Support mouth as needed. Provide oral or nasopharyngeal airway. Maintain lie down. Minimize discomfort. patient in upright position: do not force a distressed patient to B \200\224use respiratory support for breathing \200 Identify appropriately (e.g. bronchodilators). Assist achieved with nasopharyngeal continuo us +ve airway pressure (see bronchiolitis, b p.288), or \200\223ve pressure ventilation. I ntubation the level of respiratory involvement: treat speci \201 c problems work of breathing with non-invasive support: this can be and mechanical ventilation. C \200\224assess circulation; establish IV access \200 \200 Start Provide \202 uid intake to an amount ranging from restricted to just below maintena nce. pulse oximetry and cardiac monitoring. IV \202 uids: when the circulation is good it is advisable to limit 05_McClure_05.indd 46 11/15/2012 12:18:57 AM THE ABC OF HIGH DEPENDENCY 47 05_McClure_05.indd 47 11/15/2012 12:18:57 AM CHAPTER 5 Emergency and high dependency care 48 Respiratory distress Respiratory distress is de \201 ned as increased work of breathing th at causes a sense of altered well-being. The hallmarks are use of accessory muscles and tac hypnoea. Distress can be caused by disorders of gas exchange (O2 absorption, or CO2 elimina tion), respiratory drive, neuromuscular disease, and infection (see Box 5.1). Box 5.1 Differential diagnosis of respiratory distress Nasopharynx \200 \200 \200 \200 Nose: Oropharynx: Tongue: Pharynx: choanal atresia, stenosis tonsillar hypertrophy glossomegaly peritonsillar abscess, retropharyngeal abscess, diphtheria Upper airway obstruction \200 Larynx: haemangioma, croup Epiglottis: vocal cord dysfunction, laryngomalacia, papilloma, epiglottitis, foreign body Lower airway disorder \200 Trachea: artery sling Bronchi: Bronchioles: tracheitis, tracheobronchomalacia, foreign body, pulmonary \200 bronchitis, bronchomalacia asthma, bronchiolitis, pertussis Disordered gas exchange \200 carbon monoxide poisoning, methaemoglobinaemia, Hemoglobin: acidosis Shunt: Dead Other: \200 \200 pulmonary oedema, hemorrhage, atelectasis, or embolism space ventilation: asthma, bronchiol itis, pulmonary hypertension sickle chest syndrome, pneumonia, pneumothorax Respiratory drive \200 \200 Hyperventilation: Hypoventilation: psychogenic, brainstem tumor apnoea, drugs Neuromuscular \200 Respiratory muscle atrophy, central nervous system (CNS) depression muscle weakness: Duchenne muscular dystrophy, spinal Other \200 Pleural: empyema Chest pneumothorax, chylothorax, haemothorax, pleural effusion, wall: \202 ail chest, rib fractures 05_McClure_05.indd 48 11/15/2012 12:18:57 AM RESPIRATORY DISTRESS 49 De \201 nitions Broadly, we can de \201 ne the two major causes of respiratory distress a s follows. Respiratory failure \200 Hypoxaemia previously well child. Acidosis: since the child may have a chronic \200\230compensated \200\231 problem. Increasing your observations on child \200\231s breathing and mental state. despite high FiO2: arterial oxygen tension (PaO2) <8kPa in pH <7.25; no speci \201 c arterial carbon dioxide tension (PaCO2) fatigue, or absence of improvement with therapy: based on Neuromuscular weakness \200 Clinical: chest wall weakness of neurological or muscular origin. Physiological: manometry to assess maximum inspiratory force < \200\22320mmHg. bulbar dysfunction with poor or absent cough, gag, swallow, or use spirometry to assess vital capacity <12mL/kg, or 05_McClure_05.indd 49 11/15/2012 12:18:57 AM CHAPTER 5 Emergency and high dependency care 50 Respiratory distress: management Clinical assessment Assess the patient for the following: \200 pallor or cyanosis. \200 Color: Respiratory or brainstem cause. Inspiration obstruction produces stridor; lower airw ay obstruction leads to cough, wheeze, and a prolonged expiratory phase. Chest \202 ail-c hest, diaphragmatic palsy, pneumothorax, or foreign body inhalation. Position Mental Heart drive: pattern and timing of breathing may re \202 ect a central and expiration of air at the mouth and nose: upper airway wall movement: chest and abdominal wall dynamics may indicate \200 \200 and level of agitation. state. rate and perfusion: these may re \202 ect impending arrest. Investigations \200 Non-invasive: saturation, pulse oximetry measurement of oxyhaemoglobi n saturation (SpO2). Arterial blood gas: assessment of acid \200\223base, PaO2, PaCO2. A ca pillary blood sample is a good alternative (for pH, PCO2) if the extremity is warm and the blood \202 ows freely. Blood CXR complications (e.g. pulmonary oedema, pneumothorax). pulse oximetry measurement of oxyhaemoglobin \200 tests: full blood count (FBC), electrolytes, glucose, and cultures. : for diagnosis (e.g. s evere pneumonia); for assessment of Monitoring \200 \200 \200 \200 \200 \200 Pulse oximetry. Continuous