Epiglottitis--an increasing problem for adults.

In a 2-year period, 9 adults were admitted to hospital with acute epiglottitis confirmed by direct laryngoscopy or lateral neck radiograph, or both. The mean age was 53 +/- 14 years, with acute epiglottitis occurring in 89% during the months of September to March. Intubation was required in 4 patients. The duration of symptoms was 7.8 +/- 2.4 hours for intubated patients versus 18.8 +/- 8.9 hours for those not intubated. For 6 patients an incorrect diagnosis was made on their first presentation. All 8 patients having laryngoscopy had typical findings, and none had respiratory obstruction precipitated by the procedure. In 5 patients blood cultures were positive, 4 for Hemophilus influenzae type b, and 1 for Streptococcus pneumoniae. In 2 patients the H influenzae was ampicillin-resistant. All patients recovered after receiving parenteral steroid therapy and appropriate antibiotics.     

Detecting breast cancer

A 7-year-old boy, diagnosed as having croup, develops an upper airway obstruction due to epiglottitis during the therapy, resulting in cerebral anoxia. Pediatricians to whom the boy is referred feel that failure to consider epiglottitis in the original diagnosis constitutes negligence. The parents suspect nothing. What should the pediatricians say or do?     

Antimicrobial immunity in patients with acute epiglottitis

Fifty-three patients with catarrhal epiglottitis and 31 patients with epiglottic abscess aged 16-60 years were examined. It was determined that development of epiglottitis is tightly related to abnormalities in reactivity of phagocytic and humoral arms of immunity. Decreased affinity of produced antibodies, opsonizing properties of serum as well as phagocytic and biocide activity of neutrophils were revealed in patients. In patients with catarrhal and necrotic epiglottitis similar abnormalities of immunoreactivity were observed although in patientswith necrotic epiglottitis they were more pronounced.     

Airway Management in Croup and Epiglottitis

Treatment techniques for airway obstruction in croup and epiglottitis are reviewed in the medical literature. Series totaling 295 nasotracheal intubations, and 591 tracheostomies were reviewed. There were two deaths attributable to airway complications in 126 patients in whom nasotracheal intubation was carried out. In three patients subglottic granulation tissue and subglottic stenoses developed from short-term nasotracheal intubation. There were no subglottic stenoses or tracheal stenoses reported in the 591 tracheostomies. From this review, it would seem feasible to use nasotracheal intubation for short-term airway treatment in croup and epiglottitis. The increasing occurrence of laryngeal and tracheal complications with long-term intubation suggests that tracheostomy be considered in such cases.     

Beware of thermal epiglottis! A case report describing ‘teapot syndrome’

Background

The type of scalding injury known as ‘teapot syndrome’, where hot liquid is grabbed by the child with the aim of ingestion and falls over a child causing burns on the face, upper thorax and arms, is known to cause peri-oral and facial oedema. Thermal epiglottitis following scalds to face, neck and thorax is rare and can occur even in absence of ingestion of a damaging agent or intraoral burns, Awareness of the possibility of thermal epiglottitis, also in scald burns, is imperative to ensure prompt airway protection.

Case presentation

We report the case of a child with thermal epiglottitis after a scalding burn from boiling milk resulting in mixed deep burns of the face, neck and chest, but no history of ingestion. Upon presentation there was a progressive stridor and signs of respiratory distress requiring intubation. Laryngoscopy revealed epiglottis oedema, confirming the diagnosis of thermal epiglottitis. Final extubation took place 5 days after initial burn.

Conclusions

Thermal epiglottitis following scalds to face, neck and thorax is rare and can occur even in absence of ingestion and intra-oral damage. Burns to the peri-oral area should raise suspicion of additional damage to oral cavity and supraglottic structures, even in absence of intra-oral injury or initial respiratory distress. Awareness of the occurrence of thermal epiglottitis in absence of intra-oral injury is important to diagnose impending upper airway obstruction requiring intubation.

