Poliomyelitis-like illness after acute asthma.

Two children had pain in one arm, followed by weakness and wasting, after an acute exacerbation of bronchial asthma. Similar cases in which a poliomyelitis-like illness was associated with acute asthma have been reported, but the relationship between the two remains conjectural.     

Poliomyelitis-like illness associated with asthma.

A 10-year-old girl with a combination of paralytic disease, resembling poliomyelitis, and asthma is described. The girl developed neurological symptoms 5 days after a severe attack of asthma. No aetiology to the flaccid paralysis could be demonstrated although Coxsackie B5 virus was isolated from a stool. A similar poliomyelitis-like illness associated with asthma has previously been reported in 13 cases from Australia and the UK.     

Poliomyelitis-like paralysis during recovery from acute bronchial asthma: possible etiology and risk factors.

A poliomyelitis-like paralytic disease during recovery from an attack of bronchial asthma is described in two young children. They presented at the age of 13 and 22 months, respectively, with acute flaccid paralysis of one or both lower limbs and preserved sensation. Cerebrospinal fluid examinations revealed mild protein elevation in both and pleocytosis in the second infant. Enteroviruses were isolated in a nasal swab and stools of the second patient. Acute onset of flaccid paralysis with absent motor action potential and normal sensory responses, detected by electrophysiologic studies, are highly suggestive of motor anterior horn cell disease in these infants. A multifactorial setup of immune suppression, stress, and neurotoxic drugs during an acute bronchial asthma attack triggered by a viral disease may render the patient vulnerable to viral invasion of the anterior horn cell with enteroviruses other than poliovirus. The overall experience of 22 patients with this serious complication is reviewed.     

Persistent increase in plasma and urinary leukotrienes after acute asthma

Leukotrienes may mediate bronchoconstriction in asthma. Cysteinyl leukotriene production rises in vivo after allergen challenge, but few reports describe leukotriene concentrations in clinical asthma or in children. Using high performance liquid chromatography/radioimmunoassay, plasma and urinary leukotrienes in asthmatic children (aged 5-10 years) were measured during an acute exacerbation (peak expiratory flow (PEF) < 65%, n = 10) and one month later (PEF 74-169%, n = 9), and in non-atopic normal children (aged 1.3-13.2 years). In the asthmatics, geometric mean (95% confidence interval) plasma leukotriene B4 (LTB4) was 746 pg/ml (398 to 1403) acutely and 1026 pg/ml (662 to 1593) in remission, compared with 369 pg/ml (167 to 728) in the normal children (n = 14). Plasma cysteinyl leukotrienes were low or undetectable, but urinary leukotriene E4 (LTE4) was higher in the asthmatics during an acute episode (210 pmol/mmol creatinine, 101 to 454) and at follow up (179 pmol/mmol, 110 to 293), compared with the normal children (98 pmol/mmol, 81 to 118, n = 41). This persistent increase in plasma LTB4 and urinary LTE4 concentrations one month after a severe asthmatic episode suggests leukotriene production is related to chronic inflammation rather than to acute bronchoconstriction.     

Persistent increase in plasma and urinary leukotrienes after acute asthma.

Leukotrienes may mediate bronchoconstriction in asthma. Cysteinyl leukotriene production rises in vivo after allergen challenge, but few reports describe leukotriene concentrations in clinical asthma or in children. Using high performance liquid chromatography/radioimmunoassay, plasma and urinary leukotrienes in asthmatic children (aged 5-10 years) were measured during an acute exacerbation (peak expiratory flow (PEF) < 65%, n = 10) and one month later (PEF 74-169%, n = 9), and in non-atopic normal children (aged 1.3-13.2 years). In the asthmatics, geometric mean (95% confidence interval) plasma leukotriene B4 (LTB4) was 746 pg/ml (398 to 1403) acutely and 1026 pg/ml (662 to 1593) in remission, compared with 369 pg/ml (167 to 728) in the normal children (n = 14). Plasma cysteinyl leukotrienes were low or undetectable, but urinary leukotriene E4 (LTE4) was higher in the asthmatics during an acute episode (210 pmol/mmol creatinine, 101 to 454) and at follow up (179 pmol/mmol, 110 to 293), compared with the normal children (98 pmol/mmol, 81 to 118, n = 41). This persistent increase in plasma LTB4 and urinary LTE4 concentrations one month after a severe asthmatic episode suggests leukotriene production is related to chronic inflammation rather than to acute bronchoconstriction.     

Immunological abnormalities in the syndrome of poliomyelitis-like illness associated with acute bronchial asthma (Hopkin's syndrome).

In recent years an unusual syndrome of poliomyelitis-like illness, associated with acute bronchial asthma, has been reported from different parts of the world. A further 3 cases are described in this paper. Although the condition resembles poliomyelitis in most respects, particularly with regard to the severe permanent residual weakness usually observed, consistent evidence of a viral aetiology has not been forthcoming. Tests of immune function suggested the presence of varying degrees of nonspecific immune deficiency in our 3 patients, but evidence of viral invasion was inconclusive. It is suggested that a combination of immune deficiency with the stress of the acute asthma attack rendered the patients susceptible to invasion of the anterior horn cells by a viral agent, which may have been of external origin, or may have existed in a latent form within the host.     

