and resuscitation. These improvements sufficed to increase oxygen delivery and consumption, despite the decreases in hematocrit induced by bleeding, transcapillary refill, and asanguinous fluid administration. Under these severe hemorrhage conditions, the acid-base imbalance was not improved by hypertonic saline dextran, and the rate of increase in acidosis was not affected by its administration. We observed a progressive decrease in base excess from +1.35+/-3.19 (mean +/- standard error) to -12.9+/-2.1 mEq/L even when resuscitation improved oxygen consumption significantly by 95+/-20%. In animals that survived as many as three bleedings and resuscitation, the depletion of buffering capacity of the blood was most predominant, and bicarbonate reached a nadir of 7.62 mEq/L with a base excess of -22.4 mEq/L. It is evident that restoration of perfusion in shock treats only a portion of the physiologic dysfunction, leaving major metabolic derangements uncorrected.

[Hyperosmolar volume replacement in heart surgery].

The ideal solution for use in volume therapy is still a matter of debate. Hypertonic sodium (HS) solutions have been advocated for resuscitation from hemorrhagic shock (small volume resuscitation). As hypertonic fluids may also be of interest in cardiac surgery, the effects of a new HS solution were studied. METHODS. In 90 patients undergoing aorto-coronary bypass grafting studies were performed at three different periods: I (n = 30) after induction of anesthesia (before onset of the operation); II (n = 30) during cardiopulmonary bypass (CPB); III (n = 30) after termination of bypass. During these periods the patients were randomly allocated to one of three groups with 10 patients in each group: group 1 received a new hypertonic solution prepared in hydroxyethyl starch (HES) solution (72 g/l NaCl, 60 g/l HES, 2400 mosmol/l; HS-HES patients), group 2 received a 6% HES solution (200/0.5; HES patients), and group 3 received no volume infusion and served as controls. RESULTS. After the induction of anesthesia, significantly less HS-HES solution (4.5 +/- 0.5 ml/kg) than 6% HES solution (10.1 +/- 1.4 ml/kg) was necessary to double the baseline PCWP. The fluid balance during CPB was negative in the patients who had received HS-HES preoperatively (-0.03 +/- 0.01 ml/kg.min CPB), whereas 6% HES (+0.06 +/- 0.02 ml/kg.min CPB) and control patients (+0.13 +/- 0.03 ml/kg.min CPB) had a positive fluid balance. Both after the induction of anesthesia and after termination of bypass, CI increased more in the HS-HES group than in the HES patients, and it even decreased in the control group. SVR decreased in the HS-HES patients, whereas it increased in the control group. Rapid infusion of HS-HES during CPB was followed by a significant, but short-lasting decrease in MAP (-40 mmHg) and an increase in the oxygenator volume. Pulmonary gas exchange (= paO2) was least compromised in the HS-HES patients; the sodium concentration increased only in the HS-HES patients, but never exceeded 150 mmol/l. DISCUSSION. Cardiac surgery procedures offer a special situation for volume therapy as there is a possibility of deterioration in the macro- and microcirculation before, after, and during the period of CPB. Hemodynamic effects of the new HS-HES solution included an increase in CI and a decrease in SVR, which were not merely transient as has been reported which hypertonic saline solution used alone. It was also observed that HS-HES patients required significantly smaller volumes of fluids, both during CPB and during the early postoperative period. This effect seems to be due to a redistribution of interstitial fluid to the intravascular space, possibly decreasing tissue edema. CONCLUSION. The hypertonic saline HES solution adds a new dimension to volume therapy for cardiac surgery patients. The improvement in hemodynamics was effective and not only transient. Fluid requirements were significantly reduced during as well as after CPB, and pulmonary gas exchange was least compromised in these patients.

[Effect of 3% hypertonic saline as early fluid resuscitation in pediatric septic shock].

The mainstay of therapy in patients with septic shock is early and aggressive intravenous fluid resuscitation. However the type of intravenous fluid that would be ideal for managing septic shock has been intensely debated. In this study, the authors observed the effects of 3% hypertonic saline solution compared with normal saline solution as early fluid resuscitation in children with septic shock. In this prospective study, 44 septic shock children seen in the intensive care unit (ICU) of the Children's Hospital Affiliated to Capital Institute of Pediatrics were enrolled from January 2012 to January 2014, of whom 33 were male and 11 were female. Patients were randomly divided into two groups: normal saline group (NS group, 24 patients) and 3% hypertonic saline group (HS group,20 patients). There were no significant differences between the 2 groups of patients in age, gender, pediatric critical illness score (PCIS), oxygenation index (OI = PaO2/FiO2), arterial lactate, initial hemodynamic parameters, serum sodium and treatment at time of admission. Patients in NS group received normal saline guided by standard therapy. Those in HS group received 6 ml/kg 3% hypertonic saline as a single bolus over 10 min to 15 min with a maximum of 2 boluses and other standard therapy. Heart rate (HR), mean arterial blood pressure (MAP), arterial lactate, oxygenation index, urine output, serum sodium, lactate clearance rate, PCIS, fluid infusion volume, vasoactive - inotropic score, mechanical ventilation time , as well as incidence of multiple organ dysfunction syndrome (MODS), and 28 days in - hospital mortality were recorded for all patients. (1) HR, MAP in both groups were significantly higher after infusion than those on admission. There were no significant difference in HR and MAP at 1h, 3h, 6h and 24h after infusion between NS group and HS group. (2) OI in HS group was significantly higher than that on admission at 3 hours after infusion [(321. 8 ± 50. 7) vs. (296. 5 ± 58. 2) mmHg, t = -2. 50, P = 0. 018 ]), and it was significantly higher at 24 hours after infusion in NS group (325. 7 ± 62. 6) vs. (304. 2 ± 70. 4) mmHg, t = -2.60, P=0.016]. There were no significant differences in OI at 1h, 3h, 6h and 24h after infusion between NS group and HS group. (3) At 1 hour after infusion, serum sodium in HS group was significantly higherthan that in NS group [(138.3 ± 3.8)vs. (135.0 ± 3.5) mmol/L, t=8.77, P=0.005], and then no significant difference at 3h, 6h and 24h after infusion between two groups. (4) At 6 hours and 24 hours after treatment, fluid infusion volume in HS group was markedly less than that in NS group [6 h: (39. 2 13. 9) vs. (60. 8 ± 22. 4) ml/kg, t = 14. 21, P =0. 000; 24 h: (102. 9 ± 27. 7) vs. (130. 6 ± 33. 2 ) ml/kg, t= 8. 85, P = 0. 005]. Urine output had not significant different between the two groups. (5) There were no significant differences in 24h PCIS, 24h lactate clearance rate, vasoactive - inotropic score and mechanical ventilation time between the two groups. The incidence of MODS (80. 0% in HS group, 70. 0% in NS group) and mortality rate(5. 0% in HS group, 8. 3% in NS group) were similar in both groups. The 3% hypertonic saline was effective as resuscitation fluid in pediatric septic shock with respect to restoration of hemodynamic stability without obvious side effects. Hypertonic saline could more rapidly improve oxygenation and need less fluid infusion volume compared with normal saline.

