European Review for Medical and Pharmacological Sciences 2006; 10: 135-151 Approach to respiratory failure in emergency department P. FORTE, M. MAZZONE, G. PORTALE, C. FALCONE, F. MANCINI, N. GENTILONI SILVERI Department of Emergency Medicine, Catholic University – Rome (Italy) Abstract. – Objectives and Background: The second mechanism (mismatch in blood The goal of this review is to provide update rec- gas exchanges) is due to the following differ- ommendations that can be used by emergency ent pathologies: physicians who provide primary cares to pa- tients with Acute Respiratory Failure (ARF), from • Adult acute respiratory distress syn- the admission to an emergency department drome; through the first 24 to 48 hours of hospitaliza- • Neonatal respiratory distress syndrome; tion. This work wants to address the diagnosis • Acute cardiogenic pulmonary oedema; and emergency medical care of ARF and the • Severe status asthmaticus; management of medical complications. • Pneumonia; State of the Art: A lot of statement has been developed for the early management and treat- • Airspace collapse (atelectasis); ment of ARF; moreover, over the last fifteen • Pulmonary embolism. years, we have assisted to the rise of a new technique of ventilation, in the Emergency De- The clinical signs and symptoms of patients partment: Non Invasive Ventilation. This kind of with ARF, refer to the two main manifesta- ventilation was firsthy applied in Intensive Care tions of pulmonary diseases: arterial hyper- and in Respiratory Care Unit. Randomized con- capnia and hypoxemia. trolled clinical trials have showed its usefulness in the early treatment of several forms of ARF, The pathophysiology of hypercapnia is together with medical therapy. based on four main mechanisms: Increase in CO2 production (for istance, Key Words: parenteral feeding with high doses of carbo- Respiratory failure, Pulmonary edema, Asthma, hydrates; high body temperature, etc.) Pneumoniae, Therapy in emergency department. Deterioration in gas exchanges as the in- crease in alveolar death space ventilation (for istance in Chronic Obstructive Pulmonary Disease – COPD –, because of mismatch in ventilation/perfusion ratio, and in pulmonary embolism); Introduction Deterioration in respiratory mechanics that involves a huge effort, an increase in res- Acute Respiratory Failure (ARF) was de- piratory work and the development of a rapid ↑ fined as the inability of the respiratory system shallow breathing CO2; to exchange gases and to oxygenate the blood Alteration in the mechanism of control of adequately1-8. We can distinguish two mecha- the ventilation (for istance, in chronic hyper- nisms at the basis of ARF: capnia, we observe a decrease in ventilatory 1. Failure in pulmonary ventilation (pump drive with an increase in tolerance threshold failure); to CO2; it happens in metabolic alkalosis 2. Failure in gas exchanges (lung failure). too). The hypoxemia is due to different patho- The first one is due to neuromuscular dis- physiological mechanisms: eases, chest wall deformities, obstructive pul- • Hypoventilation; monary diseases (Table I). • Alteration in gas diffusion; Corresponding author: [email protected]; [email protected] 135 P. Forte, M. Mazzone, G. Portale, C. Falcone, F. Mancini, N. Gentiloni Silveri Table I. Moreover he has to take an arterial blood gas sample and a peripheral venous blood Neuromuscular Drugs abuse sample to evaluate CK, CKMB, T-tropo- diseases Cervical tetraplegia Curare/strychnine/ nine, LDH, AST, ALT and hemochrome. phosphate poisoning 2. At the same time he must evaluate the Guillaine-Barré syndrome neurological state, in order to call for the Miastenia gravis; hereditary/ resuscitator if Kelly score (Table II) is acquired myopathies more than 3. Botulism/Poliomyelitis 3. If neurological state is not compromised Chest wall deformities Bilateral or hypertensive Pneumothorax patient can be managed by emergency Pneumomediastinum physician, entirely. Arterial blood gas Post-traumatism (ABG) evaluation: Obstructive diseases Severe Status Asthmaticus – Hypoxemia with hypercapnia → pump Central airways obstruction failure due to neuromuscular disease or chest wall deformities; Lung failure due to COPD or acute asthmatic status. • Mismatch in ventilation/perfusion ratio; This last situation can be treated with • Pulmonary shunt. pharmacological therapy and/or with non invasive ventilation, if indicated. Pa- Which are the clinical signs and symptoms tient must undergo endotracheal intuba- of hypoxemia and hypercapnia? The first one tion (ETI) if his clinical conditions dete- shows with shortness of breath, tachycardia, riorate. mental confusion, changes of personality, – Hypoxemia with no hypercapnia → restlessness, cyanosis, hyper/hypotension, ar- lung