Nail varnish/synthetic \201 ngernails (if a \201 nger probe is used). \200 Excessive movement. Correlate readings with clinical \201 ndings: a non-pulsatile trace (or heart r ate different from that on cardiac monitor) suggests the saturation reading is probably ina ccurate. 97 HYPERVENTILATION Hyperventilation Hyperventilation is breathing which occurs more deeply and/or more rapidly than normal. CO 2 is \200\230blown off \200\231, so that pCO 2 d . Hyperventilation may be primary ( \200\230psychogenic \200\231) or secondary. A classical secondary cause is DKA \200\224 Kussmaul \200\231s respiration represents respiratory compensation for a metabol ic acidosis. Secondary causes of hyperventilation \200 Metabolic acidosis (eg DKA, uraemia, sepsis, he patic failure). \200 Poisoning (eg aspirin, methanol, CO, cyanide, ethylene glycol). \200 Pain/hypoxia. \200 Hypovolaemia. \200 Respiratory disorders (eg PE, asthma, pneum othorax). Primary (psychogenic or inappropriate) hyperventilation Typically, the patient is agitated and distressed with a past history of panic attacks or episodes of hyperventilation. They m ay complain of dizziness, circumoral paraesthesia, carpopedal spasm, and occasionally sharp or stabbing chest pain. Initial examination reveals tachypnoea with equal air entry over b oth lung \201 elds, and no wheeze or evidence of airway obstruction. It is important to c onsider secondary causes (such as PE or DKA). Therefore, perform the following investigatio ns: \200 SpO 2. \200 ECG. \200 ABG if SpO 2 d , or if symptoms do not completely sett le in a few minutes. BMG. If symptoms do not completely settle in a few minutes, obtain: \200 CXR. \200 U&E, blood glucose, FBC. Treatment Do not sedate a patient who is hyperventilating. Once seriou s diagnoses have been excluded, use this information to help reassure the patient with prim ary hyperventilation. Often this is all that is required, but it may be helpful to try simp le breathing exercises (breathe in through nose \200\224 count of 8, out through mouth \200\224 count of 8, hold for count of 4 and repeat). Discharge the patient with arrangemen ts for GP follow-up. If these simple measures fail, reconsider the diagnosis and refer the patient to the medical team for subsequent observation and treatment. 98 CHAPTER 3 Medicine Arterial blood gasses Blood gas sampling is useful in assessing breathless patients, septic patients, diabetic patients in ketoacidosis, those who are critically ill and patients who have ingested poisons. This enables rapid measurement of blood pH, bicarbonate, O 2 and CO 2 . Most ED blood gas analysers will also measure blood glucose, K + , Hb, and lactate, so arterial or venous blood gas sampling will also test for anemia, hyperkalaemia, and hypogl ycaemia. Assessing respiratory function Arterial sampling helps in the assessment of a patient with low SpO 2 , or in patients with known lung disease (especially if they are receiving supple mental oxygen). If possible (caution required), take the \201 rst sample with the patient breathing room air. If this is not possible, document the inspired oxygen concentration. L ook speci \201 cally for: \200 Hypoxia, (pO 2 <10.6kPa on air). \200 Hypercarbia, (pCO 2 > 6.0kPa). \200 Bicarbonate retention (HCO 3 \200\223 > 28mmol/L). \200 Acidosis (p H <7.35). Differentiating between type I and type II respiratory failure In type I failure there is hypoxia with normal or d pCO 2 . In type II failure, there is hypoxia with i pCO 2 , and frequently an i HCO 3 \200\223 . In type II failure, the patient may develop life-t hreatening respiratory failure if administered high concentrations of oxygen. Aim to mainta in SpO 2 at 88 \200\22392 % , and recheck ABGs in 30min. Differentiating between acute and chronic type II respiratory failure Patients who normally have a slightly i pCO 2 will also show i HCO 3 \200\223 on ABG. The kidneys adapt over a period of days to retain bicarbonate, in attempt to buffer the respiratory acidosis (see no mogram inside front cover). Respiratory acidosis in a patient with chronic type II respira- tory failure ( i pCO 2 , i HCO 3 \200\223 and pH <7.35) indicates life-threatening impair ment of lung function. In acute respiratory failure, the lungs are unable to eliminate CO 2 (caused by d GCS or hypoventilation from any cause), which results in i pCO 2 and a respir atory acidosis. Patients may require ventilatory support. A venous blood sample will give a ccurate readings for K + , lactate, glucose, HCO 3 \200\223 , Hb and COHb. In addition, a normal venous pCO 2 will exclude hypercarbia. Other blood gas results Blood gas analysers calculate the base excess from the HCO 3 \200 \223 concentra- tion and pH. Levels < \200\2232mmol/L indicate that the patient has a metab olic acidosis. Levels > 2mmol/L indicate a metabolic alkalosis (for example, as a result of chronic bicarbonate retention in type II respiratory failure). 