Cyanide \200 \200 There are special kits for rescue that will be in Drugstore Sodium poisoning as well Sodium nitrate 3%: dose depends on Hb level, but do not give if CO thiosulphate 25%: dose depends on Hb level Digoxin \200 \200 \200 Measure serum drug level. Toxicity occurs with level >2ng/mL Check electrolytes, magnesium, thyroxine, and calcium Correct hypokalaemia (IV 0.5 \200\2231mmol/kg/dose as infusion 0.5m mol/kg/h over 2hr) If hyperkalaemic (>5mmol/L) give insulin, dextrose, sodium bicarbonate, and Kayexalate . Do not give calcium chloride or calcium gluconate because these potentiat e ventricular arrhythmias Digoxin-speci \201 c dysrhythmias, or supraventricular bradyarrh ythmias (if resistant to IV atropine 10 \200\22320micrograms/kg), hyperkalaemia, hypotensio n, heart block, and ingestion >4mg. Phenytoin may be used to improve AV conduction. Avoid q uinidine, procainamide, isoprenaline, or disopyramide if AV block present antibody (FAB fragments). Give for ventricular Ethylene glycol, methanol \200 Fomepizole 15mg/kg bd until levels (cid:1)20mg/dL): antidote for methanol and ethylene glyc ol. Indications: level (cid:2)20mg/dL, or high anion gap metabolic acidosis If not availabl e, use followed by infusion 100mg/kg/hr) Other agent: the case of methanol, also give folat e (50 \200\223100mg over 6hr) (loading 15mg/kg, then 10mg/kg bd for 4 doses, then ethanol (loading dose 0.6g/kg; load over 1hr pyridoxine 2mg/kg and thiamine 500micrograms/kg. In Iron \200 Measure serum concentration 2 \200\2236hr after ingestion. A level >350micrograms/dL is fre quently associated with systemic toxicity. If ingestion <20mg/kg no treatment needed Desfer rioxamine serious poisoning (i.e. based on symptoms, AXR, serum level >500micrograms/dL). C ontinue until symptoms have resolved : IV infusion 5 \200\22315mg/kg/hr in all cases of 05_McClure_05.indd 87 11/15/2012 12:19:01 AM CHAPTER 5 Emergency and high dependency care 88 Isoniazid For stopping seizure use pyridoxine (vitamin B6) 3 \200\2235g Lead \200 \200 (cid:2)70micrograms/dL Immediate intervention for blood level Oral chelation with dimercaptosuccinic acid (DMSA): kg/day divided every 8hr; next 14 days 20mg/kg/day divided every 12hr Parenteral chelation with British antilewisite (BAL): initial dose 75mg/ m2 deep IM; then 4hr later start CaNa2E DTA (1500mg/m2/day via continuous IV infusion for 48hr). If there is risk of cerebral oedem a, then give IM. BAL is continued simultaneously at 75mg/m2/dose IM 4-hourly for 48hr BAL i s suspended in peanut oil, and may cause haemolysis in patients with G6PD de \201 ciency \201 rst 5 days 30mg/ Methaemoglobinaemia: sulphonamides, quinines, phenacetin, nitrates, aniline dyes, naphthale ne \200 \200 Measure level and if >30% start treatment Methylene repeat dose (maximum total 7mg/kg) if s ymptoms present after 1hr Beware of methylene blue in G6PD de \201 ciency Consider hyperba ric oxygen or exchange transfusion if no response blue 1%: 1 \200\2232mg/kg (0.1 \200\2230.2mL/kg) IV over 5min. May \200 Narcotics: codeine, dextromethorphan, propoxyphene, pentazocine, butorphanol, methadone \200 Naloxone or via ETT 2mg (10micrograms/kg, if < 12yrs) inc to 100micrograms/ kg. Response is rapid and repeat doses or infusion can be used. useful for reversing coma caused by opiates. Give IV, IM, Organophosphates: pesticides \200 initial dose 20micrograms/kg (max 2mg) IV; then additional Atropine: doses if bronchorrhoea Pralidoxime: infusion for severe cases 25 \200\22350mg/kg/dose (up to 1g) IV; consider 10 \200\22315mg/kg/hr Phenothiazine \200 For extrapyramidal syndrome, IV over 5min. Also if life-threatening, IV (1 \200\2232 doses per day in children >3yrs) diphenhydramine: 1mg/kg/dose slow benzatropine 20 \200\22350micrograms/kg/dose 05_McClure_05.indd 88 11/15/2012 12:19:01 AM FLUID AND ELECTROLYTES 89 Fluid and electrolytes Normal \202 uid requirements All children with serious acute illne ss in hospital are given \202 uid and elec- trolyte solutions. It is