Fluid replacement

Optimisation phase - In this phase, the goal is to increase the oxygen delivery to tissues in order to meet the oxygen demands of the tissues. Oxygen delivery can be improved by increasing stroke volume of the heart (through fluid challenge), haemoglobin concentration (through blood transfusion), and arterial oxygen saturation (through oxygen therapy). Fluid challenge is the procedure of giving large amounts of fluid in a short period of time. However, 50% of patients do not respond to fluid challenge. Additional fluid challenges only causes fluid overload. However, there is no gold standard on determining the fluid responsiveness. Among other ways of determining the fluid responsiveness and the end point of fluid resuscitation are: Central venous oxygen saturation (ScvO2), passive leg raising test, ultrasound measurements of pulse pressure variation, stroke volume variation, and respiratory variations at superior vena cava, inferior vena cava and internal jugular vein.

Elevated Methemoglobin Levels in a Patient Treated with Hydroxocobalamin After Suspected Cyanide Exposure.

Cyanide (CN) toxicity commonly occurs during enclosed-space fires. Historically, the first step in treating CN toxicity utilized amyl nitrite and sodium nitrite to induce methemoglobinemia, which can be dangerous in this population. Hydroxocobalamin (OHCob), which binds to CN to form the nontoxic metabolite cyanocobalamin, is now the first-line antidote for CN toxicity, and has the advantage of not inducing methemoglobinemia. A 62-year-old man presented to the Emergency Department (ED) after a house fire. He was intubated for respiratory distress and hypoxia with an initial carboxyhemoglobin of 1.3%, methemoglobin 0.3%, and anion gap 19. Eleven hours after presentation, his serum lactic acid was 9 mmol/L. Given his continued deterioration, 14 h after arrival he received OHCob 5 g i.v. for presumed CN toxicity. Methemoglobin concentration 4 min prior to OHCob administration was 0.7%, and 2 h after administration was 4.2%. This subsequently increased to 14.3% (16 h after OHCob administration) and peaked at 16.3% (47 h after OHCob administration), at which time he was administered a dose of methylene blue 50 mg i.v., 60 h after ED arrival. His methemoglobin concentrations fluctuated until a consistent downward trend starting at 92 h from ED arrival. He continued to deteriorate and expired on hospital day 5 with a methemoglobin concentration of approximately 6.0%. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CN toxicity requires immediate recognition and treatment. The antidote, OHCob, is believed to not induce methemoglobinemia. However, this potential side effect must be considered by emergency physicians when treating suspected CN toxicity, especially if the patient does not improve after antidotal therapy.

[Comments on the 2010 guidelines on cardiopulmonary resuscitation of the European Resuscitation Council].

Administer chest compressions (minimum 100/min, minimum 5 cm depth) at a ratio of 30:2 with ventilation (tidal volume 500-600 ml, inspiration time 1 s, F(I)O₂ if possible 1.0). Avoid any interruptions in chest compressions. After every single defibrillation attempt (initially biphasic 120-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min independent of the ECG rhythm. Tracheal intubation is the optimal method for securing the airway during resuscitation but should be performed only by experienced airway management providers. Laryngoscopy is performed during ongoing chest compressions; interruption of chest compressions for a maximum of 10 s to pass the tube through the vocal cords. Supraglottic airway devices are alternatives to tracheal intubation. Drug administration routes for adults and children: first choice i.v., second choice intraosseous (i.o.). Vasopressors: 1 mg epinephrine every 3-5 min i.v. After the third unsuccessful defibrillation amiodarone (300 mg i.v.), repetition (150 mg) possible. Sodium bicarbonate (50 ml 8.4%) only for excessive hyperkaliemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider aminophylline (5 mg/kgBW). Thrombolysis during spontaneous circulation only for myocardial infarction or massive pulmonary embolism; during on-going cardiopulmonary resuscitation (CPR) only when indications of massive pulmonary embolism. Active compression-decompression (ACD-CPR) and inspiratory threshold valve (ITV-CPR) are not superior to good standard CPR. Most effective improvement of outcome by prevention of full cardiorespiratory arrest. Basic life support: initially five rescue breaths, followed by chest compressions (100-120/min depth about one third of chest diameter), compression-ventilation ratio 15:2. Foreign body airway obstruction with insufficient cough: alternate back blows and chest compressions (infants), or abdominal compressions (children >1 year). Treatment of potentially reversible causes: ("4 Hs and 4 Ts") hypoxia and hypovolaemia, hypokalaemia and hyperkalaemia, hypothermia, and tension pneumothorax, tamponade, toxic/therapeutic disturbances, thrombosis (coronary/pulmonary). Advanced life support: adrenaline (epinephrine) 10 µg/kgBW i.v. or i.o. every 3-5 min. Defibrillation (4 J/kgBW; monophasic or biphasic) followed by 2 min CPR, then ECG and pulse check. NEWBORNS: Initially inflate the lungs with bag-valve mask ventilation (p(AW) 20-40 cmH₂O). If heart rate remains <60/min, start chest compressions (120 chest compressions/min) and ventilation with a ratio 3:1. Maintain normothermia in preterm babies by covering them with foodgrade plastic wrap or similar. POSTRESUSCITATION PHASE: Early protocol-based intensive care stabilization; initiate mild hypothermia early regardless of initial cardiac rhythm [32-34°C for 12-24 h (adults) or 24 h (children); slow rewarming (<0.5°C/h)]. Consider percutaneous coronary intervention (PCI) in patients with presumed cardiac ischemia. Prediction of CPR outcome is not possible at the scene, determine neurological outcome <72 h after cardiac arrest with somatosensory evoked potentials, biochemical tests and neurological examination. ACUTE CORONARY SYNDROME: Even if only a weak suspicion of an acute coronary syndrome is present, record a prehospital 12-lead ECG. In parallel to pain therapy, administer aspirin (160-325 mg p.o. or i.v.) and clopidogrel (75-600 mg depending on strategy); in ST-elevation myocardial infarction (STEMI) and planned PCI also prasugrel (60 mg p.o.). Antithrombins, such as heparin (60 IU/kgBW, max. 4000 IU), enoxaparin, bivalirudin or fondaparinux depending on the diagnosis (STEMI or non-STEMI-ACS) and the planned therapeutic strategy. In STEMI define reperfusion strategy depending on duration of symptoms until PCI, age and location of infarction. TRAUMA: In severe hemorrhagic shock, definitive control of bleeding is the most important goal. For successful CPR of trauma patients a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation and excessive ventilation pressure may impair outcome in patients with severe hemorrhagic shock. Any CPR training is better than nothing; simplification of contents and processes is the main aim.