99 ARTERIAL BLOOD gasses Metabolic acidosis The usual pattern of results in metabolic acidosis is pH<7.35, HCO 3 \200\223 <24mmol/L and BE < \200\2232mmol/L. There may be compensatory hypocarbia (pCO 2 <4 .5kPa). Metabolic acidosis has many possible causes: \200 i Acid load (lactic acidosis, k etoacidosis, or ingestion of salicylates, methanol, ethylene glycol, or metformin). d Removal of acid (renal failure or renal tubular acidosis types 1 and 4). \200 Loss of b icarbonate from the body (diarrhea, pancreatic, or intestinal \201 stulas, acetazolamide, or renal tubular acidosis type 2). The anion gap The anion gap is the quantity of anions not balanced out by cations, (a measu rement of negatively charged plasma proteins). The normal value is 12 \200\22316mmol/L. It is measured by: (Na + + K + ) \200\223 (Cl \200\223 + HCO 3 \200\223 ) all measured in mmol/L Measuring the anion gap helps distinguish the cause of a metabolic acidosis. A high anion gap indicat es that there is excess H + in the body. The commonest cause of a high anion gap metabolic acidosis is lactic acidosis. Most blood gas analysers will measure lactate (normal <2.0mmol /L). Causes of a lactic acidosis \200 Tissue hypoperfusion (trauma with major hemorrhage, sept ic shock). \200 Tissue hypoxia (hypoxaemia, carbon monoxide or cyanide poisoning). \200 Hepatic failure. \200 Renal failure. \200 Ethylene glycol or methanol poisoning ( b p. 203; b p.202). \200 Cocaine or amphetamines ( b p.215). \200 Salicylate poisoning ( b p .189) or iron poisoning ( b p.201). \200 Biguanides (metformin). \200 Isoniazid. \200 Strenuous exercise. The other causes of a high anion gap metabolic acidosis are ketoacidos is (diabetic or alcohol induced) and renal failure. Causes of a normal anion gap metabolic acidosis are chronic diarrhea, pancreatic or intesti nal \201 stulas, acetazolamide, or renal tubular acidosis. The osmolal gap This is the difference between calculated serum osmolarity and laboratory m easured serum osmolality. Serum osmolarity can be calculated by: (2 \227 Na + ) + urea + glucose (all measured in mmol/L) Subtract the calculated result fr om the laboratory measured osmolality to give the osmolal gap. Normally this is <10mOsm/kg. An elevated osmolal gap can be caused by alcohol, methanol, ethylene glycol or acetone inge stion, mannitol, or sorbitol. 100 CHAPTER 3 Medicine Cardiogenic pulmonary oedema Left heart failure results ine i left ventricular end-diastoli c pressure, causing i pulmonary capillary hydrostatic pressure. Fluid collects in extravasc ular pulmonary tissues faster than the lymphatics clear it. Causes of cardiogenic pulmonary oedema Often an acute complication of MI and IHD, or exacer bation of pre-ex- isting cardiac disease (eg hypertension, aortic/mitral valve disease). Ot her causes are: \200 Arrhythmias. \200 Failure of prosthetic heart valve. \200 Ventri cular septal defect. \200 Cardiomyopathy. \200 Negatively inotropic drugs (eg B -blocke rs). \200 Acute myocarditis. \200 Left atrial (LA) myxoma (may produce syncope, fever, i ESR, but is very rare). Pericardial disease. The history is frequently dramatic. Dyspnoea and distress may prevent a full history from b eing taken. Find out the length of the history and whether there is any chest pain. Check c urrent drug therapy/allergies and establish what emergency prehospital treatment has been a dministered. Examination usually reveals a tachypnoeic, tachycardic, and anxious patient. If the pulmona ry oedema is severe, the patient may be cyanosed, coughing up frothy pink sputum and unable to talk. Check pulse and BP, auscultate the heart for murmurs, and 3rd/4th heart sounds of gallop rhythm. Look for i JVP (also a feature of PE and cardiac tamponade). Listen to the lung \201 elds \200\224 \201 ne inspiratory crepitations (crackles) may be limited to the bases or be widespread. Wheeze may be more prominent than crepitations. Cardiogenic pul monary oedema is associated with evidence of d cardiac output (sweaty, peripherally cool, a nd pale). Consider other diagnoses (eg sepsis) in patients with warm, \202 ushed extremit ies. Investigation Commence treatment before completing investigations: \200 Attach a cardiac monitor and check SpO 2 with pulse oximeter. \200 Obtain ECG. Check for arrhythmias, LAD, LVH, LBBB, recent or evolving MI. Send blood for U&E, glucose, FBC, troponin. \200 If severely ill or SpO 2 <94 % in air ob tain ABG. \200 Request old hospital notes/ECGs. \200 Obtain a CXR and look for features of cardiogenic pulmonary oedema: upper lobe diversion (distension of upper pulmonary veins) \200 cardiomegaly (LV and/or L A dilatation) \200 Kerley A, B, or C septal lines \200 \202 uid in interlobar \201 ssures \200 peribronchial/perivascular cuf \201 ng and micronodules \200 pleural effus ions \200 bat \200\231s wing hilar shadows. 