important to match w hat you prescribe to what the child actually needs. There are a number of ways of calculati ng daily requirements, but the method we most commonly use is based on patient weight (see Box 5.8). Box 5.8 Calculating \202 uid and electrolyte requirements 24-hr \202 uid requirements \200 \200 \200 100mL/kg: +50mL/kg: +20mL/kg: for the \201 rst 10kg of weight for the second 10kg of weight for the remaining weight ab ove 20kg 24-hr electrolyte requirements \200 2 \200\2234mmol/kg \200 Sodium: Potassium: 1 \200\2232mmol/kg Normal \202 uid therapy is based on the above calculations. In the fasting pa- tient, the type of \202 uid given should contain dextrose (usually 5%), sodium chloride, and added potassium chloride. Outside the neonatal period we use 0.9% or 0.45% saline with dextrose a nd additives. Do not use plain 5% dextrose in water or 5% dextrose 0.18% saline. The volume of \202 uid admin- istered should be increased in dehydration (see b p.91), and restrict ed to 50 \200\22375% of the usual maintenance volume in cases of: \200 \200 \200 \200 b pp.92, 448). SIADH ( b p.53). Fluid overload ( b p.226). Congestive heart failure ( Renal failure with oliguria or anuria ( b pp.362 \200\223365). 05_McClure_05.indd 89 11/15/2012 12:19:01 AM CHAPTER 5 Emergency and high dependency care 90 Fluid and electrolytes: dehydration Dehydration can lead to shock, severe metabolic acidosi s, and death, par- ticularly in infants. Its severity can be assessed using change in weigh t or the following physical signs. Mild dehydration (0 \200\2235%) \200 \200 \200 \200 \200 \200 \200 \200 \200 Weight Skin Mucous Urine: Heart Blood Perfusion: Skin Consciousness: loss: 5% in infants and 3% in children. turgor: may be decreased. membranes: dry. may be low. rate: increased. pressure: normal. normal. color: pale. irritable. Moderate dehydration (5 \200\22310%) \200 \200 \200 \200 \200 \200 \200 \200 \200 Weight Skin Mucous Urine: Heart BP: Perfusion: Skin Consciousness: loss: 10% in infants and 6% in children. turgor: decreased. membranes: very dry. oliguric. rate: increased. may be normal. prolonged capillary re \201 ll (capillary re \201 ll time (CRT) > 2s). color: gray. lethargic. Severe dehydration (10 \200\22315%) \200 \200 \200 \200 \200 \200 \200 \200 \200 Weight Skin Mucous Urine: Heart Blood Perfusion: Skin Consciousness: loss: 15% in infants and 9% in children. turgor: poor with tenting. membranes: parched. anuric. rate: increased. pressure: decreased. prolonged CRT. color: mottled; blue or white. comatose. After you have assessed the degree of dehydration in your patient, two problems need to be addressed \200\224water and electrolyte losses. In practice, our treatment is aimed at corr ecting both the water and electrolyte losses (Table 5.4). 05_McClure_05.indd 90 11/15/2012 12:19:01 AM FLUID AND ELECTROLYTES: DEHYDRATION 91 Table 5.4 Water and electrolyte losses in 10% dehydration Losses in 10% dehydration H2O (mL/kg) Na (mmol/kg) K (mmol/kg) Cl (mmol/kg) Isotonic dehydration (Na, 130 \200\223150mmol/L) 100 \200\223120 8 \200\22310 8 \200\22310 8 \200\22310 Hyponatraemic dehydration (Na < 130mmol/L) 100 \200\223120 10 \200\22312 8 \200\2231 10 \200\22312 Hypernatraemic dehydration (Na > 150mmol/L) 100 \200\223120 2 \200\2234 0 \200\2234 2 \200\2236 Isotonic and hyponatraemic dehydration \200 \200 \200 \200 First assess the degree of dehydration (use weight change and signs). Calculate the \202 uid de \201 cit. FBC with differential. Serum electrolytes (Na, K, Ca) with urea, creatini ne, and glucose. Emergency treatment is directed toward restoring any compromise in the circulation. (See sh ock, b p.56: use 20mL/kg IV normal saline). Monitoring should include: vital signs, losses (urine output, stool, vomitus, NG), daily weights, and blood tests. After the initial phase , \202 uid administration should be calculated to correct de \201 cits over 48hr. Overal l, take into account the de \201 cit, maintenance requirements, and any ongoing