[Haemodynamic effects following preoperative hypervolemic haemodilution with hypertonic hyperoncotic colloid solutions in coronary artery bypass graft surgery].

Using hyperoncotic colloids as volume replacement to provide haemodynamic stability appears to be a suitable approach to diminish fluid overload and subsequent interstitial edema during cardiac surgery. The aim of the present study was to investigate for the first time the haemodynamic effects following preoperative haemodilution with different hypertonic hyperoncotic colloid solutions in patients undergoing coronary artery bypass grafting. A total of 43 patients with normal left ventricular ejection fraction, undergoing elective coronary artery bypass grafting received preoperatively after induction of anaesthesia according to randomisation the following solutions: 1: 750 ml/m(2) (body surface area) NaCl 0.9% ( n=10, control group, NACL), 2: 250 ml/m(2) 10% HES 200/0.5 plus 400 ml/m(2) NaCl 0.9% ( n=9, HES), 3: 250 ml/m(2) 10% dextran 40 plus 300 ml/m(2) NaCl 0.9% ( n=8, DEX), 4: 150 ml/m(2) hypertonic NaCl (7.2%) 10% HES 200/0.5 (n=8, HYPER-HES), 5: 150 ml/m(2) hypertonic NaCl (7.2%) 10% dextran 60 ( n=8, HYPER-DEX). Haemodynamic measurements were performed immediately before and 15 min after haemodilution and up to 60 min after termination of extracorporeal circulation in 10 min intervals. Fluid balances were calculated separately, during the time period of surgery, postoperatively up to 24 h after termination of surgery, and during the course of extracorporeal circulation. After haemodilution with colloid solutions, a marked increase was observed in all patients and with HYPER-HES and HYPER-DEX a statistically significant increase in cardiac index (CI: +38%, +54%), stroke volume index (SVI: +42%, +40%), and oxygen availability (DO2: +34%; +41%), respectively, was observed during the pre-bypass period. At the same time right and left ventricular filling pressures increased slightly in all patients but these changes did not differ among the treatment groups. Heart rate and mean arterial pressure remained almost unchanged in all groups. The amount of crystalloid solutions required by the patients during surgery was markedly decreased with HES and DEX and significantly decreased with HYPER-HES and HYPER-DEX (1,013+/-341 ml/m(2), 1,096+/-234 ml/m(2)) compared to the control group NACL (1629+/-426 ml/m(2)). Serum sodium concentrations increased with HYPER-HES and HYPER-DEX to maximal values of 150+/-3 mmol/l and 149+/-4 mmol/l, respectively (baseline 141+/-3 mmol/l, 141+/-1 mmol/l) Compared to isotonic saline solution, preoperative volume replacement with hyperoncotic colloids improves haemodynamic conditions during the pre-bypass period in patients with normal left ventricular function undergoing coronary artery bypass grafting. Additionally intraoperative crystalloid solution requirements are reduced. The volume saving effects are increased with administration of hyperoncotic colloids in a preparation with hypertonic saline solution, whereas the choice of the colloid, either hydroxyethyl starch or dextran seems to be of minor importance.

Hyperbaric treatment schedules

Built in breathing system Treatment gases are generally oxygen or oxygen rich mixtures which would constitute an unacceptable fire hazard if used as the chamber gas. Chamber oxygen concentration is limited due to fire hazard and the high risk of fatality or severe injury in the event of a chamber fire. US Navy specifications for oxygen content of chamber air allow a range from 19% to 25%. If the oxygen fraction rises above this limit the chamber must be ventilated with air to bring the concentration to an acceptable level. To minimize the requirement for venting, oxygen-rich treatment gases are usually provided to the patient by built in breathing system (BIBS) masks, which vent exhaled gas outside the chamber. BIBS masks are provided with straps to hold them in place over the mouth and nose, but are often held in place manually, so they will fall away if the user has an oxygen toxicity convulsion.


Spontaneous reports of serotonergic syndrome associated with concomitant administration of linezolid and serotonergic agents, including antidepressants such as selective serotonin reuptake inhibitors (SSRIs), have been reported.

In a 35-year-old patient with a depressive syndrome on treatment with serotonin reuptake inhibitors, the use of the following antimicrobials is contraindicated:

Serotonin toxicity as a consequence of linezolid use in revision hip arthroplasty.

Linezolid is the first in a new group of antibiotics called oxazolidinones. As a potent antimicrobial, it has activity against methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus, penicillin-resistant Streptococcus pneumoniae, and macrolide-resistant streptococci. There are several documented case reports of serotonin toxicity when used with selective serotonin reuptake inhibitors. The symptoms of serotonin syndrome are alteration of mental state, autonomic dysfunction, and neuromuscular disorders. This article presents a case of an interaction of the serotonin reuptake inhibitor venlafaxine and linezolid and the possible diagnostic problems that can occur. A 58-year-old woman presented with signs of systemic infection. Her medical history included bladder resection for transitional cell carcinoma, bilateral total hip arthroplasty (THA), and depression, for which she was on venlafaxine. Serological and imaging investigations revealed MRSA infection of the bilateral THA. The patient was started on vancomycin and rifampicin intravenously. As intravenous access was becoming problematic and long-term antibiotics were needed, treatment was changed to oral linezolid and oral rifampicin. Four days after the commencement of linezolid, the patient was acutely disorientated with generalized cerebellar signs and no autonomic dysfunction. A computed tomography scan of the head and lumbar puncture revealed no abnormal findings. A diagnosis of serotonin toxicity was made. The patient recovered when linezolid and venlafaxine were discontinued and supportive measures were provided. Linezolid is a popular choice of antibiotic, especially for the treatment of orthopedic-related MRSA infections. Patients who commonly require linezolid as an antimicrobial are those with complex infections where other antibiotic treatment has failed. It is therefore important to be vigilant with linezolid use. Physicians should be aware of the nonspecific presentation of serotonin symptoms and the treatment.

