Herbal intoxication: psychoactive effects from herbal cigarettes, tea and capsules

Herbal intoxication: psychoactive effects from herbal cigarettes, tea and capsules

The source and removal of microaggregates in aged human blood and human blood components. Gervin ~, Mason KG, Buckman RF, et al, Surg Gynecol Obstet 1...

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The source and removal of microaggregates in aged human blood and human blood components. Gervin ~, Mason KG, Buckman RF, et al, Surg Gynecol Obstet 141:582"586, (Oct) 1975.

Herbal intoxication: psychoactive effects from herbal cigarettes, tea and capsules. Siegel R, JAMA 236:437476, 1976. H e r b a l preparations, designed to be smoked or ingested for

The authors review the previous studies on microaggregate forsation in h u m a n blood and their removal with specialized ultrapore filters. They point out t h a t such filters are expensive ~nd usually cannot handle large blood volumes and studied alLernate ways of removing microaggregates. The first was prevention of m i c r o a g g r e g a t e f o r m a t i o n (usually d e g e n e r a t i n g platelets, white blood cells, and an amorphous matrix) by in vitro addition of various concentrations of aspirin to the blood. Both low and high concentrations of aspirin prevented microaggregate formation. Microaggregates could be removed after formation by removal of the buffy coat t h r o u g h differential centrifugation or by washing and t h e n reconstituting the blood. The authors also point out in closing t h a t glycerol frozen red blood cells and blood components such as packed red cells and plasma are free of microaggregates_ They hope studies such as this one ~ill develop safe m e a n s for administering large quantities of blood with less fear of pulmonary and vascular complications from microaggregates. Richard Ostendorf, MD

"health and happiness," are promoted as legal hallucinogens, euphoriants, and m a r i h u a n a substitutes. A total of 25 psychoactive substances have been identified in these products, and a n u m b e r of intoxications have resulted from their short- or longterm use. Physicians should be alert to the n a t u r e of these effects when taking drug histories, and consider their passible role in the cause of medical complaints. (Editor's note: As "health food" industries grow, the use of all manner of "natural" substances brings a variety of signs and symptoms to the emergency department. Rather than asking only about medications, the physician should specifically ask about drugs, vitamins, "preparations," or natural substances when appropriate_)

m i c r o a g g r e g a t e s , r e m o v a l : u l t r a p o r e filters

The effects of carotid sinus pressure in re-entrance paroxysmal supraventricular tachycardia. Josephson ME, Seides SE, Batsford WB, et al, Am Heart J 88:694697, 1974. The effects of carotid sinus pressure (CSP) on 13 patients with paroxysmal atrial tachycardia (PAT) are discussed. Classically, CSP is supposed to abruptly terminate PAT to sinus r h y t h m without any gradual slowing, whereas CSP gradually slows a sinus tachycardia. In 13 patients known to have PAT, episodes of PAT were induced with atrial pacing and monitored with His's-bundle electrodes. The PAT was initiated when a critical A-V conduction delay was achieved by the atrial pacing. CSP terminated the r h y t h m by adding an additional A-V delay which broke the re-entrance cycle. In 12 of the 13 patients, r e t u r n to sinus r h y t h m from PAT was preceded by a gradual slowing over several beats. Thus, the gradual slowing of a supraventricular tacbycardia prior to conversion to normal sinus r h y t h m does not conclusively rule out PAT, and further diagnostic measures may be needed. Martin S. Kohn. MD

cardiovasology; tachycardia, paroxysmal supraventricular Effects and distribution of acute fat embolism in spontaneously breathing dogs using radioactive carbon triolein, Shaffer JW, Sealy WC, Seaber AV, et al, Surg Gynecol Obstet 141:387-393, (Sept) 1975. The authors studied the effects of fat injection in spontaneously breathing dogs to try to understand the pathophysiology of fat embolism in man. The acute effect seen in these dogs (as contrasted with other studies where the dogs are mechanically ventilated) was a distribution of the fat in the pulmonary and systemic vascular tree without evidence of inflammation. Hypoxia was of sudden onset and progressively worsened. P u l m o n a r y hypertension developed wi~bout any evidence of h e a r t failure or Pulmonary edema. While most of the fat remained in the lungs (76%), the t e r m i n a l event seemed to be cerebral fat embolism. The dogs had respiratory arrest without cardiac decompensation, cardiac arrest, or pulmonary edema. (Editor's note: There is still much controversy as to whether the h u m a n clinical syndrome of fat embolism is a real entity or a variant of post-traumatic pulmonary insufficiency combined with cerebral hypoxia. There ~s also debate as to whether the fat is mechanically embolized or is present as a chemical deposition in the low perfusion state, This set of experiments would indicate that, however it gets to the lung, fat may be the inducing cause o f an insufficiency syndrome.) Richard Ostendorf, MD

respiratory disease, fat embolism

-"~J~P6:2 (Feb) 1977

Robert Rothstein, MD

drug ingestion, herbal preparations Phenformin and lactic acidosis. Conlay LA, Loewenstein JE, JAMA 235:1575-1578, 1976. Phenformin hydrochloride-associatod lactic acidosis is probably more common t h a n most physicians realize. It tends to occur in patients with few previous hospitalizations and with no previous episodes of ketoacidosis. The patient will present in profound acidosis with a pH as low as 6.8, negative serum acetone, elevated serum lactate, and an elevated blood urea nitrogen level indicative of prerenal azotemia, In this study of all patients adm i t t e d to a university teaching hospital d u r i n g a 17-month period with severe lactic acidosis, phenformin-associated lactic acidosis accounted for 7% of the episodes of metabolic acidoms and 27% of deaths due to metabolic acidosis in diabetics. Since several alternative methods of controlling diabetes exist, the use of phenformin should be severely restricted and removal of the drug from the m a r k e t should be considered. (Editor's note: A t the triage desk, the most common complaint of these patients is weakness. A s with many metabolic disturbances, they frequently appear sicker than their complaints would indicate.)

Vincent Markovchick, MD

lactic acidosis, phenformin-associated Physical signs in childhood asthma. Commey JO, Levison H, Pediatrics, (Oct) 1976. The presence of seven physical signs of acute airway obstruction (dyspnea, wheezing, rhonchi, prolonged expiration, scalene contraction, supraclavicular i n d r a w i n g and sternocleidomastoid contraction) was correlated with the results of pulmonary function tests in 62 asthmatic children admitted to the emergency department with an acute flaring of their symptoms. All patients had some impairment of pulmonary function, with forced e x p i r a t o r y volumes (FEV1), m a x i m u m m i d e x p i r a t o r y flow (MMEF), and m a x i m u m expiratory flow rate (MEFR) below predicted normal values, and had expanded lung volumes with elevated functional residual capacity (FRC) and total lung capacity (TLC) values. However, only supraclavicular indrawing and sternocleidomastoid contraction consistently predicted the presence of severe obstructive disease, as determined by final vital capacity (FVC), FEV1, and MEFR values of less t h a n 50% of predicted normal. When present, these two signs should alert t h e e m e r g e n c y p h y s i c i a n to t h e p o s s i b i l i t y of a d i f f i c u l t therapeutic course. (Editor's note: Most asthmatic attacks are broken as outpatients. These clinical signs suggest those children who might benefit from early admission.)

Michael D. McGehee, MD

respiratory disease, acute airway obstruction, pediatric; asthma, pediatric Tachyarrhythmias in Wolff-Parkinson-White syndrome treatment and prevention. Tonkin AM, Gallagher JJ, -r~allace AG, JAMA 235:947-949, (Mar) 1976. Patients with Wolff-Parkinson-White (WPW) syndrome are most

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