failure due to ARDS or cardio- rhythmias and palpitations. Hypercapnia, in- genic pulmonary oedema or pulmonary stead, shows with sleepiness, mental confu- embolism or pulmonary infection. If sion, cephalea, convulsions, arrhythmias, oxygen saturation in more than 90% miosis, papilledema, peripheral vasodilation, continue to administer O2 with face hypotension and coma. mask and high flows. If oxygen satura- The first goal of the initial diagnostic eval- tion is less than 90% consider the use uation is to understand the underling causes, of Non Invasive Ventilation (NIV), to- and so to do differential diagnosis among all gether with medical therapy. pathologic conditions that showed the most 4. Clinical evaluation must be associated important clinical symptom of this illness: with radiological evaluation (Chest X- dyspnoea. Rays) and with continuous ABG evalua- tions (after 1 hour and after each chang- ing in clinical conditions). Patient must undergo endotracheal intubation if his A – Approach to Patients clinical conditions deteriorate. with Dyspnoea Evidence and Information Sources Clinical Evaluation A comprehensive literature search was A patient with ARF usually presents with performed in order to select the latest rec- signs of respiratory distress: dyspnoea, cyanosis, tachypnea, accessory muscle use, paradoxical breathing and tachycardia. Pri- Table II. Kelly scale. mary care physician must apply the algorithm •Awoke patient, he executes 3 complex orders A-B-C-D, in order to exclude an Acute Up- •Awoke patient, he only executes simple orders per Airway Obstruction (AUAO), first of all, • Sleepy patient, he can be awaken under verbal and then he must operate as following: orders 1. He has to administer high flows of oxy- • Sleepy patient, he can be awaken under physical gen, to measure blood pressure, to take stimulus • Coma with no brainsteam alteration heart rate, respiratory rate, oxygen satu- • Coma with brainsteam alteration ration, to make an electrocardiogram. 136 Approach to respiratory failure in emergency department Table III. Infectious Viral laryngotracheitis (croup) Bacterial epiglottiditis Bacterial tracheitis Neoplasm Subglottic hemangioma Tracheal and endobronchial neoplasms Thyroid and mediastinal tumors Traumatic External bodies aspiration Anaphylaxis Obstructive Sleep Apnea Syndrome (OSAS) Neurogenic diseases Bilateral paralysis of recurrent nerve Modified by G. Garetto, La Nuova Medicina d’Urgenza, Ed. C.G. Torino11. ommendations for the early diagnosis and ryngeal obstruction). We usually observe the therapy of the pathologies below. asymmetries in diaphragmatic ranges, in res- In developing of the present guidelines we piratory movements, in the intercostal and considered the latest evidences in the man- supraclavicular re-entrances. agement of dyspnoea, asthma, COPD, ARDS If the physician suspects an epiglottiditis, he and we applied the ATS Consensus Confer- should be cautious in carrying out clinical ex- ence indications9 and the BTS guidelines10 for amination: in fact he could provoke a com- the use of NIV in ARF. plete obstruction stimulating with the tongue depressor. Moreover, if respiratory distress continues and the patient is stable (rapid shal- low breathing, valid cough, conscious, lucid B – Approach to Patients with and alert patient but with no cardiovascular al- Acute Upper Airway Obstruction terations) physician should take blood pres- (AUAO) sure and oxygen saturation, continuously, and often control ABG. If patient presents with respiratory arrest he should follow the Ad- Etiology vanced Life Support Algorithm. In a second The causes of AUAO can be summarized time physician should make differential diag- in Table III11. nosis between epiglottiditis and viral croup. Anaphylaxis: if patients present with glot- Clinical Evaluation tis’ oedema should be immediately intubated We distinguish two different types of upper before developing complete obstruction of airway obstruction: the extra thoracic pre- upper airways. Then they should be submit- sents inspiratory stridor, because of the col- ted to infusion therapy with adrenaline (1 mg lapse of upper extra thoracic airways, during in bolus repeatable), corticosteroids (hydro- the inspiration when tracheal pressure is mi- cortisol – methylprednisolone) at high doses, nor than atmospheric one. The intra thoracic fluids. one that presents expiratory stridor, because the extrathoracic airways collapse during the expiration, when the intrapleural pressure is Table IV. Infectious AUAO. greater than atmospheric one. The stridor is the main symptom of Supraglottic Severe tonsillitis (> 10 years) AUAO (Table IV), and it’s often associated Peritonsillar abscess (> 10 years) with cyanosis, loss of consciousness, nape’s