     

Haemophilus Epiglottitis: Nine Recent Cases in Oxford

Recent experience of epiglottitis in Oxford confirms the need for doctors in this country—especially family doctors and casualty officers—to be aware of this disease and to be able to recognize it and to take appropriate action immediately. Some important diagnostic and therapeutic implications both of the anatomy of the supraglottic lesion and of the septicaemic component of the illness are discussed.     

INTESTINAL OBSTRUCTION COMPLICATING ACUTE PERFORATIVE APPENDICITIS

Upon preoperative diagnosis of acute small bowel obstruction, without an obvious cause, acute perforative appendicitis must be considered. Reevaluation of the history and careful reexamination of the physical findings with that diagnosis in mind should be carried out. If appendiceal disease is likely, maximum antibiotic therapy must be begun immediately along with the administration of fluids, electrolytes and other corrective therapy. A mercury-weighted small bowel tube should be inserted and every effort made to advance it into the small bowel before operation. Operative treatment should be restricted to the least possible. A McBurney incision is best unless wider operation is indicated. If an abscess is present, drainage alone may be the procedure of choice. Severely distended and decompensated small bowel must be decompressed, for if not relieved it can be the cause of death in acute perforative appendicitis. Decompression may be accomplished either by small bowel intubation with continuous suction or by enterotomy and aspiration. If not relieved, small bowel distention will be the mechanism responsible for death in a large percentage of patients with acute perforative appendicitis.     

流感嗜血杆菌的研究进展

流感嗜血杆菌是嗜血杆菌属(Haemophilus influenzae)中对人有致病性的常见细菌,可引起小儿脑膜炎、中耳炎、会厌炎等原发化脓性感染及呼吸道继发感染。现就流感嗜血杆菌病的流行情况、实验室检查及其预防措施等方面的研究进展进行综述。     

Unusual acute effects of antidepressants and neuroleptics on S2-serotonergic receptors

The antidepressants mianserin and amoxapine, and the neuroleptic loxapine caused significant decreases in the number of rat frontal cortex S2-serotonergic receptors after a single acute injection. The affinity of serotonin for this site was also decreased after acute mianserin. Daily injections of loxapine and amoxapine for 2, 7 or 28 days resulted in decreased receptor density but no change in Kd. Down-regulation of S2 sites by mianserin was not dependent on endogenous serotonin stores or occupation of the S2 recognition site since chronic PCPA or acute ketanserin preadministration did not affect the mianserin-induced decreases. The results suggest that mianserin may be acting on other sites which it does not share in common with other S2-antagonists such as ketanserin.     

Artificial and Bioartificial Liver Support

The liver is a complex organ with various vital functions in synthesis, detoxification and regulation; its failure therefore constitutes a life threatening condition1. Liver failure (LF) can either occur without preceding liver disease (acute liver failure, ALF), usually caused either by intoxication (Amanita phalloides, acetaminophen, methylendioxymethamphteamine) or as acute decompensation of chronic liver-related illness (acute-on-chronic liver failure, AoCLF). In both cases, its symptoms include icterus, hepatic encephalopathy and impairment of coagulation status and may result in multi organ failure. Exceptionally, liver failure may also be triggered by certain diseases (Budd-Chiari-syndrome, Morbus Wilson) or pregnancy. The only long-term therapy in most cases is orthotopic liver transplantation, unless the liver is able to regenerate. Many patients, especially those who are not listed for high urgency transplantation, may not survive until a suitable donor organ is available, since donor organs are rare. In other cases, contraindications do not permit liver transplantation. For these indications, extracorporeal liver assist devices have been developed in order to either bridge the patient to transplantation or temporarily support the failing organ until it is able to regenerate.     

Long-Term Outcome of Critically Ill Adult Patients with Acute Epiglottitis

BackgroundAcute epiglottitis is a potentially life threatening disease, with a growing incidence in the adult population. Its long-term outcome after Intensive Care Unit (ICU) hospitalization has rarely been studied.