ECG. BP. Temperature. Fluid balance. Conscious level. Therapy There are speci \201 c therapies for each condition listed in the \200\230Differe ntial diagnoses \200\231 on b p.48 (see individual sections). With regard to \202 uid the r- apy, we generally restrict total volume to 80% maintenance for the fol- lowing reasons. \200 with retraction: high \200\223ve intrathoracic pressure will pull \202 uid Distress out of capillaries into the interstitial space and will aggravate breathing with p ulmonary oedema. Syndrome common problem in moderate to severe respiratory distress. Diures is is limited: in the hydrated patient consider using furosemide (0.5 \200\2231mg/kg, IV). It may help the patient with extra-interstitial water without overt oedema. of inappropriate antidiuretic hormone (SIADH): this is a 05_McClure_05.indd 50 11/15/2012 12:18:57 AM FOREIGN-BODY INHALATION 51 Foreign-body inhalation Foreign-body (FB) aspiration is more common in toddlers and infants , who tend to put objects in their mouths. FBs can be inhaled into the airway, or they may get caught in the esophagus and compress the trachea. Symptoms The symptoms of a FB in the aerodigestive tract range from no symptoms to complete airway obstruction. \200 Larynx: usually causes hoarseness, cough, dysphonia, haemoptysis, stridor, wheezing, dyspno ea, cyanosis, or apnoea due to complete obstruction. Trachea there may be an asymptomatic p eriod followed by features of pneumonia (see b p.290). Esophagus: trachea is compressed, ma y produce dyspnoea, stridor, respiratory failure, or apnoea (see b pp.256, 258). and bronchus: can cause chest pain. After initial symptoms, will produce drooling, dysphagia, or vomiting and, if the Etiology Inhaled FB should be considered in all patients with a history of choking or gaggi ng. Diagnosis \200 A monophonic chest may be noted on examination. Chest and neck identifying the location of an object. Inspiratory and expiratory \201 lms may show an area of hyperin \202 ation. A rterial blood gas distress. wheeze or absent breath sounds on one side of the radiographs, with lateral views, may be helpful in analysis is indicated when the patient is in severe Initial treatment Follow a standard protocol. \200 FB \200 ABC . removal: if the child is calm with good air exchange, removal of the FB should take place under controlled circumstances; manipulation may change the pos ition of the object, inducing more severe obstruction. If the child is in distress, but mai ntaining good air exchange, back blows and chest thrusts may be performed as per the standa rd technique for pediatric advanced life support (ALS). An unconscious child with poor air entry should be given oxygen (FiO 2 100%) via a face mask until rigid bronchoscopy and obje ct removal can be performed. 05_McClure_05.indd 51 11/15/2012 12:18:57 AM CHAPTER 5 Emergency and high dependency care 52 Drowning Drowning is caused by submersion in water. When water has been aspi- rated into th e lungs it is usually a small amount (<22mL/kg). In (cid:1)10% there has been laryngospasm without aspiration of water. The location \200\224sea, freshwater, brackish water \200\224i s of little consequence. However, the tem- perature of the water is important, and the inci dent is classi \201 ed as warm, cold, and very cold when the water temperature is 20 C, 6 \200\22319 C, and (cid:1)5 C, respectively. Symptoms Respiratory acidosis occurs with inadequate ventilation. \200 If there has been a hypoxic \200\223ischaemic insult, brain swelling, and raised intracrani al pressure (ICP) may develop. Hypoxaemia and inadequate perfusion will cause acidosis, arr hythmia, and shock. Etiology Children under 3yrs old and teenagers are most at risk. Young children may have ac cidents in pools and bathtubs if left unattended. Assess the duration of submersion, water temperature, and presence of cyanosis or apnoea. Emergency staff should provide details of resuscitation and the time taken to establish a pulse and cardiac output. Consider: \200 \200 \200 \200 head and neck injuries from diving; pre-existing cardiac arrhythmia; pre-existing seizure d isorder; drug and alcohol abuse. Initial treatment Follow a standard protocol. \200 AB: the neck may be injured and the airway may be obstructed by material from the water. Cl ear the mouth and immobilize the neck. If there is no gagging, hypoxaemia, or apnoea, then endotracheal intubation is needed. At the time of intubation use in-line traction. C: injur y or pulmonary oedema. Temperature: remove all wet clothing in order to avoid cooling. Warm the child to achieve a core temperature >35 C (use a heating blanket). In profound hypoth ermia, more invasive methods of warming may be used on the intensive care unit (e.g. heart \200\223lung bypass or internal bladder and gastric lavage). poor perfusion occurs in children with severe hypoxic \200\223ischaemic After resuscitation \200 \200 \200 \200 Assess Start ECG. Look closely for signs of lower respiratory tract involvement: use of acc essory respiratory muscles, nasal \202 aring, tachypnoea, cough, wheeze, and crackles. : vital signs, chest, heart, and the central nervous system. : pulse oximetry and cardiac monitoring. 