Linezolid interaction with serotonin reuptake inhibitors: report of two cases and incidence assessment.

Prompted by the advent of potentially life-threatening neuromuscular symptoms following initiation of linezolid therapy in two patients receiving treatment with a serotonin reuptake inhibitor antidepressant, an evaluation was conducted to determine the incidence and characteristics of symptomatic serotonin toxicity among hospitalized patients receiving combined treatment with these medications. Patients admitted between January 1, 2006 and August 30, 2008 who received linezolid concurrently with citalopram or escitalopram were identified and their medical records were examined. Patients were judged to have serotonin toxicity if their records contained documentation of clinical evidence adequate to fulfill requisites of the Hunter Serotonin Toxicity Criteria. Severity of serotonin-related symptoms was graded according to previously established criteria. During the period of observation, 24 patients received concurrent treatment with linezolid and citalopram or escitalopram. Of these, one patient (4%) treated with citalopram met evidentiary requirements for diagnosis of serotonin toxicity. The severity of symptoms in this patient was graded as mild. No evidence of serious harm related to a possible drug interaction was identified. Severe symptoms associated with serotonin toxicity were shown to be uncommon in patients receiving linezolid and selected serotonin reuptake inhibitors. Nonetheless, serious interaction-related toxicity has been observed at our institution and reported in detail by others. Accordingly, concurrent use of these medications is categorized as contraindicated. Alternative antimicrobial therapy should be instituted in most cases. If no suitable alternative is available, recipient patients should be hospitalized for expectant observation and rigorous monitoring.

Drug interactions between linezolid and selective serotonin reuptake inhibitors: case report involving sertraline and review of the literature.

A 47-year-old woman developed confusion, incoordination, and hypertension after she was given linezolid in addition to sertraline for 5 days. Her symptoms resolved within 4 days of discontinuing linezolid. One and a half months later, she received a second course of linezolid; sertraline was discontinued on day 1 of linezolid therapy. On day 9 of therapy, the patient developed confusion, myoclonus, and incoordination, and cardiopulmonary arrest occurred, leaving the patient in a coma. Diarrhea, hypertension, and tachycardia developed after cardiopulmonary arrest. Linezolid was discontinued on day 10, and cyproheptadine was given. Linezolid is a weak monoamine oxidase inhibitor and has been reported to interact with selective serotonin reuptake inhibitors (SSRIs). Several cases of serotonin syndrome in patients taking linezolid and SSRIs have been reported, including two reports with sertraline, one with paroxetine, four with citalopram, and two with fluoxetine. One abstract of a retrospective analysis reported that serotonin syndrome did not occur in patients who received linezolid and fluoxetine, paroxetine, or sertraline. Because of several limitations, however, no conclusions can be drawn from that retrospective analysis. A drug interaction involving escitalopram and linezolid has not been documented. Caution should be used when linezolid is used in patients receiving an SSRI. Other antibiotic options should be considered first, and linezolid should be reserved as the last resort if possible. If the infection requires linezolid, the SSRI should be discontinued, and the patient should be monitored closely for serotonin syndrome.

Linezolid-associated hypoglycemia in a 64-year-old man with type 2 diabetes.

Older diabetic patients are at increased risk for skin infections, often with methicillin-resistant Staphylococcus aureus (MRSA). Linezolid offers oral therapy with MRSA coverage. We present a case of linezolid-associated hypoglycemia in a 64-year-old diabetic patient with presumed MRSA cellulitis. A 64-year-old man with diabetes was treated for cellulitis. Linezolid was started when amoxicillin/clavulanate failed. Within 7 days, he developed frequent diaphoresis and tremulousness, with glucoses of 30 to 60 mg/dL. Hypoglycemia worsened despite decreasing insulin use, discontinuing glyburide, and increasing caloric intake. The day of admission, he awoke with a glucose level of 30 mg/dL. He took no medications, ate a large breakfast, and presented to clinic. He was symptomatic with a glucose level of 35 mg/dL. Hypoglycemia persisted despite IV dextrose. Linezolid was discontinued immediately in favor of vancomycin. Dextrose was weaned and his diabetes medications were resumed without further hypoglycemia. Linezolid has monoamine oxidase (MAO) inhibitory properties, and MAO inhibitors have been reported to contribute to hypoglycemia. The use of linezolid in older diabetic patients, especially those patients already taking agents with the potential to cause hypoglycemia, represents an area of concern. Increased comorbidities and polypharmacy in geriatric patients adds to this concern.

Serotonin syndrome after concomitant treatment with linezolid and citalopram.

Linezolid, a new synthetic antimicrobial, is an important weapon against methicillin-resistant Staphylococcus aureus (MRSA). Although there are reports of serotonin syndrome developing after concomitant use of linezolid and the selective serotonin reuptake inhibitor paroxitene, this report concerns a patient receiving citalopram who developed thrombocytopenia, serotonin syndrome, and lactic acidosis and died following long-term linezolid therapy.

Incidence of Serotonin Syndrome With Combined Use of Linezolid and Serotonin Reuptake Inhibitors Compared With Linezolid Monotherapy.

Linezolid is a monoamine oxidase inhibitor that may increase the risk of serotonin syndrome in patients receiving combination selective serotonin reuptake inhibitors (SSRIs) or serotonin norepinephrine reuptake inhibitors (SNRIs). The objective of this study was to compare the incidence of serotonin syndrome when linezolid was administered alone and in combination with SSRIs or SNRIs. This was a retrospective case-control study of adult inpatients admitted to the University of Iowa Hospitals and Clinics who received linezolid between January 2010 and December 2014. Patients who received linezolid with or within 14 days of an SSRI or SNRI were eligible for inclusion in the combination therapy group. Patients who received linezolid alone were matched by age and gender to patients in the combination therapy group, and 3 monotherapy patients were included for each combination therapy patient. Clinical features consistent with serotonin syndrome were assessed using the Sternbach and Hunter criteria. A total of 348 patients were included in this study, of which 87 received combination therapy and 261 received linezolid monotherapy. One patient given combination therapy (1.1%) and 1 patient given linezolid monotherapy (0.4%) were determined to have a diagnosis of serotonin syndrome (P = 0.438; relative risk, 3.00; 95% confidence interval, 0.19-47.45). In both cases, signs and symptoms of serotonin syndrome reversed upon discontinuation of linezolid therapy. There was no significant difference in the incidence of serotonin syndrome when linezolid was used alone or in combination with an SSRI or SNRI, and the overall incidence of serotonin syndrome was low.