losses: Hourly rate = (24hr maintenance + de \201 cit \200\223 resuscitation \202 uids)/24 Hypernatraemic dehydration \200 Water losses exceed sodium loss. \200 Cerebral oedema i s a risk during rehydration, so correction of the de \201 cit should be achieved slowly an d evenly, over 48hr. Emergency treatment of shock is treated with 10 \200\22320mL/kg IV sal ine. Thereafter, calculate the de \201 cit and restore patient \200\231s needs. Monitor as above, with at least 8-hourly electrolyte studies. Use 0.9% saline so that sodium correcti on occurs slowly. \200 Seizures and cerebral oedema may complicate the rehydration phase of hypernatraemic dehydra tion. If these occur, treat symptomatically and refer to an intensive care unit. There may be a number of causes of these problems \200\224your initial role in this emergency is to d o the ABCs. Further investigations and CT scan may be needed. 05_McClure_05.indd 91 11/15/2012 12:19:01 AM CHAPTER 5 Emergency and high dependency care 92 Fluid and electrolytes: abnormalities Hyponatraemia (<130mmol/L) Assess the problem. Is the patient hypovolaemic or overloaded? Sodium depletion \200 Associations: \200 Causes: \200 Treatment: \200 therapy (<120 mmol/L): if there are seizures, the serum Na Symptomatic level should be acutely raised by 5 \200\22310mmol/L in about 1hr. Use 3mmol NaCl/kg IV over 30 \200\22360min. hypovolaemia and low urine Na (<10mmol/L). inadequate Na intake, excessive Na losses. restore circulation, replace water and salt de \201 cits. Dilution \200 Associations: urine Na (usually >300mmol/L), and sometimes cerebral oedema. Causes: Treatme nt: (furosemide 0.5 \200\2231.0mg/kg IV). Provide oxygen and inotropes if required. Restric t \202 uids to less than maintenance. SIADH: volume and high urine osmolality in the abse nce of hypovolaemia, renal disease, and adrenal disease. Urine Na is paradoxically high (20 \200\22330mmol/L) in the presence of hyponatraemia secondary to volume overload (see b p.4 48). normovolaemia (occasionally overload), paradoxically high \200 impaired water excretion; excess water given. correct the volume overloaded circulation with diuretics There are many causes of SIADH. The features are low urine Hypernatraemia (>150mmol/L) Besides hypernatraemic dehydration and salt poisoning, you will see hypernatraemia in diabetes insipidus (DI), where there is excess renal water loss. The urine is 5 \200\22310 times usual volume, with low osmolality (50 \200\223100mOsm/L), in t he absence of glycosuria. So, assess the underlying problem, and restore compromised circul ation (see b p.91). Anti-diuretic hormone (ADH) de \201 ciency \200 \200 severe asphyxia, and CNS trauma, surgery, or infection. Causes: Treatment: replacement of insensible losses; the other for replacing urine losses. Check urine Na/K and prepare IV replacement solution to match. Hormone therapy is reasonabl e. However, if this problem is established, hormonal replacement is needed: nasal deamino-8 d-arginine vasopressin (DDAVP) 1 \200\22340micrograms/day in 1 or 2 doses; parenteral (IV) DDAVP 2 \200\2234micrograms/day in 2 doses. You should see a response within 1hr. use two IV solutions \200\224one at 30 \200\22340% maintenance for replacement: DI is sometimes transient and so initial \202 uid 05_McClure_05.indd 92 11/15/2012 12:19:01 AM FLUID AND ELECTROLYTES: ABNORMALITIES 93 Hypokalaemia (<3mmol/L) \200 ECG waves; ST segment depression; atrioventricular block. Dysrhythmias Neuromuscular: GI: changes: \202 attened, prolonged, or inverted T waves; prominent U \200 \200 , hypotension. weakness; hypotonia; hypore \202 exia; paraesthesiae. ileus; constipation. Correction \200 Urgent: \200 Treatment. should not exceed 20mmol, and should not be mor e concentrated than 40mmol/L KCl/L. Monitor with continuous ECG and repeat serum K level af ter 1 \200\2232hr. ECG changes, children on digoxin, or serum <2.5mmol/L. use 0.5mmol KCl/kg IV over 1hr via a central line. The bolus Hyperkalaemia (>5.5mmol/L) \200 