Improving follow-up for children with asthma after an acute Emergency Department visit

OBJECTIVE: To improve follow-up with primary care providers after acute Emergency Department (ED) asthma visits for children from low-income urban families. STUDY DESIGN: A prospective, randomized, controlled trial evaluated combined telephone asthma coaching and monetary incentive. The primary outcome was asthma-planning visits with primary care providers within 15 days of index ED visits. The subjects were urban parents whose children were treated for asthma in the ED and had Medicaid or no insurance. RESULTS: We enrolled 527 parents (264 control and 263 intervention). There was a significant difference ( P < .0001) between the intervention (35.7%) and control (18.9%) groups in the proportion of children who had asthma-planning visits and decreased mean nights/days with asthma symptoms by 4.36 intervention and 3.31 control at 2 weeks. The proportions of children with asthma-planning visits and acute asthma care visits during the 16-day to 6-month period were similar for both groups. CONCLUSIONS: Telephone coaching and a monetary incentive significantly increased the proportion of low-income urban parents who brought their children for asthma-planning visits, and decreased asthma symptoms shortly after asthma ED visits. The intervention did not increase subsequent asthma-planning visits or decrease ED visits or hospitalizations.     

Management of acute asthma

Hospitalization due to acute severe asthma represents a failure in the preventive, long-term as well as home care of asthma. Recognition of danger signs and prompt treatment can prevent the risk of morbidity and mortality of an acute asthma episode. The principle pharmacological management is use of inhaled beta2 sympathomemetrics and systemic steroids given with monitoring of respiratory status with the help of clinical parameters and pulmonary function tests. In patients non responsive to routine management, there is a role of inhaled cholinergic compounds, intravenous magnesium sulphate, and beta2 sympathomemetic infusion. Patients in respiratory failure need intensive care. Carefully managed prognosis of an acute attack of asthma is good.     

Inhaled budesonide in acute asthma

OBJECTIVE: To evaluate the efficacy of aerosolized budesonide therapy (with metered dose inhaler and spacer) early in the emergency room treatment of acute moderate exacerbations of bronchial asthma in children. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Paediatric Emergency Service of an urban teaching hospital and a tertiary case referral centre. STUDY POPULATION: Sixty children between 3 and 12 years of age with an acute moderate exacerbation of asthma. INTERVENTION: All patients received humidified oxygen (5-8 L/min by Venturi(R) mask; Hudson Respiratory Care, Temecula, CA, USA), nebulized salbutamol (0.15 mg/kg in 3 mL saline) and were randomized to receive either budesonide (400 microg) or placebo inhalation (MDI and spacer) at half hourly intervals for three doses. If there was an inadequate response or no response to treatment at the end of 2 h, oxygen and salbutamol therapy were continued and the patient was given one of dose intravenous hydrocortisone and was started on an aminophylline infusion. If there was no response at the end of a further 4 h, the patient was hospitalized. INITIAL EVALUATION AND MONITORING: Colour, respiratory rate (RR), heart rate, accessory muscle usage, chest retraction, wheeze, oxygen saturation (by pulse oximetery) and peak expiratory flow rate (PEFR) was recorded at admission and thereafter at hourly intervals for 3 h or until till the child recovered. The need for oxygen therapy after 2 h and need for hospitalization were recorded. MAIN RESULTS: Both groups showed a significant improvement in respiratory status at the end of 2 h. However, children in the intervention group showed greater improvements in RR and PEFR (P < 0. 05) and respiratory distress score (P < 0.1). A significantly lower proportion of the intervention group patients required oxygen therapy for more than 2 h (23% vs 50%; P < 0.05) and aminophylline infusion and systemic corticosteroid therapy (7% vs 27%; P < 0.05). None of the children in the budesonide group, in contrast to 23% of those in the placebo group, required hospitalization (P < 0.05). The length of hospital stay (i.e. time taken to recover from acute asthma) was significantly shorter in the intervention group (3.2 +/- 2.5 h) than in the placebo group (7.8 +/- 11.3 h; P < 0.01). CONCLUSION: Aerosolized budesonide therapy (with MDI and spacer) together with nebulized salbutamol early in the emergency room treatment of acute moderate exacerbations of asthma helped in early recovery and decreased the need for hospitalization. It may be worthwhile calculating this regimen for home-based early treatment of acute exacerbations.     

Magnesium sulfate in acute asthma

Conclusion Intravenous magnesium sulfate in dose of 50–100 mg/kg disolved in 30–50 ml normal saline, infused over about 30 minutes is a promising drug for acute severe exacerbations of chilhood asthma, not responding to conventional therapy.     

Managing acute asthma in children

Acute asthma is the most common medical emergency in children. Despite the widespread distribution of national guidelines∩ treatment is variable and often suboptimal. Audit has shown that clinical guidelines improve the outcome of children treated in emergency departments with asthma. The assessment of children with asthma is different from that in adults and this may lead to the severity being underestimated. Core therapies including oxygen, high-dose inhaled β₂gonists and oral steroids should be initiated without delay following assessment. Second-line therapies including inhaled ipratropium and parenteral aminophylline may be considered if the child is not improving. If there is no clear improvement, failure of treatment needs to be considered as children may deteriorate rapidly.Children presenting to an emergency department with asthma, often have poor background control and the opportunity to review chronic therapy and provide education should not be missed.