Methodology and Principal Findings

Thirty-four adult patients admitted for acute epiglottitis were included in this retrospective multicentric study. The mean age was 44±12 years (sex ratio: 5.8). Sixteen patients (47%) had a history of smoking while 8 (24%) had no previous medical history. The average time of disease progression before ICU was 2.6±3.6 days. The main reasons for hospitalization were continuous monitoring (17 cases, 50%) and acute respiratory distress (10 cases, 29%). Microbiological documentation could be made in 9 cases (26%), with Streptococcus spp. present in 7 cases (21%). Organ failure at ICU admission occurred in 8 cases (24%). Thirteen patients (38%) required respiratory assistance during ICU stay; 9 (26%) required surgery. Two patients (6%) died following hypoxemic cardiac arrest. Five patients (15%) had sequelae at 1 year. Patients requiring respiratory assistance had a longer duration of symptoms and more frequent anti inflammatory use before ICU admission and sequelae at 1 year (p<0.05 versus non-ventilated patients). After logistic regression analysis, only exposure to anti-inflammatory drugs before admission was independently associated with airway intervention (OR, 4.96; 95% CI, 1.06-23.16).

Conclusions and Significance

The profile of the cases consisted of young smoking men with little comorbidity. Streptococcus spp. infection represented the main etiology. Outcome was favorable if early respiratory tract protection could be performed in good conditions. Morbidity and sequelae were greater in patients requiring airway intervention.     

Metabolic effects of cigarette smoking.

The inverse relationship between cigarette smoking and body weight, a potent obstacle to stopping smoking, may be due in part to effects of smoking on increasing whole body metabolism. Studies examining chronic and acute metabolic effects of smoking, as well as its constituent nicotine, are reviewed. Evidence suggests the absence of a chronic effect; most studies indicate that smokers and nonsmokers have similar resting metabolic rates (RMR) and that RMR declines very little after smoking cessation. Although an acute effect due to smoking is apparent, its magnitude is inconsistent across studies, possibly because of variability in smoke exposure or nicotine intake. In smokers at rest, the acute effect of smoking (and nicotine intake) appears to be significant but small (less than 10% of RMR) and transient (less than or equal to 30 min). However, the specific situations in which smokers tend to smoke may mediate the magnitude of this effect, inasmuch as smoking during casual physical activity may enhance it while smoking after eating may reduce it. Sympathoadrenal activation by nicotine appears to be primarily responsible for the metabolic effect of smoking, but possible contributions from nonnicotine constituents of tobacco smoke and behavioral effects of inhaling may also be important. Improved understanding of these metabolic effects may lead to better prediction and control of weight gain after smoking cessation, thus increasing the likelihood of maintaining abstinence.     

Lipid management after acute coronary syndrome

PURPOSE OF REVIEW: Despite advances in medical therapy and percutaneous revascularization, patients with acute coronary syndrome face a high risk of early, recurrent cardiovascular events. Interventions targeting atherogenic lipoproteins may favorably modify this risk. RECENT FINDINGS: Two randomized clinical trials, MIRACL and PROVE-IT, demonstrated efficacy of early, intensive statin therapy after acute coronary syndrome. Recent observational and meta-analyses corroborate the findings of these trials. The benefit of intensive statin treatment appears to apply broadly to elderly as well as younger patients, and to patients with or without diabetes or metabolic syndrome. Randomized trials demonstrating the efficacy of early, intensive statin treatment after acute coronary syndrome employed fixed statin dosages, and there does not appear to be an initial or achieved LDL-cholesterol level below which benefit is absent. As such, broad application of intensive statin therapy after acute coronary syndrome may be preferable to titration of statin dose to achieve specific LDL goals. Low HDL-cholesterol predicts risk after acute coronary syndrome; therefore, pharmacologic interventions to raise HDL concentration or mimic its function may help reduce that risk. SUMMARY: Early, intensive statin therapy is safe and effective after acute coronary syndrome. Future research will determine whether drugs that raise or mimic HDL-cholesterol are effective adjuncts to statin therapy.     