ECG progressing to increasingly aberrant ECG complexes; Dysrhythmias: changes: peaked T waves; widened QRS; depressed ST segments bradycardia; VT; VF; cardiac arrest. Approach Treatment guided by the level, but \201 rst repeat a venous sample in case of ha emolysis. Stop all potassium and monitor the ECG, while you wait for the result. Symptomatic treatment (>8.0mmol/L or ECG changes) \200 Protect maximum rate 100mg/min; 1.5 \200\2233.3mL/min, 50mg/mL) and monitor for bradycardia and hypotension. intracellular K uptake: NaHCO3 (1 \200\2232mmol/kg IV over Increase 5 \200\22310min); insulin with glucose (0.1unit/kg IV with dextrose 25% 0.5g/kg IV over 30min ). Induce Decrease 20% sorbitol). the myocardium: calcium gluconate 10% (100mg/kg/dose IV at \200 kaluresis: salbutamol nebulizer. total load of K: Kayexalate (1g/kg/dose PR 2-hourly with 5mL Hypocalcaemia (<1.1mmol/L) See also b p.442. Low ionized values of Ca can result in: \200 \200 \200 ECG Shock CNS changes: prolonged QT, AV block; . effects: seizures, tetany, and weakness. Symptomatic therapy \200 \200 Calcium gluconate 10% for seizures, tetany, hypotension, arrhythmias. Monitor HR and BP dur ing treatment. Refractory hypocalcaemia \200 Check IV magnesium sulfate over 30min, 6-hourly for 3 doses). If these are normal, with and use phosphate binders. Check renal function. magnesium level and serum albumin: if low, correct (25 \200\22350mg/kg. raised phosphate, decrease phosphate intake 05_McClure_05.indd 93 11/15/2012 12:19:01 AM CHAPTER 5 Emergency and high dependency care 94 Renal insuf \201 ciency Acute renal failure is the sudden reduction or cessation of renal function to the point where body \202 uid homeostasis is compromised, leading to ac- cumu lation of nitrogenous waste products, with or without reduced urine output. Children in thi s state need immediate attention and transfer to a specialized renal unit. More commonly, w e see patients with a degree of renal insuf \201 ciency that is complicating an acute medi cal illness \200\224it may be present at the time of presentation or it may evolve during h ospital admis- sion. The causes of renal insuf \201 ciency are discussed on b p.362. Clinical assessment Take a thorough history and do a full examination. Assess whether there is hypertension or hypotension. Check the urine output (oliguria <0.5mL/ kg/hr) and if anu ric suspect obstruction. The particular points you should consider are the following: \200 Whether there has been any preceding throat infection (streptococcus), gastroenteritis (hae molytic-uraemic syndrome (HUS)), or exposure to drugs or toxins. Is there any evidence of g eneral illness with pallor, anorexia, oedema, weakness, and fatigue? Is there a rash, and i s it petechial or purpuric? Is there hypertension or signs of heart failure? Is there tachy noea, cough, or haemoptysis? Is there any nausea, vomiting, bleeding, \202 ank mass, or a scites? Is there any evidence of altered consciousness? \200 \200 \200 \200 Investigations The following tests are required in acute care: \200 \200 Blood: Serum or capillary blood gas. Urine: check for any protein, blood, or active sedimen t (red cell casts, tubular cells, white cell casts, or other evidence of urinary tract infe ction (UTI)). Imaging: (US) examination with Doppler studies of renal vessel blood \202 o w. Other C4), serum titres (e.g. anti-streptolysib O (ASO) titres). FBC with differential. biochemistry: electrolytes with urea and creatinine, and arterial organize a CXR, AXR, and abdominal and renal ultrasound tests: consider taking blood samples for complement levels (C3, Monitoring The form and type of monitoring will be dictated by the patient \200\231s condi- tion. Start with: \200 \200 \200 \200 Continuous pulse oximetry. ECG monitoring. Intermittent BP monitoring. Insert a urinary cat heter and follow hourly output. 