101 CARDIOGENIC PULMONARY OEDEMA Treat urgently. Provide the following within the \201 rst few minutes: \200 Check that the airway is clear. \200 Raise the back of the trolley to sit the patient up and support with pillows if necessary. Provide high \202 ow O 2 by tight- \201 tting face mask. \200 If systolic BP > 90mmHg, give 2 puffs of GTN SL (800mcg) and com- mence GTN IVI, starting at 10mcg/min, i every few minutes according to clinical response (monitor BP closely; take special care to avoid hyp otension). Alternatively try buccal GTN (3 \200\2235mg). Give IV furosemide 50mg. Larger doses may be needed in patients already taking oral furosemide. If the patient has chest pain or is distressed, give very small titrated increments of IV o pioid (with anti-emetic). Do not give opioids to patients who are drowsy, confused. or exha usted as this may precipi- tate respiratory arrest. Consider inserting a urinary catheter and monitor urine output. \200 Treat underlying cau se and associated problems (arrhythmias, MI, cardiogenic shock, acute prosthetic valve failure). Monitor the SpO 2 and the clinical response to this initial treatment. Rapid improvement ma y occur, due to venodilatation and reduction of preload. If the patient does not improve, r echeck ABG and consider: \200 Non-invasive ventilation (continuous positive airway pressu re (CPAP) or bilevel positive airway pressure (BiPAP). Non-invasive ventilation (NIV) appea rs safe in acute cardiogenic pulmonary oedema and may avoid the need for intubation. If hypotensive refer to ICU for treatment of cardiogenic shock ( b p.77). An intra- arteria l line, Swan \200\223Ganz catheter and inotropic support (dobutamine) are likely to be requ ired. Echocardiography may help to exclude valve or septal rupture and guide treatment. Rapid sequence intubation in the presence of cardiogenic pulmonary oedema may be associated with cardiovascular collapse. Stop nitrates prior to administering anesthesia and be ready to give pressors \202 uids immediately post-induction. Prosthetic valve failure Always consider valve failure in patients with prosthetic valves, of which a large variety are in common use. All are associated with some risks (eg embolism , failure, obstruction, infection, hemorrhage from associated anticoagulation), which vary according to design. Acute failure of a pros- thetic aortic or mitral valve results in dram atic acute onset pulmonary oedema with loud murmurs. The patient may deteriorate rapidly an d not respond to standard drug treatment. Resuscitate as described above. CXR will show a p rosthetic heart valve pulmonary oedema. Call urgently for expert help (ICU team, cardiol ogist, and cardiothoracic surgeon). Emergency transthoracic or transoesphageal echocardiogr aphy con \201 rms the diagnosis. Immediate valve replacement is required. 102 CHAPTER 3 Medicine Non-cardiogenic pulmonary oedema Pulmonary oedema may occur in the absence of i pulmonary v enous pressure. The following mechanisms may be responsible: \200 i Capillary permeabilit y. \200 d Plasma oncotic pressure. \200 i Lymphatic pressure. Changes in capillary perm eability, secondary to a variety of triggers, is the mechanism most frequently implicated i n non-cardiogenic pulmonary oedema, when it occurs as the Adult Respiratory Distress Syndro me (ARDS). Since the mechanisms producing cardiogenic and non-cardiogenic pulmonary oedema differ, so the approach to treatment differs. Causes of non-cardiogenic pulmonary oedema \200 ARDS (sequel to sepsis, trauma, pancreati tis). \200 Intracranial (especially subarachnoid) hemorrhage. \200 IV \202 uid overlo ad. \200 Hypoalbuminaemia (liver failure, nephrotic syndrome). \200 Drugs/poisons/chemi cal inhalation. \200 Lymphangitis carcinomatosis. \200 Smoke inhalation. \200 Near dr owning incidents. \200 High altitude mountain sickness. Approach Distinguishing non-cardiogenic from cardiogenic pulmonary oedema is usually appare nt from the history. Evaluate the patient and resuscitate according to ABCs. Direct treatme nt towards the underlying cause and according to the physiological disturbance. To estimate the latter, invasive monitoring may be required (urinary, intra-arterial, central venous a nd pulmonary artery catheters). Involve ICU early and provide appropriate IV \202 uids, i notropes, tracheal intubation, IPPV and positive end expiratory pressure (PEEP) as required . 