05_McClure_05.indd 52 11/15/2012 12:18:57 AM CIRCULATION: CARDIOVASCULAR DIFFICULTY 53 Circulation: cardiovascular dif \201 culty Shock The failure to deliver adequate oxygen to the tissues: \200 \200 Heart Decreased contractility. rate disturbance: bradycardia, dysrhythmias. stroke volume: hypovolaemia; vasodilatation; poor Congestive heart failure Cardiac fatigue due to: \200 Excess defect (VSD), patent ductus arteriosus (PDA), atreriovenous (AV) canal), AV \201 s tula, severe anemia, hypervolaemia. Excess coarctation of the aorta, or hypertension) or pu lmonary vascular system (pulmonary stenosis, pulmonary hypertension, chronic hypoventilatio n, or severe upper airway obstruction). Myocardial problems: including cardiomyopathy, myoc arditis, myocardial ischaemia (anomalous coronary artery, cardiac thrombosis in Kawasaki), metabolic disorders (b p.962). Excess volume load: from left-to-right cardiac lesions (ventricular septal pressure load: from systemic vascular system (aortic stenosis, myocardial demand: due to fever, thyrotoxicosis. Dysrhythmia See also b pp.42 \200\22343, 55 \200\22357, 250; uncommon, but consider: \200 \200 Supraventricular Congenital tachycardia. heart block. Hypertension See also b pp.55, 390; causes of hypertension are: \200 Renal: glomerulonephritis; haemolytic \200\223uraemic syndrome; pyelonephritis; obstructive nephropathy; vascular disease. Cardiac: Neurological: Endocrine: hyperthyroidism. Toxins P rimary essential hypertension. \200 \200 coartation of the aorta. infection; drugs; tumor; cerebral oedema. phaeochromocytoma; Cushing \200\231s syndrome; corticosteroids; \200 and poisons. Anaphylactic shock See also b p.64; main causes are food, medication, and insect bites. Lif e- threatening problems are: \200 airway narrowing of upper and lower airway. \200 shoc k, vasodilatation, and increased vascular permeability. Pericarditis See b p.246 The causes include infection, rheumatologi- cal disorders, trauma, malignancy, and post-pericardiotom y syndrome. Congenital heart disease See b pp.232 \200\223241 Respiratory: CVS: 05_McClure_05.indd 53 11/15/2012 12:18:57 AM CHAPTER 5 Emergency and high dependency care 54 Cardiovascular system dif \201 culty: assessment See also b pp.226 \200\223231. Shock In early shock, \201 ndings can be subtle. Hypotension is a late sign, so look for a decreased stroke volume (decreased pulse amplitude) and increased systemic vascular resis tance (perfusion changes to skin and muscle). In classic shock there are features of decomp ensation. Late shock is a pre- arrest phenomenon. Shock Early shock \200 Pulse: \200 BP: \200 Breathing: \200 Limbs: \200 CNS: \200 Lab oratory: tachycardia normal but postural drop tachypnoea cool and mottled agitated mild metabolic acidosis Classic shock \200 \200 \200 \200 \200 \200 Pulse: BP: Breathing: Limbs: CNS: Laboratory: tachycardia and weak pulses hypotension tachypnoea and grunting cool, clammy, and pale or blue depressed level of consciousness metabolic acidosis Late shock \200 Pulse: \200 BP: \200 Breathing: \200 Limbs: cold (blue to white) \200 CNS: coma \200 Laboratory: tachycardia and thready pulses; bradycardia is pre-arrest profound hypotension tachypnoea; bradypnoea signi \201 es pre-arrest metabolic acidosis, multisystem derangement Congestive heart failure The patient may have: sweating on exertion or feeding; malaise and irrita- bility; decreased appetite. The physical \201 ndings include: \200 \200 \200 \200 \200 \200 gallop rhythm on auscultation. wheeze and crackles on auscultation. Tachycardia: Tachypnoea: Raised Pale Hypotension . Features anemia. jugular venous pressure: hepatosplenomegaly and oedema. or mottled and cool extremities. of the underlying cause: e.g. murmur in VSD or pallor in 05_McClure_05.indd 54 11/15/2012 12:18:57 AM CARDIOVASCULAR SYSTEM DIFFICULTY: ASSESSMENT 55 CXR: pulmonary oedema. showing cardiomegaly, and pulmonary vascular congestion to Arrhythmias A 12-lead ECG and BP are needed for diagnosis. Bradycardia If there is haemodynamic instability (i.e. hypotension or poor perfusion), sign i \201 cant bradycardia is present if the HR is: \200 \200 \200 <80/min in neonates. <50/min in infants. <40/min in older children. Tachydysrhythmia These may be: \200 complex: QRS duration <0.1s in children or <0.12s in Narrow adolescents (e.g. supraventricu lar tachycardia (SVT) and atrial \202 utter). There are no P waves in