05_McClure_05.indd 94 11/15/2012 12:19:02 AM RENAL INSUFFICIENCY 95 Acute therapy In the acute setting \201 rst assess the ABCs. Then, to assess intravascula r volume, come to a decision about whether the patient is hypovolaemic or hypervolaemic. Hypovolaemia \200 Administer 20mL/kg 0.9% normal saline as an IV bolus, and repeat if necessary. If the cause of anuria is \202 uid depletion, \202 uid resuscitation should restore urine \202 ow within 6hr. Give blood if necessary and continue to monitor. Acute tubular necrosis is lik ely if there is no response to the above. Repeat the \202 uid bolus with furosemide (1 \200\2235mg/kg IV), but do not use if obstructive uropathy is suspected \200\224refer to a urologist. If the patient produces urine, expect large amounts (which will need to be repla ced) as polyuric renal failure may be present. \200 Hypervolaemia \200 \200 Consider a single dose of furosemide (1 \200\2235mg/kg IV). If the urine output is minimal then treat as acute renal failure. Acute renal failure and kidney injury A child in acute renal failure will need to be transf erred to a renal unit. Hypertension, hyperkalaemia, hyponatraemia, and seizures will need t o be treated. You should continue to monitor volume state, BP, ECG, and electrolytes. Stand ard treatment includes the following. BP \200 \200 \200 b pp.391 \200\223392). Hypertension is present if BP >95th centile (see Restrict salt intake. Consider antihyperte nsive drugs. Fluids \200 \200 Continue to correct and replace volume loss with normal saline. Thereafter, restrict \202 uids to urine replacement and insensible losses (300 \200\223400mL/m2/day). Electrolytes \200 \200 Correct hyponatraemia if causing seizures. Correct hypocalcaemia if symptomatic \200\224do this before correcting any acidosis. Discontinue any potassium administration. (Remember th at for every 0.1 fall in pH, potassium will rise by 0.4mmol/L, so you may need to treat aci dosis if pH <7.2 and bicarbonate <10mmol/L.) Diet Limit protein to 0.5 \200\2231.0g/kg/day. 05_McClure_05.indd 95 11/15/2012 12:19:02 AM CHAPTER 5 Emergency and high dependency care 96 Glucose: hypoglycaemia In infants and children this emergency is de \201 ned as a blood va lue <2.2 \200\2232.6mmol/L (see also b pp.132, 412, 967). Etiology Hypoglycaemia is a sign of an underlying disease process that interferes with carb ohydrate intake or absorption, gluconeogenesis, or glycogenoly- sis. These conditions are d iscussed in detail in Chapter 26 (see b p.967). Outside the neonatal period, in the acute s etting, the causes of hypogly- caemia can be grouped as follows. Endocrine \200 \200 \200 \200 \200 Hyperinsulinism. Hypopituitarism. Growth hormone de \201 ciency. Hypothyroidism. Congenita l adrenal hyperplasia. Metabolic \200 \200 \200 \200 \200 \200 Glycogen storage disease. Galactosaemia. Organic acidaemia. Ketotic hypoglycaemia. Carnitin e de \201 ciency. Acyl CoA dehydrogenase de \201 ciency. Toxic \200 \200 \200 \200 Salicylates. Alcohol. Insulin. Valproate. Hepatic \200 \200 \200 Hepatitis. Cirrhosis. Reye syndrome. Systemic \200 \200 \200 \200 Starvation. Malnutrition. Sepsis. Malabsorption. Clinical assessment Take a thorough history and identify the timing of hypoglycaemia in rel a- tion to feeding and medication. On examination assess for: \200 \200 \200 \200 b p.466). Short stature ( Failure to thrive ( Hepatomegaly ( Features of any generalized metabolic di sorder ( b p.308). b p.960). b p.954). 05_McClure_05.indd 96 11/15/2012 12:19:02 AM GLUCOSE: HYPOGLYCAEMIA 97 Investigation If possible, during an acute episode you should try to: \200 \200 \200 \200 \200 Save blood and urine for metabolic and endocrine testing. Check blood glucose in the labora tory. Blood electrolytes, urea, liver function, and osmolality. Blood gas. Toxicology scree n. Monitoring Ensure ABCs. Then start with continuous pulse oximetry and ECG moni- toring, and intermittent BP monitoring. Treatment Asymptomatic child Oral glucose drink or gel. Symptomatic child \200 \200 Glucose: Followed (6 \200\2238mg/kg/min), e.g. 0.45% saline and 5% glucose. If If there is These patients will need advice from a specialist. 