InternalMed_Harrison

Linezolid is a weak monoamine oxidase inhibitor and can be associated with the serotonin syndrome when given concomitantly with serotonergic drugs (primarily antidepressants such as selective serotonin-reuptake inhibitors). A recent meta-analysis showed that ~80% of patients with MDRor XDR-TB can be successfully treated with linezolid-containing anti-TB regimens; however, significant adverse events attributed to linezolid were reported. For MDR-TB treatment, linezolid is usually administered at a dose of 600 mg (or less in some cases) once daily, which appears to be effective. The single daily dose is associated with fewer adverse events than twice-a-day dosing.

InternalMed_Harrison

Linezolid is a bacteriostatic agent and is indicated for serious infections due to resistant gram-positive bacteria, such as MRSA and VRE. The intrinsic resistance of gram-negative bacteria is mediated primarily by endogenous efflux pumps. Linezolid has excellent oral bioavailability. Adverse effects include myelosuppression and ocular and peripheral neuropathy with prolonged therapy. Peripheral neuropathy may be irreversible. Linezolid is a weak, reversible monoamine oxidase inhibitor, and coadministration with sympathomimetics and foods rich in tyramine should be avoided. Linezolid has been associated with serotonin syndrome when coadministered with selective serotonin-reuptake inhibitors. Tedizolid has properties similar to those of linezolid, but with lower dosing it may be less likely to cause adverse hematologic and neuropathic effects.

Obstentrics_Williams

For women with severe disease according to criteria in Table 51-3, Mandell and associates (2007) summarized IDSAI ATS guidelines, which call for either: (1) a respiratory luoroquinolone-Ievofloxacin, moxifloxacin, or gemiloxacin; or (2) a macrolide plus a preferred �-lactam-either high-dose amoxicillin or amoxicillin-clavulanate. �-Lactam alternatives include ceftriaxone, cefpodoxime, or cefuroxime (see Table 51-4). In areas in which the resistance of pneumococcal isolates to macrolides is great, these latter regimens are preferred. he teratogenicity risk of luoroquinolones is low, and these should be given if indicated (Briggs, 2015). IfCA-MRSA is suspected, then vancomycin or linezolid is added (Mandell, 2015; Moran, 2013; Wunderink, 2013).

WHO Model List of Essential Medicines for Children

Antifilarials Albendazole Diethylcarbamazine Ivermectin Antischistosomals and other antinematode medicines Praziquantel Triclabendazole Oxamniquine Antibiotics Access group antibiotics Amikacin Amoxicillin Amoxicillin/clavulanic acid (amoxicillin + clavulanic acid) Ampicillin Benzathine benzylpenicillin Benzylpenicillin Cefalexin Cefazolin Chloramphenicol Clindamycin Cloxacillin Doxycycline Gentamicin Metronidazole Nitrofurantoin Phenoxymethylpenicillin (penicillin V) Procaine benzylpenicillin Sulfamethoxazole/trimethoprim (sulfamethoxazole + trimethoprim) Watch group antibiotics Azithromycin Cefixime Cefotaxime Ceftriaxone Cefuroxime Ciprofloxacin Clarithromycin Piperacillin/tazobactam (piperacillin + tazobactam) Vancomycin Ceftazidime Meropenem Vancomycin Reserve group antibiotics Ceftazidime/avibactam (ceftazidime + avibactam) Colistin Fosfomycin Linezolid Polymyxin B Antileprosy medicines Clofazimine Dapsone Rifampicin

Serotonin–norepinephrine reuptake inhibitor

Contraindications SNRIs are contraindicated in patients taking MAOIs within the last two weeks due to the increased risk of serotonin syndrome, which can be life-threatening. Other drugs and substances that should be avoided due to increased risk of serotonin syndrome when combined with an SNRI include: other anti-depressants, anti-convulsants, analgesics, antiemetic agents, anti-migraine medications, methylene blue, linezolid, Lithium, St. John's worts, ecstasy, and LSD. Signs and symptoms of serotonin syndrome include: hyperthermia, rigidity, myoclonus, autonomic instability with fluctuating vital signs, and mental status changes that include extreme agitation progressing to delirium and coma.

Serotonin syndrome and linezolid.

We present a case of serotonin syndrome in a patient who initiated linezolid therapy shortly after discontinuation of therapy with a selective serotonin reuptake inhibitor (paroxetine).

Linezolid

In the treatment of diabetic foot infections, linezolid appears to be cheaper and more effective than vancomycin. In a 2004 open-label study, it was as effective as ampicillin/sulbactam and amoxicillin/clavulanic acid, and far superior in patients with foot ulcers and no osteomyelitis, but with significantly higher rates of adverse effects. A 2008 meta-analysis of 18 randomized controlled trials, however, found that linezolid treatment failed as often as other antibiotics, regardless of whether patients had osteomyelitis. Some authors have recommended that combinations of cheaper or more cost-effective drugs (such as co-trimoxazole with rifampicin or clindamycin) be tried before linezolid in the treatment of SSTIs when susceptibility of the causative organism allows it.

Ventilator-associated pneumonia

Risk factors for infection with an MDR strain include ventilation for more than five days, recent hospitalization (last 90 days), residence in a nursing home, treatment in a hemodialysis clinic, and prior antibiotic use (last 90 days). Possible empirical therapy combinations include (but are not limited to): vancomycin/linezolid and ciprofloxacin, cefepime and gentamicin/amikacin/tobramycin vancomycin/linezolid and ceftazidime Ureidopenicillin plus β-lactamase inhibitor such as piperacillin/tazobactam or ticarcillin/clavulanate a carbapenem (e.g., imipenem or meropenem) Therapy is typically changed once the causative bacteria are known and continued until symptoms resolve (often 7 to 14 days). For patients with VAP not caused by nonfermenting Gram-negative bacilli (like Acinetobacter, Pseudomonas aeruginosa) the available evidence seems to support the use of short-course antimicrobial treatments (< or =10 days).