SVT; ventricular : prolonged QRS. Hypertension To diagnose hypertension strict criteria should be followed: three mea- sureme nts in non-stressful circumstances with values >2 standard devia- tions above mean for age and sex. Standard charts should be consulted (b p.391 \200\223392), but, by age, the upper limits of normal BP are: \200 : systolic BP, 110mmHg; diastolic BP, 65mmHg; \200 : syst olic BP, 120mmHg; diastolic BP, 70mmHg; \200 : systolic BP, 130mmHg; diastolic BP, 75mmHg ; \200 : systolic BP, 140mmHg; diastolic BP, 80mmHg. <2yrs 3 \200\2236yrs 7 \200\22310yrs 11 \200\22315yrs Pericarditis There may be chest pain or features of the underlying cause. Look for: \200 \200 \200 Congestive heart failure. Friction rub. Pulsus paradoxus (>10mmHg). When cardiac tamponade is present there are classic signs: \200 \200 \200 \200 \200 Shock. Distended jugular veins. Heart sounds appear distant. ECG: CXR: decreased voltage, elevated ST segments, T-wave inversion. the heart will look enlarged if an effusion is present. Congenital heart disease In cyanotic babies the history and examination can be used to excl ude respiratory causes of cyanosis. The assessment also includes the hyperoxia test (measur ement of PaO2 in FiO2 100%). \200 \200 2 < 13.3kPa (100mmHg): possible cyanotic heart disease. 2 13.3 \200\22326.7kPa (100 \200 \223200mmHg): possible heart disease with PaO PaO complete mixing and increased pulmonary blood \202 ow. PaO 2 > 33.3 kPa (>250mmHg): cyanotic heart disease unlikely. 05_McClure_05.indd 55 11/15/2012 12:18:57 AM CHAPTER 5 Emergency and high dependency care 56 Cardiovascular system dif \201 culty: therapy \200\2241 Shock Initial therapy includes the following. \200 \200 provide supplemental oxygen, FiO2 100%. Intubate if required. in shock, elevate the legs to improve venous return. In Oxygen: Position: congestive heart failure elevate the head. IV \200 access: central access may be required, particularly when using inotropes. Temperature: Metabolic respiratory cause should be controlled with ventilation. \200 control fever with antipyretics (paracetamol 15mg/kg). state: correct hypoglycaemia and hyp ocalcaemia. Acidosis of Fluid volumes for shock \200 Hypovolaemia: give 40 \200\22360mL/kg of normal saline, with additional increments of 10mL/ kg to restore volume if small heart size on CXR, and CVP <5 \200\22310mmHg. Stop resuscitat ion with volume: \200 \200 \200 IV 20mL/kg of normal saline. In severe volume depletion when clinical improvement is achieved; when clinical signs of improvement fail to appear; i f there are signs of volume overload: hepatosplenomegaly, JVP distension, gallop rhythm, wh eeze and crackles. Inotropes for shock \200 Start inotropes: \200 when circulation remains unsatisfactory and CXR shows large heart, pulmonary vascular conge stion, pulmonary oedema, or pleural effusion; when CVP >10 \200\22315mmHg; once initiated, titrate dose upward to produce the effect required. Hypotension with tachycardia: \200 \200 dopamine dobutamine Can use peripheral IV. \200\2241 \200\22320microgram/kg/min (start at 5microgram/kg/min). \200\2242 \200\22320microgram/kg/min (start at 5microgram/kg/min). Dysrhythmias See also b pp.42 \200\22343, 250 \200\223251. Sinus bradycardia and heart bloc k \200 \200 Do not treat if haemodynamically stable (i.e. BP and perfusion). Consider other treatable c auses of bradycardia, such as raised ICP, acidosis, or hypercapnia. Atropine: 0.02mg/kg IV (min 0.1mg; max 1mg). 05_McClure_05.indd 56 11/15/2012 12:18:57 AM CARDIOVASCULAR SYSTEM DIFFICULTY: THERAPY \200\2241 57 Intensive care treatments for shock Hypotension with normal or low HR \200 Adrenaline: kg/min) Noradrenaline: microgram/kg/min) Amrinone: kg/min 0.05 \200\2231microgram/kg/min (start at 0.05 \200\2230.10 microgram/ 0.05 \200\2231microgram/kg/min (start at 0.05 \200\2230.10 load 0.75mg/kg IV over 3min, then give 5 \200\22310microgram/ Hypotension refractory to volume and single inotrope \200 Seek intensive care advice as these patients will usually need intubation and ventilation, and steroids (see b p.714) Combinations of inotropes are used in this instance Afterload re duction may be required with sodium nitroprusside: 0.5 \200\2237micrograms/kg/min (start 0. 