10% 5 \200\22310mL/kg IV, or 25% 2 \200\2234mL/kg IV. by: continuous infusion of salt solut ion with 5 \200\22310% glucose hypoglycaemia persists increase the glucose to 10 \200\22312mg/kg/min. \200 no response consider glucagon, hydrocortisone, or diazoxide. 05_McClure_05.indd 97 11/15/2012 12:19:02 AM CHAPTER 5 Emergency and high dependency care 98 Diabetic ketoacidosis See also b p.413. Diabetic ketoacidosis (DKA) is a diabetic emergency and such patients can die from hypovolaemic shock, cerebral oedema, hypokalaemia, or aspir a- tion pneumonia. DKA is de \201 ned as: \200 Hyperglycaemia (>11mmol/L). \200 pH < 7 .3. \200 Bicarbonate <15mmol/L. \200 Urinary ketones. Patients who meet the above criteria, who are more than 5% dehydrated, or who have altered level of consciousness require careful supervision and treatment. Some patients may need re ferral to an intensive care unit (e.g. pH < 7.1, severe dehydration with shock, <2yrs of ag e). Clinical assessment \200 \200 \200 \200 b p.90). b pp.74 \200\22377). Degree of dehydration ( Level of consciousness ( Full examination for evidence of cerebral oedema, infection, and ileus. Weight. Investigations The key tests are as follows. Blood \200 \200 \200 \200 \200 \200 \200 FBC with differential. Serum electrolytes with urea and creatinine. Glucose. LFTs (transami nases). Arterial or capillary blood gas. Lactate level. Ketone level. Urine \200 \200 \200 \200 \200 Urinalysis. Ketones. Reducing substances. Organic and amino acids. Drug screen. Monitoring \200 Ensure dictated by the patient \200\231s condition. CNS: consciousness, t reat as though raised ICP has developed. Continuous alert you to hypokalaemia or hyperkalae mia. Intermittent BP monitoring. Hourly the ABCs: after that the form and type of monitoring will be follow the neurological state. If there is headache or altered pulse oximetry and ECG monitoring: T-wave changes should \200 urine output: test for ketones. 05_McClure_05.indd 98 11/15/2012 12:19:02 AM DIABETIC KETOACIDOSIS 99 05_McClure_05.indd 99 11/15/2012 12:19:02 AM CHAPTER 5 Emergency and high dependency care 100 Diabetic ketoacidosis: treatment Fluid therapy We have already discussed the management of dehydration (b pp.90 \200\223 93). Our therapy is similar in DKA, with the following caveat s. Resuscitation \202 uid \200 \200 \200 Use 0.9% saline for resuscitation of the circulation. This alone will bring down the glucos e level. Remember to include the initial resuscitation volume in your calculation of total \202 uid replacement to be given in the 48hr. Calculation of de \201 cit \200 \200 Never use more than 10% dehydration in the calculations. Restore de \201 cit over 48hr. Type of \202 uid \200 \200 Use normal saline initially. When glucose has fallen to 14mmol/L add glucose to the \202 uid. If this fall occurs within 6hr, the child may still be sodium depleted. In this instan ce add glucose to 0.9% saline. Usually the fall in glucose occurs after 6hr and it is safe to change the \202 uid type to 0.45% saline with 5% glucose. Potassium should be started with the rehydration \202 uids after the \201 rst 500mL provided the patient is passing urine. Add 40mmol KCl/L (i.e. 20mmol KCl to each 500mL bag). Bicarbonate and phosphate \200 \200 1 There is no evidence for using bicarbonate/phosphate in DKA. However, under extreme condi tions and in critical illness these are sometimes considered. Electrolytes Check these 2-hourly after resuscitation, and then 4-hourly. Oral \202 uids \200 \200 Initially nil by mouth NGT. Juices and rehydration solutions should only be given after substantial clinical improvement. These \202 uids should be added to the overall calculat ion of \202 uid intake. Insulin therapy Once the rehydration \202 uids and potassium have been started insulin sh ould be used to switch off ketogenesis and reverse DKA. There is no need for an initial bol us dose; continuous low-dose IV insulin is the pre- ferred method of administration. 