103 PLEURAL EFFUSION Pleural effusion Under normal circumstances, each pleural cavity contains <20mL \202 uid. Causes An exudate is diagnosed if the pleural \202 uid:serum protein > 0.5, \202 uid:se rum LDH > 0.6, or \202 uid LDH > 2/3 the upper limits of laboratory normal value for seru m LDH. Exudates \200 Pneumonia (bacterial, viral, mycoplasma). \200 Malignancy (bronchial carc inoma, mesothelioma, lymphoma). \200 TB. \200 PE with pulmonary infarction. \200 Coll agen vascular disease (SLE, rheumatoid arthritis). \200 Subphrenic abscess. \200 Amoebi c liver abscess. \200 Pancreatitis. \200 Chylothorax (thoracic duct injury \200\224 ra re). Transudates \200 Cardiac failure. \200 Nephrotic syndrome. \200 Hepatic failure. \200 Ovarian hyperstimulation. \200 Ovarian \201 broma (Meig \200\231s syndrome \200\224 rare). \200 Peritoneal dialysis. Clinical presentation Symptoms are usually due to the underlying disease process. A mild du ll ache and dyspnoea (initially on exercise, later at rest) may occur if the effusion is la rge. A history of vomiting followed by chest pain points to a ruptured esophagus \200\224 a surgical emergency. Signs of an effusion are not apparent until > 500mL are present. Dyspnoea, stony dullness t o percussion, with absent breath sounds over the effusion are characteristic. Bronchial bre athing may be heard just above the effusion. Very large unilateral effusions may produce ev idence of mediastinal shift (away from the collection of \202 uid). Investigations CXR can demonstrate pleural effusions as small as 250mL, as blunting of the costophrenic angle. Other investigations depend on likely cause. Treatment Provide O 2 and resuscitate as necessary, according to the underlying pathology. Emergency therapeutic pleural aspiration is rarely required in the ED, except where haemoth orax is suspected. Refer to the medical team for further investigation (including ultrasoun d guided diagnostic pleural aspiration). 104 CHAPTER 3 Medicine Acute asthma: assessment Follow the British Thoracic Society guidelines ( www.brit-thoracic .org. uk ) to assess and manage adults presenting with asthma, b p.106. The guidelines re \202 ect continuing concern over asthma deaths. Patients with severe asthma and one or more adverse psychosocial factors (psychiatric illness, alcohol or drug abuse, unemployment) ha ve i mortality. Measure the peak expiratory \202 ow rate and compare it against that expe cted (see Fig. 3.22 ). The peak \202 ow acts as an immediate triage tool: remember that p atients with life-threatening asthma may be too dyspnoeic to do this. Make an initial assessment of the severity of acute asthma based upon a combination of clin ical features, peak \202 ow measurement and pulse oximetry as outlined below. Moderate exacerbation of asthma \200 Increasing symptoms. \200 Peak \202 ow 50 \200 \22375 % best or predicted. \200 No features of acute severe asthma (below). Acute severe asthma Any 1 of: \200 Inability to complete sentences in 1 breath. \200 Re spiratory rate \211 25/min. \200 Heart rate \211 110/min. \200 Peak \202 ow 33 \200 \22350 % best or predicted. Life-threatening asthma A patient with severe asthma with any 1 of: \200 Cyanosis. \200 Exhaustion, confusion, coma. \200 Feeble respiratory effort. \200 SpO 2 <92 % . \200 Silent chest. \200 Bradycardia, arrhythmia, hypotension. \200 pO 2 <8kPa. \200 Norma l pCO 2 (4.6 \200\2236.0kPa). \200 Peak \202 ow <33 % best or predicted. Near fatal asthma \200 i pCO 2 and/or requiring mechanical ventilation with i in \202 at ion pressures. Other investigations Obtain ABG if SpO 2 <92 % or if there are other features of life-threa tening asthma. Obtain a CXR (without delaying treatment) if there is: \200 Suspected pneumomediastinum o r pneumothorax. \200 Suspected consolidation. \200 Life-threatening asthma. \200 Fail ure to respond to treatment satisfactorily. \200 Requirement for ventilation. 105 ACUTE ASTHMA: ASSESSMENT 660 650 640 630 620 610 600 590 580 570 560 550 540 530 520 510 500 490 480 470 460 450 440 430 420 410 400 390 380 660 650 640 630 620 610 600 590 580 570 560 550 540 530 520 510 500 490 480 470 460 450 440 430 420 410 400 390 380 190 183 175 75 72 69 66 MEN 167 160 Ht. (cms) 63 Ht. (ins) 48 = litres/min 42 = litres/min STANDARD DEVIATION MEN STANDARD DEVIATION WOMEN n m / L i F E P 69 66 63 60 175 WOMEN 167 160 152 145 Ht. (cms) 57 Ht. (ins) IN MEN, VALUES OF PEF UP TO 100 LITRES/MIN, LESS THAN PREDICTED, AND IN WOMEN LESS THAN 85 LITRES/MIN, LESS THAN PREDICTED, ARE WITHIN NORMAL LIMITS. 15 20 25 30 35 40 45 50 55 60 65 70 AGE IN YEARS Fig. 3.22 Peak expiratory \202 ow rates in normal adults. Nunn AJ, Gregg I. (1989). New r egression equations for predicting peak expiratory \202 ow in adults. Br Med J 298 : 1068 \200\22370. 