Clinical application of therapeutic erythrocytapheresis (TEA)

Valbonesi, M; Bruni, Renato

doi:10.1016/s0955-3886(00)00042-4

Cited by 48 publications

(29 citation statements)

References 45 publications

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“…TREX has been used in toxicology for poisoning from aniline, arsine, chloramines, salicylates (infants), theophylline (neonates), sodium chlorate, carbon monoxide, cyanide and, methemoglobinemia [57,[63][64][65][66][67][68][69][70]. TREX is performed either manually or is automated with the addition of replacement fluids that include crystalloids, albumin and/or plasma.…”

Section: What Therapeutic Modalities Exist To Treat Acute H 2 S Exposmentioning

confidence: 99%

“…TREX is performed either manually or is automated with the addition of replacement fluids that include crystalloids, albumin and/or plasma. Plasma exchange is another possibility at the time of red blood cell exchange [65, 67,70]. The American Society for Apheresis considers exchange transfusion in poisonings as a category II intervention: generally acceptable, but best used as an adjuvant to primary therapy [65].…”

Section: What Therapeutic Modalities Exist To Treat Acute H 2 S Exposmentioning

confidence: 99%

“…Complications from the procedure include volume shifts, hypocalcemia from excess citrate, hypothermia, dilutional coagulopathy, and transfusion reactions, including anaphylaxsis. Contraindications to TREX include severe anemia, pre-existing coagulapathy, or severe hypotension [65, 67,70].…”

Section: What Therapeutic Modalities Exist To Treat Acute H 2 S Exposmentioning

confidence: 99%

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Case files of the university of cincinnati fellowship in medical toxicology: Two patients with acute lethal occupational exposure to hydrogen sulfide

Policastro

Otten

2007

J. Med. Toxicol.

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We are presenting cases of 2 employees of a chemical plastics manufacturing plant who experienced acute, brief, inhalational exposure to lethal concentrations of hydrogen sulfide in a confined space. Eight other coworkers not present in the immediate exposure area also presented to local health care facilities with mild complaints of headache, nausea, and dizziness, but they suffered no significant sequelae.Patient #1 was a 55-year-old man who, while working in a confined space, uncoupled a nozzle from a steam pipe, collapsed within one minute, and suffered cardiopulmonary arrest. He had a prior history of asthma, hyperlipidemia, coronary artery disease, and was taking lisinopril, aspirin, and lipitor. Following chest compressions and rescue breathing, both by on-scene responders and EMS, the patient's blood pressure was 210/110 mmHg, the pulse was 100 bpm, and ventilation was assisted at 14/minute. On examination, the patient was minimally combative, with a Glasgow coma score of 6 (E1, V1, M4), with pupils 3 mm bilaterally and reactive to light. The patient had a small partial-thickness burn to the right chest, presumed to be a thermal burn from steam or the hot pipe. No cyanosis or pulmonary crackles were noted. Because of respiratory distress, the patient was intubated on-scene using fentanyl, diazepam, and vecuronium by the combined nurse-physician Air EMS flight team. Post-intubation vital signs were as follows: blood pressure 130/69 mmHg, pulse 95 bpm, respirations 14/min (assisted), and oxygen saturation 98% on 100% FiO 2 . The patient's temperature on arrival to the Emergency Department (ED) was 98.2°F (36.8°C), where his examination remained unchanged.Diagnostic studies were obtained in the ED. Arterial blood gas analysis on 100% O 2 showed: pH 7.24, pCO 2 58 mmHg, pO 2 284 mmHg, oxyhemoglobin 97.2%, deoxyhemoglobin 2.0%, methemoglobin 0.3%, and carboxyhemoglobin 0.0%. The blood appeared red. An electrocardiogram revealed a narrow complex tachycardia, without Q waves, ST-segment abnormalities, or interval changes. Serum chemistries were as follows: a sodium of 139 mEq/L, potassium of 4.2 mEq/L, chloride of 105 mEq/L, bicarbonate of 25 mEq/L, BUN of 15 mg/dL, creatinine of 0.9 mg/dL, and glucose of 156 mg/dL. Creatinine kinase (CK) was 299 IU/L, CK-MB 2.2 IU/L, and troponin-I was 0.05 IU/L. A complete blood count showed: white blood cells at 9.0 k/mm 3 , hemoglobin at 13.0 g/dL, hematocrit at 38.2%, and platelets at 130/mm 3 . Coagulation studies were normal, and a chest radiograph showed adequate endotracheal tube placement, absence of pulmonary edema, and a widened mediastinal silhouette, likely due to projection artifact on an antero-posterior film.Patient #2 was a 53-year-old male co-worker, with a history of hypertension, but he was not receiving medical therapy. He was

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Section: What Therapeutic Modalities Exist To Treat Acute H 2 S Exposmentioning

confidence: 99%

Section: What Therapeutic Modalities Exist To Treat Acute H 2 S Exposmentioning

confidence: 99%

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Case files of the university of cincinnati fellowship in medical toxicology: Two patients with acute lethal occupational exposure to hydrogen sulfide

Policastro

Otten

2007

J. Med. Toxicol.

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“…Patients with polycythemia vera or, less commonly, secondary polycythemia are also at risk of thrombotic events caused by hyperviscosity associated with uncontrolled erythrocytosis. Urgent red cell depletion, by phlebotomy or automated erythrocytapheresis, is warranted in severely affected patients [14,55,81,96,137].…”

Section: Hematologic Disordersmentioning

confidence: 99%

“…Babesiosis, caused by the tick-born parasite Bebesia, can also cause severe hemolysis and multiplesystem complications in immunocompromised, asplenic, or elderly patients. As in fulminant malaria, these patients quickly respond to red cell exchange of 1 to 1.5 blood volumes [14,96,137,150,151].…”

Section: Hematologic Disordersmentioning

confidence: 99%

Use of Cellular and Plasma Apheresis in the Critically Ill Patient: Part II: Clinical Indications and Applications

Linenberger

Price

2005

J Intensive Care Med

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Apheresis is the process of separating the blood and removing or manipulating a cellular or plasma component for therapeutic benefit. Such procedures may be indicated in the critical care setting as primary or adjunctive therapy for certain hematologic, neurologic, renal, and autoimmune/rheumatologic disorders. In part I of this series, the technical aspects of apheresis were described and the physiologic rationale and clinical considerations were discussed. This review highlights the pathophysiologic basis, specific clinical indications, and treatment parameters for disorders that more commonly require management in the intensive care unit. The choice of plasma or cellular apheresis in these cases is guided by well-accepted, evidence-based clinical treatment guidelines. For some disorders, such as liver failure, severe sepsis, and multiple-organ dysfunction syndrome, apheresis treatment approaches remain experimental. Ongoing studies are investigating the potential utility of conventional plasma exchange, ex vivo plasma manipulation, and newer technologies for these and other disorders in severely ill patients.

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