Antibiotic-induced serotonin syndrome.

Due to its broad spectrum of clinical presentations and to the large number of available serotonergic medications, serotonin syndrome (SS) remains an elusive diagnosis to many clinicians. SS results from the over-stimulation of serotonin receptors by a variety of mechanisms. New medications with the potential to cause SS are released regularly, and among them is the antibiotic linezolid. We present a case of SS in a 36-year-old woman that occurred after linezolid was added to a drug regimen that included lithium, venlafaxine, and imipramine.

Lyme disease

Antibiotics are the primary treatment. The specific approach to their use is dependent on the individual affected and the stage of the disease. For most people with early localized infection, oral administration of doxycycline is widely recommended as the first choice, as it is effective against not only Borrelia bacteria but also a variety of other illnesses carried by ticks. People taking doxycycline should avoid sun exposure because of higher risk of sunburns. Doxycycline is contraindicated in children younger than eight years of age and women who are pregnant or breastfeeding; alternatives to doxycycline are amoxicillin, cefuroxime axetil, and azithromycin. Azithromycin is recommended only in case of intolerance to the other antibiotics. The standard treatment for cellulitis, cephalexin, is not useful for Lyme disease. When it is unclear if a rash is caused by Lyme or cellulitis, the IDSA recommends treatment with cefuroxime or amoxicillin/clavulanic acid, as these are effective

Linezolid-associated serotonin syndrome: what we can learn from cases reported so far.

To study the characteristics of the linezolid-associated serotonin syndrome cases. Database search for linezolid-associated serotonin syndrome. Twelve cases were found. The mean age of patients was 52.8 years. All patients received linezolid concomitantly with selective serotonin re-uptake inhibitor drugs (SSRID). The onset of syndrome was 9.5 days after linezolid introduction and was directly correlated to patients' age (P = 0.024). The symptoms resolved in 2.9 days. Citalopram was associated with a delayed resolution (P = 0.018). A trend was observed towards longer resolution time the longer the half-life of the interacting drug (P = 0.096). Patients are at risk when receiving SSRID concomitant with linezolid. The syndrome onset could be delayed in older patients. The resolution could be delayed when citalopram is involved in the syndrome.

Serotonin Syndrome A serious, but rare, side effect of SNRIs is serotonin syndrome, which is caused by an excess of serotonin in the body. Serotonin syndrome can be caused by taking multiple serotonergic drugs, such as SSRIs or SNRIs. Other drugs that contribute to serotonin syndrome include MAO inhibitors, linezolid, tedizolid, methylene blue, procarbazine, amphetamines, clomipramine, and more. Early symptoms of serotonin syndrome may include nausea, vomiting, diarrhea, sweating, agitation, confusion, muscle rigidity, dilated pupils, hyperthermia, rigidity, and goose bumps. More severe symptoms include fever, seizures, irregular heartbeat, delirium, and coma. If signs or symptoms arise, discontinue treatment with serotonergic agents immediately. It is recommended to washout 4 to 5 half-lives of the serotonergic agent before using an MAO inhibitor.

Linezolid-Associated Serotonin Syndrome. A Report of Two Cases.

Linezolid, a mild monoamine oxidase inhibitor, is a commonly used antibiotic drug for the treatment of complicated skin and skin structure infections, including diabetic foot infections. Use of linezolid has been associated with serotonin syndrome, a potentially life-threatening condition typically caused by the combination of two or more medications with serotonergic properties, due to increased serotonin release. The goals of this article are to highlight the risk factors associated with the development of serotonin syndrome related to the use of linezolid and to aid in its prevention and early diagnosis. In this case series we report on two hospitalized patients who, while being treated with linezolid for pedal infections, developed serotonin syndrome. Both individuals were also undergoing treatment with at least one serotonergic agent for depression and had received this medication within 2 weeks of starting the antibiotic drug therapy. In these individuals, we noted agitation, confusion, tremors, and tachycardia within a few days of initiation of linezolid therapy. Owing to the risk of serotonin toxicity, care should be taken when prescribing linezolid in conjunction with any other serotonergic agent. Although serotonin syndrome is an infrequent complication, it can be potentially life threatening. Therefore, risks and benefits of therapy should be weighed before use.

The challenge of antibiotic selection in prosthetic joint infections due to Corynebacterium striatum: a case report.

Corynebacterium striatum is a gram-positive facultative anaerobe found in the environment and human flora that has historically been considered a contaminant. More recently, Corynebacterium striatum has been implicated in human infections, including respiratory infections, endocarditis, and bone and joint infections, particularly those involving hardware or implanted devices. A 65-year-old man presented for washout of his left total knee arthroplasty following a revision 20 days prior. The patient underwent debridement of his left total knee and revision of the left total femur arthroplasty. Daptomycin was initiated empirically due to a previous rash from vancomycin. Operative tissue cultures grew Staphylococcus haemolyticus, Staphylococcus epidermidis and Corynebacterium striatum. Given concern for daptomycin resistance and the reliability of vancomycin susceptibility, daptomycin was discontinued and vancomycin initiated following a graded challenge. Within a few days, the patient developed a diffuse, blanching, erythematous, maculopapular rash and daptomycin was restarted. Over the next 72 h, his rash progressed and he met criteria for drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome. Daptomycin was stopped and oral linezolid initiated; rash improved. C. striatum returned with susceptibility to gentamicin, linezolid, vancomycin and daptomycin. Due to concern for adverse effects on long-term linezolid, daptomycin was restarted and was tolerated for 20 days, at which point purulent drainage from incision increased. The patient underwent another arthroplasty revision and washout. Operative cultures from this surgery were again positive for C. striatum. Repeat C. striatum susceptibilities revealed resistance to daptomycin but retained susceptibility to linezolid. Daptomycin was again changed to linezolid. He completed six weeks of linezolid followed by linezolid 600 mg daily for suppression and ultimately opted for disarticulation. C. striatum has historically been regarded as a contaminant, particularly when grown in tissue culture in the setting of prosthetic joint infection. Based on the available literature and susceptibility patterns, the most appropriate first-line therapy is vancomycin or linezolid. Treatment with daptomycin should be avoided, even when isolates appear susceptible, due to the risk of development of high-level resistance (MIC > 256 µg/mL) and clinical failure.

Serotonergic antidepressants and linezolid: a retrospective chart review and presentation of cases.