106 CHAPTER 3 Medicine Acute asthma: management Initial treatment Follow BTS/SIGN guidelines ( www.brit-thoracic.o rg.uk ) summarized as follows: \200 Provide high \202 ow O 2 . \200 Put the trolley b ack and side rails up so the patient is sitting up and holding on to the side rails (to use pectoral muscles as accessory muscles of respiration). If the patient cannot talk, start treatment, but get senior ED and ICU help in case intubation and ventilation are required. Check trachea and chest signs for pneumothorax. \200 Ask about previous admissions to ICU . \200 Administer high dose nebulized B 2 agonist (eg salbutamol 5mg or terbu- taline 10m g), or 10 puffs of salbutamol into spacer device and face mask. For severe asthma or asthma that reponds poorly to the initial neb- ulizer, consider continuous nebulization. Give a corticosteroid: either prednisolone 40 \200\22350mg PO or hydrocorti- sone (preferably as sodium succinate) 100mg IV. Add nebulized ipratropium bromide (500mcg) to B 2 agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to B 2 agonist the rapy. Consider a single dose of IV magnesium sulfate (1.2 \200\2232g IVI over 20min) after consul tation with senior medical staff, for patients with acute severe asthma without a good init ial response to inhaled bronchodi- lator therapy or for those with life-threatening or near fatal asthma. \200 Use IV aminophylline only after consultation with senior medical staf f. Some individual patients with near-fatal or life-threatening asthma with a poor response to initial therapy may gain additional bene \201 t. The loading dose of IVI aminophylline is 5mg/kg over 20min unless on maintenance therapy, in which case check blood theophylline level and start IVI of aminophylline at 0.5 \200\2230.7mg/kg/hr. IV salbutamol is an alternative in severe asthma, after consultation with senior staff. Dra w up 5mg salbutamol into 500mL 5 % dextrose and run at a rate of 30 \200\22360mL/hr. A patient who cannot talk will be unable to drink \202 uids and may be dehydrated. Avoid \200\230routine \200\231 antibiotics. \200 Repeat ABG within an hour. \200 Hypok alaemia may be caused or exacerbated by B 2 agonist and/or steroid therapy. 107 ACUTE ASTHMA: MANAGEMENT Criteria for admission Admit patients with any features of \200 A life-threatening or nea r-fatal attack. \200 Severe attack persisting after initial treatment. Management of discharge Consider for discharge those patients whose peak \202 ow is > 75 % best or predicted 1hr after initial treatment. Prescribe a short course of oral pred- nis olone (eg 40 \200\22350mg for 5 days) if initial peak expiratory \202 ow rate (PEFR) <50 % , and ensure adequate supply of inhalers. If possible arrange for review by an asthma lia ison nurse before discharge. At a minimum, inhaler technique and peak expiratory \202 ow monitoring should be reviewed. Arrange/advise GP/asthma liaison nurse follow-up within 2 da ys. Fax or email the discharge summary to GP. Advise to return to hospital if symptoms wors en/recur. Referral to intensive care unit Refer any patient requiring ventilatory support or with acu te severe or life-threatening asthma failing to respond to therapy, evidenced by: \200 Dr owsiness, confusion. \200 Exhaustion, feeble respiration. \200 Coma or respiratory arre st. \200 Persisting or worsening hypoxia. \200 Hypercapnoea. \200 ABG showing d pH. \200 Deteriorating peak \202 ow. Cardiac arrest in acute asthma The underlying rhythm is usually PEA. This may re \202 ect one or more of the following: prolonged severe hypoxia (secondary to severe bronchospasm an d mucous plugging), hypoxia-related arrhythmias or tension pneumothorax (may be bilateral). Give advanced life support according to the guidelines in b Cardiac arrest, p.46 and treat tension pneumothorax if present ( b p.328). Aim to achieve tracheal intubation early in vi ew of the higher than normal required lung in \202 ation pressures and the attendant risk of gastric in \202 ation in the absence of a tracheal tube. 108 CHAPTER 3 Medicine COPD Chronic obstructive pulmonary disease (COPD) is characterized by chronic air \202 ow limitation due to impedance to expiratory air \202 ow, mucosal oedema, infection, bronchos pasm and bronchoconstriction due to d lung elasticity. Smoking is the main cause, but other s are chronic asthma, -1 antitrypsin de \201 ciency and chronic infection (eg bronchiect asis). History Exertional dyspnoea, cough, and sputum are usual complaints. Ask about: \200 Pres ent treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, opiate analgesia, and home O 2 treatment. Past history: enquire about previous admissions and co-morbidity. \200 Exercise tolerance : how far can they walk on the \202 at without stopping? How many stairs can they climb? Do they get out of the house? Recent history: ask about wheeze and dyspnoea, sputum volume and color. Chest injuries, abd ominal problems and other infections may cause respiratory decompensation. Read the hospital notes: have there been prior ICU assessments? Has the respiratory consult ant advised whether ICU would be appropriate? Examination Examine for dyspnoea, tachypnoea, accessory muscle use, and lip-pursing. Look f or hyperin \202 ation ( \200\230barrel chest \200\231) and listen for wheeze or coarse cra ckles (large airway secretions). Cyanosis, plethora (due to secondary polycythaemia) and ri ght heart failure (cor