5microgram/kg/min) \200 Diuresis for volume overload \200 Start diuretics: 1mL/kg/hr If oliguria or anuria use furosemide 0.5 \200\2231mg/kg IV or ma nnitol 0.5 \200\2231g/kg IV after circulation is restored expected urine volume is Tachydysrhythmia \200\224SVT Treatment will require consultation with a cardiac specialist. If haemody- namically stable, consider the following: \200 Vagal massage or Valsalva maneuver. Do not compress orbits. Adenosine : 50 \200\223100micro grams/kg initially, as rapid IV push. DC haemodynamically unstable. Intubation and appropri ate analgesia and sedation are required. Other drugs: maneuvers: ice bag to face for 15 \200\22320s or unilateral carotid \200 shock: synchronized countershock 1J/kg should be reserved for the amiodarone, procainamide, \202 ecainide. Ventricular tachycardia If haemodynamically stable and pulse, consider the following after advice from cardiac specialist: \200 \200 amiodarone 5mg/kg; synchronized shock. b Chapter 41, p.41). If pulse present: Pulseless (see 05_McClure_05.indd 57 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 58 Cardiovascular system dif \201 culty: therapy \200\2242 Congestive heart failure Use \202 uid restriction and inotropic support after cardiological advice. Digoxin may be used for primary cardiac problem (total digitalizing dose, TDD). By age TDDs are as follows. \200 \200 \200 \200 Neonate <2yrs 2 \200\22310yrs 10yrs : 30micrograms/kg PO or 20micrograms/kg IV. : 40 \200\22350micrograms/kg PO or 30 \200\2234 0micrograms/kg IV. : 25 \200\22335micrograms/kg PO or 20 \200\22330micrograms/kg IV. : 0.75 \200\2231.25mg PO or 0.5 \200\2231mg IV. Digoxin administration Split the TDD at the following times: \200 \200 \200 Initial 8hr 16hr : give 50% of TDD. : give 25% of TDD. : give 25% of TDD. Hypertension See b pp.390 \200\223397. For severe, symptomatic hypertension, the BP should be lowered by 20 \200\22325%. Do not aim for normal levels. Patients should be monitored in a high-dependency area. Discuss with nephrologist. Hypertensive encephalopathy is an emerg ency and too rapid lowering of BP may lead to stroke. Short-acting antihypertensives are th e treatment of choice. Consider: \200 \200 Diazoxide: Hydralazine: 20mg). May repeat dose in 20 \200\22330min. Sodium 1 \200\2233mg/kg IV by rapid infusion; repeat after 5 \200\22315min. 100 \200\223500micrograms/kg IV over several minutes (max dose nitroprusside. Congenital heart disease: alprostadil See also b p.232. In neonates, consider alprostadil ( prostaglandin E1 (PGE1) infusion if: PaO \200 \200 \200 \200 2 <4 \200\2235.3kPa (30 \200\22340mm/kg). Oxygen saturation <70% in FiO Femoral pulses are diminished or absent with poor perfusion. Metabolic acidosis persisting after volume and in otropes. 2 100%. PGE1 dose 0.01 \200\2230.20micrograms/kg/min (start at 0.05micrograms/kg/min, increase in 0 .05micrograms/kg/min increments if response is not adequate). Be aware that apnoea may deve lop. 05_McClure_05.indd 58 11/15/2012 12:18:58 AM CARDIOVASCULAR SYSTEM DIFFICULTY: THERAPY \200\2242 59 05_McClure_05.indd 59 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 60 Cyanosis: assessment Cyanosis is the result of deoxygenated hemoglobin or abnormal haemo- g lobin in the blood. Cyanosis is apparent when there is 4g/dL of reduced hemoglobin or 0.5g/ dL of methaemoglobin. Anemic patients may not become cyanotic even in the presence of marke d arterial desaturation. In light-skinned patients, cyanosis is usually noted with arterial saturation <85%. In dark-skinned patients, the saturation must be lower. Cyanosis is cause d by the following problems. \200 Lung pump: \200 \200 \200 Cardiovascular pump: Hematological: alveolar hypoventilation; ventilation \200\223perfusion inequality; impairment of oxygen di ffusion. \200 right-to-left shunting. decreased af \201 nity of hemoglobin for oxygen. Differential diagnosis for cyanosis Alveolar hypoventilation \200 CNS: ischaemia; drugs Hypothermia seizures; cerebral oedema; hemorrhage; infection; hypoxia \200\223 Ventilation \200\223perfusion inequality \200 bronchiolitis; pneumonia, pneumothorax; pleural effusion; Lung: respiratory muscle dysfunct ion (muscular dystrophy, myasthenia gravis, Guillain \200\223Barr ); tracheal compression Cardiac: decreased pulmonary blood \202 ow (tricuspid atresia, pulmonary atresia with int act septum, critical pulmonary stenosis, tetralogy of Fallot); decreased systemic perfusion (coarctation of the aorta, sepsis) Impairment of oxygen diffusion \200 Lung: bronchopulmonary dysplasia; hypoplasia; diaphragmatic hernia Right-to-left shunting \200 congenital heart defect; Eisenmenger syndrome; AV \201 stula \200\224 Cardiac: pulmonary or systemic Decreased Methaemoglobinaemia: compounds and nitrites Carbox yhaemoglobinaemia \200 oxygen af \201 nity for hemoglobin hereditary; aniline dyes; nitrobenzene; azo 05_McClure_05.indd 60 11/15/2012 12:18:58 AM CYANOSIS: ASSESSMENT 61 Clinical assessment Also see b pp.31 \200\22332. The key part of the assessment is respirat ory and cardiovascular. Vital and general signs \200 \200 \200 \200 Record the temperature. Record HR. Record BP in all four limbs. Is there evidence of failur e to thrive? Clubbing This sign may be present in the older infant or child. It should be looked for in the \201 ngers and toes. The causes can be: \200 \200 \200 \200 \200 \200 hereditary; idiopathic; congenital heart disease (CHD); infective endocarditis; pulmonary c onditions (e.g. cystic \201 brosis); GI disease (e.g. Crohn \200\231s, ulcerative colitis , cirrhosis). Respiratory In the neonate increased respiratory rate (usually <80breaths/min) with no resp iratory distress suggests cyanotic heart disease, but with respiratory distress pulmonary d isease is suggested. In the older child a full respiratory examination is required \200\224 look at all components of the examinations. Cardiovascular The absence of a murmur does not exclude congenital heart disease. Is the li ver enlarged? 