Janet Shapiro

Management of respiratory failure in status asthmaticus.

Status asthmaticus is a life-threatening episode of asthma that is refractory to usual therapy. Recent studies report an increase in the severity and mortality associated with asthma. In the airways, inflammatory cell infiltration and activation and cytokine generation produce airway injury and edema, bronchoconstriction and mucus plugging. The key pathophysiological consequence of severe airflow obstruction is dynamic hyperinflation. The resulting hypoxemia, tachypnea together with increased metabolic demands on the muscles of respiration may lead to respiratory muscle failure.The management of status asthmaticus involves intensive pharmacological therapy particularly with β-adrenoceptor agonists (β-agonists) and corticosteroids. Albuterol (salbutamol) is the most commonly used β2-selective inhaled bronchodilator in the US. Epinephrine (adrenaline) or terbutaline, administered subcutaneously, have not been shown to provide greater bronchodilatation compared with inhaled β-agonists. Corticosteroids such as methylprednisolone should be administered early. Aerosolized corticosteroids are not recommended for patients with status asthmaticus. Inhaled anticholinergic agents may be useful in patients refractory to inhaled β-agonists and corticosteroids. In patients requiring mechanical ventilation, the strategy aims to avoid dynamic hyperinflation by enhancing expiratory time to allow complete exhalation. Complications of dynamic inflation are hypotension and barotrauma. Sedation with opioids, benzodiazepines or propofol is required to facilitate ventilator synchrony but neuromuscular blockade should be avoided as myopathy has been a reported complication.Overall, in the management of patients with status asthmaticus, the challenge to the pulmonary/critical care clinician is to provide optimal pharmacological and ventilatory support and avoid the adverse consequences of dynamic hyperinflation.

Efficacy of deep venous thrombosis prophylaxis in the medical intensive care unit.

The purpose of this study was to determine the incidence of deep venous thrombosis in medical intensive care unit patients receiving deep venous thrombosis prophylaxis. This was a prospective cohort study of 141 consecutive adult patients anticipated to remain in the medical intensive care unit for >48 hours. Deep venous thrombosis prophylaxis was provided using subcutaneous unfractionated heparin or a sequential compression device according to risk-stratified protocol. Compression ultrasound was performed. Fourteen patients (9.9%) developed deep venous thrombosis on follow-up studies. Incidence of deep venous thrombosis was 7.9% per person year (95% confidence interval, 4.8-12.8). Two of 14 developed pulmonary embolism. Eight patients required full anticoagulation with intravenous heparin or coumadin. In-hospital mortality was similar in both groups. Patients with deep venous thrombosis had a statistically higher risk of pulmonary embolism: 14.2% (95% confidence interval, 2.0-43.0) versus 0.0% (95% confidence interval, 0-3; P = .009). Incidence of deep venous thrombosis is high in medical intensive care unit patients receiving standard prophylaxis. Adherence to strict deep venous thrombosis prophylaxis protocol and exploration of other prophylaxis regimens should be pursued.

Myopathy in Status Asthmaticus: Relation to Neuromuscular Blockade and Corticosteroid Administration

Myopathy is a rare complication that arises during management of status asthmaticus that may be related to administration of corticosteroids and neuromuscular blocking agents. We present 4 patients with myopathy and a review of the 31 previously reported patients in the literature. All patients received corticosteroids, and 33 of the 35 patients received neuromuscular blocking agents. Muscle weakness was often diffuse and, in several patients, involved the muscles of respiration. Creatine kinase values ranged from normal to markedly elevated. Diagnosis was obtained by electromyogram and muscle biopsy in most patients. Resolution of the muscle weakness occurred over a period of days to months. Patients in whom myopathy developed required mechanical ventilation for longer periods than patients intubated for status asthmaticus without myopathy.

Effect of Bronchoalveolar Lavage on Gas Exchange in Patients with Diffuse Lung Disease and Respiratory Failure

The effect of fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) on arterial oxygenation was examined in 22 patients with acute respiratory failure requiring mechanical ventilatory support. Arterial blood gases were determined immediately prior to BAL and at 15, 60, 120, and 360 minutes following BAL. PaO2/FIO2 decreased at 15 minutes and continued to decrease to approximately 33% below the baseline value at 2 hours. PaO2/FIO2 then remained constant over the remainder of the 6-hour study period. No substantial changes in FIO2, level of positive end-expiratory pressure, or intravenous pressor requirements occurred during the period of observation. Patients with lower pre-BAL PaO2/FIO2 ratios showed the least reduction in PaO2/FiO2 following BAL The BAL was diagnostic in 9 of 22 (41%) patients (Pneumocystis carinii pneumonia in 5, bacterial pneumonitis in 2, and neoplastic involvement of the lung in 2). BAL was associated with mild deterioration of gas exchange but did not require significant changes in ventilatory or hemodynamic support for the 6-hour interval studied.

Complications of Therapeutic Hypothermia Following Cardiac Arrest

Randomized clinical trials and observational studies have shown that therapeutic hypothermia improves neurologic outcomes and survival in patients following cardiac arrest [1–3]. As the benefit is impressive, with the number needed to treat as low as six patients, therapeutic hypothermia should be applied to more and more patients [4]. At the same time, therapeutic hypothermia is a complex and expensive therapy requiring appropriate equipment, trained personnel, and close patient monitoring. A systematic approach to coordinate care at multiple levels is required for proper patient selection, effective implementation of therapy, and monitoring for possible complications. In our institution, we use a unified pathway-based approach to therapeutic hypothermia [5]. The pathway outlines patient management in a stepwise manner: from the field through the emergency department into the cardiac catheterization laboratory and to the critical care unit (step 1); induced invasive hypothermia protocol in the critical care unit (step 2); and management following the re-warming phase including decisions for future care based on neurologic outcome (step 3). Figure 8.1 shows the pathway for the management of the survivors of out-of-hospital cardiac arrest as implemented at St Luke’s Roosevelt Hospital Center, New York. The current chapter focuses on recognition and management of potential complications of hypothermia.