pulmonale) suggest advanced disease. Look for evidence of hypercarbi a: tremor, bounding pulses, peripheral vasodilatation, drowsiness, or confusion. Check for evidence of other causes of acute dyspnoea, particularly: asthma ( b p.104), pulm onary oedema ( b p.100), pneumothorax ( b p.114), PE ( b p.120). Remember that these condit ions may co-exist with COPD. Investigations \200 SpO 2 , respiratory rate, pulse rate, BP, T o , and peak \202 ow (i f possible). \200 CXR (look for pneumothorax, hyperin \202 ation, bullae, and pneumonia) . \200 ECG. \200 ABG (or capillary blood gas), documenting the FiO 2 . Use pCO 2 to gui de O 2 therapy. FBC, U&E, glucose, theophylline levels and, if pneumonia is suspected and/or pyrexial, blood cultures, CRP, and pneumococcal antigen. Send sputum for microscopy and culture if purulent. Treatment Give O 2 \200\224 remember that hypercapnoea with O 2 is multifactorial. The aim is to maintain SpO 2 88 \200\22392 % without precipitating respiratory acidosis or worseni ng hypercapnoea (see b Oxygen, p.95 and b Arterial blood gasses, p.98). If the patient is k nown to have COPD and is drowsy or has a documented history of previous hypercapnoeic respi ratory failure, give FiO 2 of 28 % via a Venturi mask and obtain ABG. Titrate up the FiO 2 with serial ABG sampling until the minimum FiO 2 that achieves SpO 2 88 \200\22392 % . Redu ce inhaled oxygen concentration if SpO 2 > 92 % . 109 COPD Give bronchodilators and steroids \200 Give nebulized salbutamol 5mg or terbutaline 5 \200\22310mg. \200 Consider adding nebulized ipratropium 0.5mg. \200 Use O 2 driven neb ulizers unless the patient has hypercapnoeic, acidotic COPD, in which case use nebulizers d riven by compressed air, supple- mented by O 2 via nasal prongs at 1 \200\2234L/min. Give steroids (eg prednisolone 30mg PO stat or IV hydrocortisone 100mg). Other drug treatments \200 Give antibiotics (eg amoxicillin, tetracycline, or clarithromy cin) if the patient reports i purulent sputum, or there is clinical evidence of pneu- monia and/or consolidation on CXR. Consider IV aminophylline or salbutamol if there is an inadequate response to nebulized bronchodilators. Consider naloxone if the patient is taking an opioid analgesic that may cause respiratory depression. See NICE guideline on COPD, 2010 ( www.nice.org.uk ). Non-invasive ventilation (NIV) NIV is recommended as standard early therapy for hypercapnoe ic ventila- tory failure during exacerbations of COPD. NIV will improve the blood gas measu rements in the ED, d intubation rates, d mortality, and length of hospital stay. NIV takes two forms \200\224 CPAP and BiPAP, (which may be more suitable for treating type II respiratory failure in COPD). Both CPAP and BiPAP have been used to treat acute cardiog enic pulmonary oedema. Patients with sleep apnoea use CPAP at night. The positive airway pr essure is delivered by a tightly adhered face mask, which is sized to \201 t the patient. The patient is awake, and must be compliant with wearing the mask. Unlike tracheal intubation, NIV does not protect the airway. Therefore, contraindications i nclude coma and vomiting. Absolute contraindications include apnoea and cardiac arrest. A p neumothorax will be converted into a tension pneuomthorax with NIV. Severe agitation may ma ke effective NIV impossible. The patient should always be cared for by staff who are familiar with the ventilator and ma sk, in the resuscitation room. Start BiPAP at 10cmH 2 O inspiratory positive airway pressur e (IPAP)/ 5cmH 2 O expiratory positive airway pressure (EPAP), and titrate upwards: \200 To treat persistent hypercapnoea, increase IPAP by 2cm at a time. \200 To treat persisten t hypoxia, increase IPAP and EPAP by 2cm at a time. \200 The maximum IPAP/EPAP is 25/15cm H 2 O. \200 For CPAP, commence treatment at 5 \200\2238cmH 2 O. 110 CHAPTER 3 Medicine Pneumonia Pneumonia involves symptoms and signs of lower respiratory tract infection (breat hlessness, productive cough, and fever) usually associated with CXR abnormalities. Pneumocy stis pneumonia may occur with minimal or no CXR changes. Consider pneumonia in patients wit h septicaemia or acute confusional states. Causes Bacterial (80 \200\22390 % ) Streptococcus pneumoniae is the commonest cause of comm unity-acquired pneumonia. Others include Mycoplasma pneumoniae , Haemophilus in \202 uenza e , Legionella , Chlamydia psittaci , Staphylococcus aureus (can cause fulminant pneumonia in patients with in \202 uenza). Gram \200\223ve and anaerobic infections are rare. Alway s consider TB, particularly in chronic alcoholism, poor social circumstances, immigrants an d those traveling to developing countries, or individuals not BCG vaccinated. Immunosuppres sed patients (eg HIV, steroid therapy) are at i risk of TB and Pneumocystis jirovecii pneum onia. Viral (10 \200\22320 % ) Predominantly in \202 uenza