05_McClure_05.indd 61 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 62 Cyanosis: management Investigations Blood tests \200 \200 \200 \200 FBC with differential. Blood cultures. Glucose. Bedside diagnosis of methaemoglobinaemia: p lace a drop of blood on a piece of \201 lter paper. After 30s exposure to air, normal blo od turns red, while blood taken from a patient with methaemoglobinaemia remains chocolate b rown. Infection \200 \200 Lumbar puncture as indicated. Urinary culture. Arterial blood gas In the older child a single measurement is needed. In the neonate, asses s the change in PaO2 in response to FiO2 100% for 5 \200\22310min (see hyperoxia test, b p. 55). Chest X-ray See also b p.231. In the neonate the lung \201 elds should be assessed f or signs of increased vascularity, pulmonary congestion, or oligaemia. Characteristic radio graphic \201 ndings are: \200 \200 Egg on a string: Boot-shaped heart: ventriculoseptal defect. Snowman sign: drainage. Wall-t o-wall heart: transposition of the great arteries. tetralogy of Fallot (Box 5.2), pulmonary atresia, supracardiac total anomalous pulmonary venous Ebstein \200\231s anomaly. Electrocardiogram See also b p.231. Characteristic \201 ndings include: \200 Superior left axis: atrial septal defect. Left axis deviation: Marked right atrial hypertro phy: tricuspid atresia; endocardial cushion defect; primum \200 pulmonary atresia atrial atresia. Ebstein \200\231s anomaly. Echocardiography Assessment for speci \201 c cardiac lesions. Monitoring Standard cardiorespiratory monitoring (see b p.50). Therapy Therapies for speci \201 c cardiac, respiratory, and poisoning conditions are disc ussed elsewhere. 05_McClure_05.indd 62 11/15/2012 12:18:58 AM CYANOSIS: MANAGEMENT 63 Box 5.2 Tetralogy of Fallot ( \200\230tet spell \200\231) See also b p.235 Patients may hav e attacks of paroxysmal hyperpnoea and increased cya- nosis that occur spontaneously or aft er early morning feeds, prolonged crying, or defecation Emergency treatment \200 \200 \200 Place the patient in the knee-to-chest position Administer oxygen Insert IV line and admini ster phenylephrine, morphine sulfate, and propranolol Prolonged attacks require sodium bica rbonate Refer to cardiac center \200 05_McClure_05.indd 63 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 64 Anaphylaxis Anaphylaxis is a life-threatening allergic event. It is the extreme clinical ex ample of an immediate hypersensitivity reaction. Symptoms The reaction includes involvement of: \200 : urticaria and angioedema. \200 Skin Respiratory bronchospasm. Gastrointestinal Systemic : acute airway obstruction with laryngeal oedema and \200 : severe abdominal cramping and diarrhea. : hypotension and shock. Etiology The symptoms of anaphylaxis are abrupt, often within minutes of expo- sure to an a ntigen. The causes are: \200 : penicillin, aspirin. \200 \200 \200 Drugs Injections Stings Foods : radiographic contrast dyes. : bites and envenomations. : shell \201 sh, nuts, peanuts, eggs. Diagnosis Take a careful history and aim to determine the time between onset of symptoms an d exposure to the potential precipitating cause. Initial treatment Follow a standard protocol \200 \200 ABC Epinephrine 0.5mL). Repeat every 15min if required. Hypotension: position) and give IV normal saline (20mL/kg bolus). IV epinephrine may be given over 2 \200\2235min (0.1mL/kg, 1 :10,000), while an infusion is being prepared. Salbutamol: give nebulized salbutamol 0.05 \200\2230.15mg/kg in 3mL normal saline. Approximately 2.5mg for child <30kg and 5mg for chi ld >30kg, every 15min if required Antihistamine Steroid: be followed by IV methylprednis olone 2mg/kg/day (divided every 6hr), or oral prednisolone 2mg/kg (bolus once a day). . (adrenaline): give SC 0.01mL/kg (1:1000, maximum dose put the patient head-down at 30 (Trendelenburg \200 give IV bolus methylprednisolone (2mg/kg). This dose should 05_McClure_05.indd 64 11/15/2012 12:18:58 AM HYPOVOLAEMIC SHOCK 65 Hypovolaemic shock Shock is characterized by inadequate systemic perfusion. The most com- m on type, hypovolaemic shock, is related to abnormally low circulating blood volume. Symptoms See b p54. Etiology The causes of hypovolaemia are: \200 \200 \200 \200 \200 \200 Trauma. GI bleeding ( Burns ( Peritonitis. Diarrhea ( Diabetic ketoacidosis. ( b pp.312 \200\223313). b pp.66 \200\22368). b pp.302 \200\223303). b pp.98 \200\223101) Diagnosis Perform a rapid clinical examination and direct your initial treatment to- ward t he patient \200\231s vital signs. Initial treatment Follow a standard protocol \200 \200 Airway, Breathing, Circulation, Disability (ABCD) . in patients with signi \201 cant blood loss, transfusion will be Blood: required (about 2mL/kg to increase hemoglobin concentrati on by 1g/dL). (Patient may need O \200\223ve unmatched blood in an emergency). Monitor the response with laboratory testing. acutely, blood pressure and perfusion need to be restore d Fluid: with crystalloid infusion. IV bolus of normal saline, 20mL/kg, can be given over 1 5min and repeated if necessary. If more than 60mL/kg is required consider endotracheal intu bation and ventilatory support. In the patient who is dehydrated, the water and electrolyte de \201 cit needs to be replaced (see, b pp.90 \200\22393). Refractory therapy are requir ed (see b p.714). hypotension: intubation and intensive care monitoring and 05_McClure_05.indd 65 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 66 Burns There are different forms of thermal injury to the body: \200 \200 \200 \200 \200 \200 Contact with \201 re. Scalding \202 uids. Chemicals. Electricity. Inhalation of \202 ame, heated vapor, and toxic fumes. Cold: freezing injury. The severity of a burn to the skin is assessed according to its severity and total surface area. Severity Severity of the burn site is categorized according to the degree of involve- ment of the skin: \200 \200 First Second painful, and deep is white and painless. Third degree: limited to epidermis; painful and erythematous. degree: epidermis and dermis. Super \201 cial is blistered and degree: epidermis and all of the dermis; painless and leathery. Surface area The extent of the burn as a proportion of the body surface area (% body surfac e area) can be calculated by making a sum of the individual areas involved in the injury. T able 5.1 gives the percentage of the body surface area taken up by the individual areas at different ages. Table 5.1 Contribution of different body parts to total body surface area at different ages Body part area/total body surface (%) at ages Body part <1yr 1 \200\22311yrs >11yrs Head 18 13 9 Trunk (front) 18 18 18 Trunk (back) 18 18 18 Arm 9 9 9 Leg 14 16 18 Genitalia 1 1 1 Symptoms Features of hypovolaemia, pain, and signs of inhalation injury may be present. 05_McClure_05.indd 66 11/15/2012 12:18:58 AM BURNS 67 Symptoms of inhalation in the lung \200 \200 \200 \200 \200 \200 \200 Tachypnoea. Stridor. Crackles. Wheeze. Cough. Respiratory distress. Black sputum. Other burn symptoms Brain \200 \200 \200 \200 \200 \200 Confusion. Dizziness. Headache. Restlessness. Coma. Seizures. Skin \200 \200 \200 Facial burns. Nasal burn. Cherry-red color. Etiology You should \201 nd out the following about the injury: \200 \200 \200 \200 Its mechanism. The duration of exposure. Environmental factors (closed or open space). Loss of consciousness during the accident. Investigations Minor burns There is no need for routine investigations in children with min or burns, i.e. burns that are: \200 \200 partial thickness and <5% body surface; full thickness and <2cm or 2 (unless hands, face, genitals, joints involved). Major burns \200 \200 \200 \200 Arterial blood gas. Carboxyhaemoglobin level. Blood count and cross-match. Blood urea, crea tinine, and electrolytes may be tested. Consider child protection issues! 05_McClure_05.indd 67 11/15/2012 12:18:58 AM CHAPTER 5 Emergency and high dependency care 68 Burns: treatment Initial treatment Follow a standard protocol \200 ABC: endotracheal intubation may be needed. Assume that there is carboxyhaemoglobin level a nd PaO2. Give humidi \201 ed 100% oxygen until results are available. Follow serial arteri al blood gasses and CXRs. Consider almonds, or if the accident is \201 re-related, or if there is metabolic acidosis with raised anion-gap. In infants with burns >10% of body surfa ce area, or children with >15% burns, consider an IV bolus of normal saline (10 \200\22320m L/kg). Further \202 uid resuscitation should be directed toward maintaining a urine outpu t of 0.5 \200\2232mL/kg/h. In patients with >25% burns use the Parkland \200\231s formula a s a guide to \202 uid therapy Box 5.3. if there is evidence of inhalation then pulmonary toilet with carbon monoxide poisoning and measure \200 cyanide exposure and poisoning if the breath smells of Box 5.3 Parkland \200\231s formula 0 \200\22324hr after burn Crystalloid \200 \200 4mL/kg per 1% burn Use 50% of this volume in the \201 rst 8hr 24 \200\22348hr after burn Crystalloid + colloid \200 \200 Use 50 \200\22375% of \202 uid requirements on day 1 Add albumin (1g/kg/day) to maintain serum level above 2g/dL Analgesia: pain must be treated. First ensure that ventilation, oxygenation, and perfusion are adequate. Use IV analgesics if required. injuries: do a secondary survey of associated traumatic injuries. Other Assess for cardiac and skeletal muscle injury in electrical accid ents. In chemical burn, wash and neutralize the chemical. Place a Pulse limitations in carb on monoxide poisoning. Eyes: antibiotics if required. Give tetanus \200 nasogastric tube (NGT) and urinary catheter. Follow outputs. oximetry and cardiac monitorin g are useful, but remember their examine the eyes for burn or abrasion, and treat with topical immunoprophylaxis if required. 05_McClure_05.indd 68 11/15/2012 12:18:59 AM BURNS: TREATMENT 69 05_McClure_05.indd 69 11/15/2012 12:18:59 AM CHAPTER 5 Emergency and high dependency care 70 Sepsis Sepsis is bacterial infection of the bloodstream accompanied by signs of systemic to xicity. In this section we will consider the recognition and spe- ci \201 c treatment for sepsis. Shock and respiratory failure are covered else- where in the chapter (see b pp.48, 54). Clinical assessment Clinically, there may be fever in the older child, but be aware that fe ver or hypothermia can be the presenting feature in the infant. Perfusion is usually poor a nd there may be evidence of shock and coagulopathy (i.e. petechiae or purpura). Investigations All organ systems may be involved in sepsis so it is important to perform th e following tests. Blood \200 \200 \200 \200 \200 \200 FBC with differential. Coagulation state. Serum electrolytes with urea and creatinine. Live r function tests. Arterial or capillary blood gas. In \202 ammatory markers (e.g. CRP and erythrocyte sedimentation rate (ESR)). Urine Urinalysis. Imaging \200 CXR. \200 Abdominal X-ray (AXR). Sepsis screen \200 Blood culture: that blood cultures may not be positive, so repeat when there is fever). Uri ne culture. Stool swab. CSF. Other cultures: catheters. bacteria (aerobic and anaerobic), virus, fungi. (Remember \200 \200 \200 respiratory; wound; and all ports of any indwelling Monitoring Ensure the ABCs. Then, the form and type of monitoring will be dictated by the p atient \200\231s condition. Start with: \200 \200 \200 \200 Continuous pulse oximetry. ECG monitoring. Intermittent BP monitoring. Hourly urine output. 05_McClure_05.indd 70 11/15/2012 12:18:59 AM SEPSIS 71 Therapy Antibiotics \200 When: trying to get a blood culture \201 rst. Should I do a lu mbar puncture? This can wait until you have stabilized the child \200\224you may even have to defer it if there is any coagulopathy. What: patient, as well as your local microbial \202 ora. In general, you can start with a third generation cephalosporin and use the follo wing antibiotics for speci \201 c groups of patients. do not delay the \201 rst dose because of tests, but it is worthwhile the choice of antibiotics you should use will depend on the Age <8 weeks Consider group B streptococcus \200\224ampicillin. Indwelling catheter Consider Staphylococcus aureus \200\224anti-staphylococcal cover that i s appro- priate in your institution. Intra-abdominal cause Consider gut anaerobes \200\224metronidazole, gentamicin. Immunosuppressed or oncological \200 \200 \200 Pseudomonas Fungi: Herpes, Varicella: : ceftazidime, gentamicin. amphotericin B. aciclovir. Cellulitis or fasciitis Consider group A streptococcus \200\224penicillin. 05_McClure_05.indd 71 11/15/2012 12:18:59 AM CHAPTER 5 Emergency and high dependency care 72 Altered level of consciousness See also b p.552. The brain can be injured in many ways. Its responses to injury, however, are uniform and include any combination of: \200 Altered l evel of consciousness (LOC). \200 Seizures or dystonia. \200 Impaired respiratory funct ion. \200 Loss of cardiovascular autoregulation. \200 Cerebral swelling. \200 SIADH. \200 Weakness. Take a note of: \200 When symptoms started, and their progression (gradual versus sudden). Possible ingestion or exposure to medication or toxins. Possible recent trauma, illness, or exposure to infectio n. History: seizures; diabetes; allergies; chronic illness. Family history/consanguinity. P revious altered LOC. \200 \200 \200 \200 Etiology Infectious causes \200 \200 \200 b pp.78 \200\22379, 720 \200\223721). Meningitis, encephalitis ( b p.719). Toxic shock ( Subdural empyema, cerebral abscess. Autoimmune Acute disseminated encephalomyelitis (ADEM) b p.520. Toxins See poisoning (b pp. 82 \200\22388). Neoplastic causes Brain tumors (b pp.662 \200\223665). Trauma \200 \200 concussion or contusion. Head injury: Hemorrhage: epidural; subdural; brain. Vascular causes \200 \200 AV malformation. Aneurysm, venous thrombosis.