Extracorporeal photopheresis (photochemotherapy) in the treatment of acute and chronic graft versus host disease: immunological mechanisms and the results from clinical studies

Extracorporeal photopheresis (ECP) is an immunomodulatory alternative for treatment of graft versus host disease (GVHD). The blood is then separated into its various components through apheresis; buffy coat cells are thereafter treated with 8-methoxypsoralen before exposure to ultraviolet light and finally reinfused into the patient. There is a general agreement that this treatment has an anti-GVHD effect, but the mechanisms of action behind this effect are only partly understood. However, altered maturation of dendritic cells (DC) and thereby indirect modulation of T-cell reactivity seems to be one important mechanism together with DC-presentation of antigens derived from apoptotic donor T cells and induction of regulatory T cells. The treatment has been best studied in patients with chronic GVHD (both pediatric and adult patients), but most studies are not randomized and it is difficult to know whether the treatment is more effective than the alternatives. The clinical studies of ECP in adults with acute GVHD are few and not randomized; it is not possible to judge whether this treatment should be a preferred second- or third-line treatment. There is no evidence for increased risk of leukemia relapse or suppression of specific graft versus leukemia reactivity by this treatment, so specific antileukemic immunotherapy may still be possible. Thus, even though the treatment seems effective in patients with GVHD, further clinical (especially randomized) as well as biological studies with careful standardization of the treatment are needed before it is possible to conclude how ECP should be used in acute and chronic GVHD.     

The artificial kidney and related procedures; a report on clinical experience

The Skeggs-Leonards artificial kidney and related methods were applied by the author in about thirty instances in patients with various kinds of renal disease. The treatment brought about clinical improvement of varying degree and appeared to be life-saving in four of five patients with acute renal failure. Treatment with the artificial kidney is indicated for patients with acute renal failure who develop clinical signs of uremia. The artificial kidney should be applied before the patient's condition has become irreversible. Removal of edema fluid is possible with modern artificial kidney equipment and appears to extend the therapeutic possibilities of the procedure. The artificial kidney may be of help in barbiturate and other intoxications. It affords temporary palliation in certain patients with chronic uremia; it may be used to overcome acute exacerbations of chronic renal disease; it may make it possible to operate on uremic patients who otherwise could not withstand operation.     

HIV-associated diseases: Acute and regressive encephalopathy in seropositive man

We observed the development of acute encephalopathy in a healthy human-immunodeficiency-virus(HIV)-seropositive man. HIV was isolated from cerebrospinal fluid but not from peripheral blood. Signs and symptoms resolved quickly without treatment. This viral isolate could be propagated only in umbilical cord lymphocytes, but not in peripheral blood T lymphocytes or in continuous lymphoblastoid cell lines such as CEM. The absence of the virus in the patient's T lymphocytes or infectivity of the virus for T lymphocytes may explain the unusual presentation of HIV-associated encephalopathy without immunodeficiency in an asymptomatic carrier. Moreover, it raises the possibility that acute expression of HIV can be controlled by natural host defence mechanisms and that clinical manifestations may be reversible despite the fact that the patient remains seropositive.     

A hassle a day may keep the pathogens away: The fight-or-flight stress response and the augmentation of immune function