To report the results from a retrospective chart review looking at the combination of linezolid and serotonergic antidepressants and to report two cases of serotonin syndrome which were identified at our hospital. During the retrospective chart review one case of serotonin syndrome was identified. A 65-year-old female was receiving escitalopram for the treatment of depression prior to admission. Linezolid therapy was initiated on admission and two days later the patient had a tonic-clonic seizure. Escitalopram was discontinued and the patient did not have any further seizure activity. In a second case, a 37-year-old male was receiving citalopram during hospitalization and was started on concomitant linezolid. The patient had myoclonus and was observed to be tremulous throughout therapy with linezolid. Ten days after discontinuation of linezolid the patient continued to have symptoms until the withdrawal of citalopram. The Naranjo probability scale scores the first case as possibly related and the second case as probably related to the combination. It has been well documented in the literature that the combination of linezolid and serotonergic antidepressants may cause serotonin syndrome. In this retrospective chart review only one patient of 53 (1.8%) had symptoms highly suggestive of serotonin syndrome. A second patient continued to have symptoms of serotonin syndrome even after withdrawal of linezolid. This retrospective review and subsequent case reports confirm the rare, but serious, potential of serotonin syndrome associated with the combination of linezolid and serotonergic antidepressants.

Selective Serotonin Reuptake Inhibitors -- Contraindications

SSRIs are contraindicated with the concurrent use of MAOIs, linezolid, and other medications that increase serotonin levels and could put patients at risk for life-threatening serotonin syndrome.

WHO Model List of Essential Medicines

Antischistosomals and other antinematode medicines Praziquantel Triclabendazole Oxamniquineα Cysticidal medicines Albendazoleα Mebendazoleα Praziquantelα Antibacterials Access group antibiotics Amikacin Amoxicillin Amoxicillin/clavulanic acid (amoxicillin + clavulanic acid) Ampicillin Benzathine benzylpenicillin Benzylpenicillin Cefalexin Cefazolin Chloramphenicol Clindamycin Cloxacillin Doxycycline Gentamicin Metronidazole Nitrofurantoin Phenoxymethylpenicillin (penicillin V) Procaine benzylpenicillin Spectinomycin Sulfamethoxazole/trimethoprim (sulfamethoxazole + trimethoprim) Trimethoprim Watch group antibiotics Azithromycin Cefixime Cefotaxime Ceftriaxone Cefuroxime Ciprofloxacin Clarithromycin Piperacillin/tazobactam (piperacillin + tazobactam) Vancomycin Ceftazidimeα Meropenemα Vancomycinα

Dermabacter hominis: a usually daptomycin-resistant gram-positive organism infrequently isolated from human clinical samples.

During a 12-year period, Dermabacter hominis was isolated from 21 clinical samples belonging to 14 patients attending a tertiary hospital in León, Spain. Samples included blood cultures (14), peritoneal dialysis catheter exit sites (three), cutaneous abscesses (two), an infected vascular catheter (one) and a wound swab (one). Identification was made by API Coryne™ V2.0, Biolog™ GP2 and 16S rRNA gene amplification. Six febrile patients had positive blood cultures (one, two or three sets) and all of them were treated with teicoplanin (two patients), vancomycin, ampicillin plus gentamicin, amoxicillin/clavulanic acid and ciprofloxacin (one each). An additional patient with a single positive blood culture was not treated, the finding being considered non-significant. In the remaining seven patients the organism was isolated from a single specimen and three of them received antimicrobial treatment (ciprofloxacin, ceftriaxone plus vancomycin and amoxicillin/clavulanic acid). At least ten patients had several underlying diseases and conditions, and no direct mortality was observed in relation to the isolated organism. All isolates were susceptible to vancomycin, rifampin and linezolid. Resistance to other antibiotics varied: erythromycin (100%), clindamycin (78.5%), ciprofloxacin (21.4%) and gentamicin, quinupristin-dalfopristin, benzylpenicillin and imipenem 7.1% each. Thirteen isolates were highly resistant to daptomycin with MICs ranging from 8 to 48 (MIC90 = 32 mg/L); only one was daptomycin-sensitive (MIC = 0.19 mg/L).

InternalMed_Harrison

Ceftriaxone and calcium-containing solutions can be given to infants >28 days of age provided they are given sequentially and the lines are thoroughly flushed between infusions. Decreased levels of valproic acid. Monitor valproic acid levels closely if drugs are given concomitantly. Increased levels of serotonergic and adrenergic agents. Monitor for serotonin syndrome. Tedizolid may have less potential than linezolid to cause this drug interaction. Can result in increased levels of interacting drug. Erythromycin and clarithromycin are more potent CYP3A4 inhibitors than azithromycin. Avoid concomitant administration if possible. Can result in subtherapeutic fluoroquinolone levels. Administer fluoroquinolone 2 h before or 6 h after interacting drug. Can result in increased levels of tizanidine and hypotensive, sedative effects. Monitor for side effects if drugs are given concomitantly.

InternalMed_Harrison

Cefoxitin, 2 g q6h; A combination of metronidazole (500 mg q8–12h) plus cefazolin (1–2 g q8h) or cefuroxime (1.5 g q8h) or ceftriaxone (1–2 g q12–24h) or cefotaxime (1–2 g q6–8h) A carbapenem (imipenem, 1 g q8h; meropenem, 1 g q8h; doripenem, 500 mg q8h); Piperacillin-tazobactam, 3.375 g q6hf; A combination of metronidazole (500 mg q8–12h) plus an antipseudomonal cephalosporin (cefepime, 2 g q8–12h; ceftazidime, 2 g q8h) or an antipseudomonal fluoroquinolone (ciprofloxacin, 400 mg q12h; levofloxacin, 750 mg q24h) — Dexamethasone (0.15 mg/ kg IV q6h for 2–4 d) should be added for patients with suspected or proven pneumococcal meningitis, with the first dose administered 10–20 min before the first dose of antibiotics. If MRSA is a consideration, add vancomycin (15 mg/kg q12hb) or linezolid (600 mg q12h); daptomycin should not be used in patients with pneumonia. If MRSA is a consideration, add vancomycin (15 mg/kg q12hb). 159, 201, and pathogen-specific chapters

Triptan

There is a theoretical risk of coronary spasm in patients with established heart disease, and cardiac events after taking triptans may rarely occur. Interactions Combination of triptans with other serotonergic drugs such as ergot alkaloids, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs) or St John's wort has been alleged to induce symptoms of a serotonin syndrome (a syndrome of changes in mental status, autonomic instability, neuromuscular abnormalities, and gastrointestinal symptoms), whereas scientific studies indicate there is no potential for life-threatening serotonin syndrome in patients taking triptans and SSRI or SNRIs at the same time, although the FDA has officially stated otherwise. Combining triptans with ergot alkaloids is contraindicated because of the danger of coronary spasms.