A&B, respiratory synctal virus (RSV), rarely varicella and severe acute respiratory syndrome (SARS). Rickettsial (1 % ) Rarely, Coxiella burnetti . Signs and symptoms Fever, cough, and production of sputum are common complaints. Breathless ness, pleuritic chest pain, myalgia, rigors, or haemoptysis may occur. Pneumonia can presen t without obvious chest signs: Mycoplasma pneumonia may present in children and young adult s with sore throat, headache, nausea, abdominal pain and diarrhea. Legionella can present w ith constitutional upset, diarrhea or confusion, particularly in the elderly. Pneumocystis pneumonia in immunosuppressed patients may present with cough, dyspnoea, and marked hypoxia , with relatively few other \201 ndings. Examination and investigation \200 Check respiratory rate, pulse, and BP. \200 Ausculta tion may reveal a patch of inspiratory crackles, signs of consoli- dation are present in <25 % . Check BMG, SpO 2 (obtain ABG if <94 % , or known to have COPD). \200 Assess for signs of SIRS (2 or more of RR > 20, HR > 90, temp > 38.3 o C or <36.0 o C, WCC<4 or > 12 \227 10 1 2 /L, confusion, glucose > 8.3mmol/L), which in combination with signs of pneumonia signify sepsis. Assess for signs of severe sepsis (sepsis + signs of organ dysfunction b p.59). Oxygen depe ndence, poor urine output, systolic BP<90mmHg, blood lactate > 3mmol/L. Commence \202 uid resuscitation immediately if present, take blood cultures and give IV antibiotics. Obtain CXR. Look for patchy or lobar opaci \201 cation, mass lesions, or an air bronchogram. In early pneumonia the CXR may be normal. Obtain blood cultures, sputum cultures, and consider urinary pneumo- coccal and Legionella antigen testing. 111 PNEUMONIA Assessment: admit or discharge Some patients with \200\230mild \200\231 illness, good soci al circumstances, and no signi \201 - cant co-morbidity may be safely discharged with appr opriate antibiotics (eg amoxicillin 0.5 \200\2231g PO tds), simple analgesia for pleuritic pain to aid deep breathing/coughing and GP follow-up. Patients with CURB-65 score \211 3 h ave severe pneumonia with a high risk of death; those who score 2 are at i risk of death an d should be considered for inpatient treatment or hospital-supervised outpatient care; pati ents with CURB-65 score 0 or 1 are at low risk of death and may be suitable for home treatm ent ( www.brit-thoracic.org.uk ; see Table 3.4 ). Table 3.4 CURB-65 score for pneumonia Score Confusion 1 Urea > 7mmol/L 1 Respiratory rate \211 30/min 1 Low BP (systolic <90mmHg or diastolic \211 60mmHg) 1 Age \211 65 years 1 Treatment Patients deemed suitable for discharge Provide simple analgesia, oral antibiotics , and GP follow-up. Patients admitted, but not severely unwell Start either oral or IV antibiotics, as follows: \200 Either amoxicillin 0.5 \200\2231g PO tds + erythromycin 500mg PO qds (or clarithromycin 500mg bd). Or if IV therapy is needed: ampicillin 500mg IV qds + erythromycin 500mg IV qds (or clarith romycin 500mg bd). Local guidelines will apply. Monitor SpO 2 and provide O 2 accordingly. \200 Provide simple analgesia. Patients with s epsis or severe sepsis (see b p.59) Commence IV crystalloid \202 uids, take blood culture s and administer IV antibiotics (eg co-amoxiclav 1.2g IV tds + clarithromycin 500mg IV bd) immediately. Contact ICU and make preparations for arterial line, central line and urinary catheter insertion. Aim for CVP > 8mmHg, MAP > 65mmHg and urine output > 0.5mg/kg/hr. See s evere sepsis guidelines ( www. surviving sepsis.org ). Differential diagnosis Pneumonia-like presentations can occur with pulmonary oedema, pulmon ary infarction, pulmonary vasculitis (eg SLE, PAN, Churg \200\223Strauss and Wegener \200 \231s), aspergillosis, allergic alveolitis, bronchial or alveolar cell carcinoma, acute pan creatitis, and subphrenic abscess. 112 CHAPTER 3 Medicine Pulmonary aspiration Aspiration of solid or liquid material into the upper and lower airway s is likely when one or more of the following features are present: \200 d GCS : head inj ury, stroke, overdose, seizures, sedation, anesthesia. \200 d Cough and/or gag re \202 e xes : related to above factors and/or bulbar dysfunction, intubation/extubation, Guillain \200\223Barr syndrome, multiple sclerosis, myasthenia gravis. Tendency to regurgitate/vomit: alcohol, full stomach, upper GI tract pathology (including h iatus hernia, oesophageal obstruction, pregnancy). May occur in in \201 rm or elderly fed via nasogastric tube. Clinical features Large food particles suf \201 cient to cause complete airway obstruction cause choking, inability to speak, i respiratory effort, cyanosis, loss of consciousness, and death. Smaller particles may pass through the vocal cords causing coughing, stridor, ta chypnoea, and wheeze. 