Stress is known to suppress or dysregulate immune function and increase susceptibility to disease. Paradoxically, the short-term fight-or-flight stress response is one of nature's fundamental defense mechanisms that galvanizes the neuroendocrine, cardiovascular, and musculoskeletal systems into action to enable survival. Therefore, it is unlikely that short-term stress would suppress immune function at a time when it may be critically required for survival (e.g., in response to wounding and infection by a predator or aggressor). In fact, studies have shown that stress can enhance immune function under certain conditions. Several factors influence the direction (enhancing versus suppressive) of the effects of stress on immune function: (1) Duration: acute or short-term stress experienced at the time of activation of an immune response enhances innate and adaptive immune responses. Chronic or long-term stress can suppress or dysregulate immune function. (2) Leukocyte distribution: compartments (e.g., skin), that are enriched with immune cells during acute stress show immuno-enhancement, while those that are depleted of leukocytes (e.g., blood), show immuno-suppression. (3) The differential effects of physiologic versus pharmacologic stress hormones: Endogenous hormones in physiological concentrations can have immuno-enhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immuno-suppressive. (4) Timing: immuno-enhancement is observed when acute stress is experienced during the early stages of an immune response while immuno-suppression may be observed at late stages. The type of immune response (protective, regulatory/inhibitory, or pathological) that is affected determines whether the effects of stress are ultimately beneficial or harmful for the organism. Arguments based on conservation of energy have been invoked to explain potential adaptive benefits of stress-induced immuno-suppression, but generally do not hold true because most mechanisms for immuno-suppression expend, rather than conserve, energy. We propose that it is important to study, and if possible, to clinically harness, the immuno-enhancing effects of the acute stress response that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve.     

The anticancer drug cytarabine does not interact with the human erythrocyte membrane

Cytarabine, an analog of deoxycytidine, is an important agent in the treatment of ovarian carcinoma, acute myeloid and lymphoblastic leukemia. Its mechanism of action has been attributed to an interference with DNA replication. The plasma membrane has received increasing attention as a possible target of antitumor drugs, where the drugs may act as growth factor antagonists and receptor blockers, interfere with mitogenic signal transduction or exert direct cytotoxic effects. Furthermore, it has been reported that drugs that exert their antiproliferative effect by interacting with DNA generally cause structural and functional membrane alterations which may be essential for growth inhibition by these agents. This paper describes the studies undertaken to determine the structural effects induced by cytarabine to cell membranes. The results showed that cytarabine, at a concentration about one thousand times higher than that found in plasma when it is therapeutically administered, did not induce significant structural perturbation in any of these systems. Therefore, it can be unambiguously concluded that this widely used anticancer drug does not interact at all with erythrocyte membranes.     

ON THE DIFFERENTIAL CYTOTOXICITY OF ACTINOMYCIN D

Actinomycin D (AMD) at concentrations that inhibit cellular RNA synthesis by 85% or more causes an acute phase of lethal cell degeneration in HeLa cultures beginning as early as 3 hr after drug exposure, resulting in the nearly complete loss of viable cells by 12 hr. The loss of cells during this acute phase of lethality is closely dose dependent. Vero, WI38, or L cells are not susceptible to this early acute cyto-intoxication by AMD, and may begin to die only after 1–2 days. Differential susceptibility to acute cyto-intoxication by AMD, or other inhibitors of RNA synthesis (daunomycin or nogalamycin), among different types of cultured cells is analogous to that observed in vivo in certain tissues and tumors, and cannot be accounted for by differences in the effect of AMD on RNA, DNA, or protein syntheses, or by the over-all loss of preformed RNA. Actinomycin D in a dose that inhibits RNA synthesis causes an equivalent loss of the prelabeled RNA in all the cell types studied. Inhibition of protein synthesis with streptovitacin A or of DNA synthesis with hydroxyurea does not cause acute lethal injury in HeLa cells as does inhibition of RNA synthesis. Furthermore, since Vero or L cells divide at about the same rate as HeLa cells, no correlation can be drawn between the rate of cell proliferation and susceptibility to the cytotoxicity of AMD. Susceptibile cells are most vulnerable to intoxication by AMD in the G₁-S interphase or early S phase. Inhibition of protein synthesis (which protects cells against damage by other agents affecting DNA) does not protect against AMD-induced injury. Although HeLa cells bind more AMD at a given dose than Vero or L cells, the latter cell types, given higher doses, can be made to bind proportionally more AMD without succumbing to acute cyto-intoxication. It is suggested that the differential susceptibility of these cell types to acute poisoning by AMD may reflect differences among various cells in the function or stability of certain RNA species not directly involved in translation whose presence is vital to cells. In HeLa cells, these critical species of RNA are presumed to have a short half-life.