Linezolid and serotonergic drug interactions: a retrospective survey.

Linezolid is a reversible, nonselective monoamine oxidase inhibitor. There are currently 11 published case reports of serotonin syndrome being associated with linezolid and selective serotonin reuptake inhibitors (SSRIs). Controversy exists regarding whether linezolid and SSRIs can be given concomitantly. The purpose of this study was to report the incidence of serotonin syndrome in patients receiving linezolid and SSRIs. This study was a retrospective chart review of inpatients at the Mayo Clinic (Rochester, MN) with concomitant orders or therapy within 14 days for linezolid and an SSRI from 2000 to 2004. The Sternbach criteria and Boyer criteria for diagnosis of serotonin syndrome were used to identify clinical features of serotonin syndrome. Seventy-two patients received linezolid and an SSRI or venlafaxine within 14 days of each other. Fifty-two patients (72%) received concomitant therapy with linezolid and an SSRI or venlafaxine, and 20 patients (28%) did not receive concomitant therapy but received linezolid and an SSRI within a 14-day period. Overall, only 2 patients (3%) had a high probability of serotonin syndrome. In both patients with high probability, symptoms reversed rapidly on discontinuation of serotonergic therapy. The Boyer criteria were much more specific than the Sternbach criteria for identification of serotonin syndrome. On the basis of our experience, we suggest that, if the clinical situation warrants use of linezolid in a patient receiving an SSRI, linezolid may be used concomitantly with SSRIs, without a 14-day washout period and with careful monitoring for signs and symptoms of serotonin syndrome. Serotonergic agents should be promptly discontinued if serotonin syndrome is suspected.

Reserve group antibiotics Ceftazidime/avibactam (ceftazidime + avibactam) Colistin Fosfomycin Linezolid Polymyxin B Antileprosy medicines Clofazimine Dapsone Rifampicin Antituberculosis medicines Ethambutol Isoniazid Isoniazid/pyrazinamide/rifampicin (isoniazid + pyrazinamide + rifampicin) Isoniazid/rifampicin (isoniazid + rifampicin) Pyrazinamide Rifampicin Rifapentine Amikacin Amoxicillin/clavulanic acid (amoxicillin + clavulanic acid) Bedaquiline Clofazimine Cycloserine Delamanid Ethionamide Levofloxacin Linezolid Meropenem Moxifloxacin P-aminosalicylic acid Streptomycin Antifungal medicines Amphotericin B Fluconazole Flucytosine Griseofulvin Itraconazole Nystatin Voriconazole Potassium iodide Antiviral medicines Antiherpes medicines Aciclovir Antiretrovirals Nucleoside/nucleotide reverse transcriptase inhibitors Abacavir (ABC) Lamivudine (3TC) Zidovudine (ZDV or AZT)

InternalMed_Harrison

NEWER ANTITUBERCULOSIS DRUGS Oxazolidinones Linezolid is an oxazolidinone used primarily for the treatment of drug-resistant gram-positive bacterial infections. However, this drug is active in vitro against M. tuberculosis and NTM. Several case series have suggested that linezolid may help clear mycobacteria relatively rapidly when included in a regimen for the treatment of complex cases of MDRand XDR-TB. Linezolid’s mechanism of action is disruption of protein synthesis by binding to the 50S bacterial ribosome. Linezolid has nearly 100% oral bioavailability, with good penetration into tissues and fluids, including CSF. Clinical resistance to linezolid has been reported, but the mechanism is unclear. Adverse effects may include optic and peripheral neuropathy, pancytopenia, and lactic acidosis. Linezolid is a weak monoamine oxidase inhibitor and can be associated with the serotonin syndrome when given concomitantly with serotonergic drugs (primarily antidepressants such as selective

Efficacy of Single and Combined Antibiotic Treatments of Anthrax in Rabbits.

Respiratory anthrax is a fatal disease in the absence of early treatment with antibiotics. Rabbits are highly susceptible to infection with Bacillus anthracis spores by intranasal instillation, succumbing within 2 to 4 days postinfection. This study aims to test the efficiency of antibiotic therapy to treat systemic anthrax in this relevant animal model. Delaying the initiation of antibiotic administration to more than 24 h postinfection resulted in animals with systemic anthrax in various degrees of bacteremia and toxemia. As the onset of symptoms in humans was reported to start on days 1 to 7 postexposure, delaying the initiation of treatment by 24 to 48 h (time frame for mass distribution of antibiotics) may result in sick populations. We evaluated the efficacy of antibiotic administration as a function of bacteremia levels at the time of treatment initiation. Here we compare the efficacy of treatment with clarithromycin, amoxicillin-clavulanic acid (Augmentin), imipenem, vancomycin, rifampin, and linezolid to the previously reported efficacy of doxycycline and ciprofloxacin. We demonstrate that treatment with amoxicillin-clavulanic acid, imipenem, vancomycin, and linezolid were as effective as doxycycline and ciprofloxacin, curing rabbits exhibiting bacteremia levels of up to 10(5) CFU/ml. Clarithromycin and rifampin were shown to be effective only as a postexposure prophylactic treatment but failed to treat the systemic (bacteremic) phase of anthrax. Furthermore, we evaluate the contribution of combined treatment of clindamycin and ciprofloxacin, which demonstrated improvement in efficacy compared to ciprofloxacin alone.

[Serotonin syndrome as a result of escitalopram and cyclosporin combination in an 84-year-old woman].

Due to the stimulation of central and peripheral 5-hydroxytryptamine receptors, the serotonin syndrome is a potentially lethal situation. The large variety of its clinical manifestations leads to a difficult diagnosis. We describe the case of a serotonin syndrome induced by the combined escitalopram and cyclosporine administration. An 84-year-old woman was hospitalized with a history of delirium associated with hyperthermia. The diagnosis of serotonin syndrome was suspected with the combination of the clinical features: the absence of infection, the selective serotonin reuptake inhibitor administration, and the absence of other metabolic and cerebral aetiology. After the discontinuation of escitalopram, the patient's condition improved rapidly. This report is a reminder of the clinical and pharmacological features of the serotonin syndrome from a recent literature review.