80 % of patients are aged <4 years, with peanuts being the classic in haled objects. Delayed presentation with cough, wheeze, haemoptysis, unresolved pneumonia, abscess formation, or empyema occurs in 830 % often days or weeks later. Vomiting/regurgita tion is often witnessed and pulmonary aspiration con \201 rmed by seeing gastric contents in the oropharynx or trachea during intubation or following suction. Gastric content is a m ixture of semi- solid and liquid material \200\224 aspiration leads to a sudden onset of s evere dypsnoea, wheeze, and cyanosis. Its acid nature causes severe damage to the alveolar- capillary membrane, with denaturation of pulmonary surfactant, i pulmonary permeability wit h oedema and atelectasis. Hydrocarbons (eg gasoline, paraf \201 n) cause severe pulmonary toxicity if aspiration occurs during ingestion or following regurgitation/vomiting. Investigations ABG These show hypoxaemia within minutes of acid aspiration. Initially, pati ents may hyperventilate with d pCO 2 until pulmonary compliance i work of breathing suf \201 cient to result in hypoventilation. CXR Abnormalities develop in > 90 % of patients, but may take hours/days. Appearances depen d on the nature of the aspirated material and the patient \200\231s position at the time of the episode (right lower lobe is most frequently and severely affected, followed by left l ower lobe and right middle lobe). In severe aspiration, diffuse bilateral in \201 ltrates and pulmonary oedema similar to ARDS appearances are present. Less severe episodes produce atelectasis followed by alveolar in \201 ltration. Intrapulmonary foreign body (including peanuts) Rarely radio-opaque. Resulting collapse, hy perin \202 ation, or consolidation is usually obvious and depends on whether obstruction i s complete or partial and if supervening infection is present. If the history strongly sug- gests an inhaled FB, but CXR is normal, consider an expiratory CXR, which may show evidenc e of air trapping distal to the obstruction. 113 PULMONARY ASPIRATION Prevention Prevention is everything. Pay meticulous attention to airway protection. This ma y involve positioning (tilt head down on the right hand side), suction to the oropharynx (Y ankauer catheter avoiding stimulation of the gag re \202 ex) and if necessary, tracheal in tubation. Tracheal intubation does not completely protect against aspiration of \202 uid into the lungs, but it is the best preventative measure. In at-risk patients, pass an NG tu be to empty the stomach. However, NG tubes can also predispose to aspiration by preventing closure of the oesophageal sphincters and interfering with coughing and clearing the pharyn x. Treatment Correct hypoxia and give nebulized salbutamol for associated bronchospasm. If par ticulate aspiration is present, refer for urgent bronchoscopy. Although secondary infection is common, the use of antibiotics or steroids is not routinely indicated. 114 CHAPTER 3 Medicine Spontaneous pneumothorax Primary spontaneous pneumothorax (PSP) may occur in previously hea lthy individuals. Secondary spontaneous pneumothorax (SSP) occurs in older patients with pr e-existing chronic lung disease (like COPD or TB) and may also occur with asthma, bronchial carcinoma, Marfan \200\231s syndrome, infection, cystic \201 brosis, and oesophageal rup ture. Presentation Most patients present with unilateral pleuritic chest pain and dyspnoea. Class ical physical signs may not be present (depending upon the size of the pneumothorax): tachy pnoea, tachycardia, normal/hyper-resonant per- cussion note withe d air entry on the affect ed side. Rarely, there may be a clicking sound at the cardiac apex. Severe symptoms (inabil ity to speak, gasping, low SpO 2 ) should prompt rapid assessment tracheal deviation, tachy pnoea, tachycardia, and hypotension. Treat tension with immediate decompression using a nee dle in the second intercostal space (just above the third rib) in the mid-clavicular line ( b p.328). Severe symptoms are also found in patients with SSP (disproportionate to the pne umothorax size). In the absence of signs of tension pneumothorax, obtain an emergency porta ble CXR and involve an experienced doctor. for tension pneumothorax: Investigation and treatment \200 Monitor pulse, SpO 2 , and BP. Ensure IV access. \200 Administer high \202 ow oxygen (aim SpO 2 90 \200\22392 % in patients with COPD). When there are no signs of tension, an ABG will help assess patients with chronic lung disease, and guide oxygen therapy. Erect CXR \200 When using digital images, always use a picture archiving and communi- cat ion system (PACS) workstation. The signs of pneumothorax may be subtle and dif \201 cult t o spot. Look for a displacement of the pleural line. \200 Do not mistake the scapular edge for th e lung edge. \200 Some patients with COPD have emphysematous bullae, which can mimic pneu mothorax. If in doubt, ask for senior review prior to treating for pneumothorax.