05_McClure_05.indd 100 11/15/2012 12:19:02 AM DIABETIC KETOACIDOSIS: TREATMENT 101 Insulin treatment in diabetic ketoacidosis Insulin infusion \200 Make up a solution of 1U/mL of human soluble insulin (50U in 50mL of 0.9% saline) Attach th is to a second IV line or \200\230piggy-back \200\231 to one line with the replacement \202 uids Give 0.1U/kg/h (i.e. 0.1mL/kg/hr) Glucose fall \200 If the rate of blood glucose fall exceeds 5mmol/L/hr, or falls to around 14 \200\22317mmol/ L, then add glucose (equivalent to 5 \200\22310%) to the IV \202 uids Insulin dose needs to be maintained at 0.1U/kg/hr in order to switch off ketogenesis \200\224do not stop it. I f the blood glucose falls below 4mmol/L, give a bolus of 2mL/kg of 10% glucose and increase the glucose concentration of the infusion Recovery \200 Once the pH is >7.3, the blood glucose <14mmol/L, and a glucose- containing \202 uid has been started, consider reducing the insulin infusion rate, but to no less than 0.05U/kg/hr Once the child is drinking well and able to tolerate food, IV \202 uids and insulin can b e discontinued Start SC insulin in the newly-diagnosed diabetic, according to local protoco l. Resume usual insulin regimen in known diabetics Discontinue the insulin infusion 60min a fter the \201 rst SC injection Treatment failure If blood glucose is uncontrolled, or the pH worsens after 4 \200\2236hr, check IV lines, dose of insulin, and consider possible sepsis Complications The most concerning complication of DKA is cerebral oedema. The warn- ing sig ns include: \200 \200 \200 \200 Headache, behavioral change with restlessness, drowsiness. Body posturing, cranial nerve pa lsy, seizures. Slowing of HR, haemodynamic instability. Respiratory arrest. Once identi \201 ed: \200 Start ABCs. \200 Emergency mannitol (1.0g/kg) IV. \200 Tra nsfer to the intensive care unit. Reference 1 Dunger DB, Sperling MA, Acerini CL, et al. (2004). ESPE/LWPES consensus stateme nt on diabe- tic ketoacidosis in children and adolescents. Arch Dis Child 89: 188 \200\22394. 05_McClure_05.indd 101 11/15/2012 12:19:02 AM CHAPTER 5 Emergency and high dependency care 102 Inborn error of metabolism Inborn errors of metabolism are rare. If such conditions are sus pected during the neonatal period, then there is a speci \201 c course of action that shou ld be followed (see b p.187, and Chapter 26). Very occasionally, however, infants or childr en present outside the neonatal period with a catabolic state induced by an intercurrent il lness such as viral infection, or fasting. The differential diagnosis at this time is broad and includes: \200 \200 \200 generalized sepsis; CNS infection. Infection: Gastrointestinal: Cardiac: pyloric stenosis; gastroenteritis. duct-dependent CHD. Clinical assessment History \200 \200 A thorough history is important. Assess whether there is any consanguinity, or death of sib lings from unknown or metabolic diseases. Identify speci \201 cally developmental progress . Has there been intermittent vomiting, sleepiness, or seizures. \200 Examination \200 \200 \200 \200 \200 \200 A full examination is needed here. Think about abnormal odors. Check on growth, failure to thrive. dermatitis or alopecia. Skin: Eyes: cataracts. Breathing pattern: Kussmaul or central hyperventilation. Investigations Until you know the diagnosis, the key tests are as follows. Blood \200 \200 \200 \200 \200 \200 \200 \200 \200 FBC with differential. Serum electrolytes with urea and creatinine. Glucose, LFTs (transami nases). Arterial or capillary blood gas. Lactate, pyruvate, ketones. Plasma amino acids. Am monia. Carnitine. Drug screen. Urine \200 \200 \200 \200 \200 \200 Urinalysis. Ketones. Reducing substances. Organic acids. Amino acids. Drug screen. 05_McClure_05.indd 102 11/15/2012 12:19:03 AM INBORN ERROR OF METABOLISM 103 Monitoring Ensure the ABCs. Then, the form and type of monitoring will be dictated by the p atient \200\231s condition. Start with continuous pulse oximetry and ECG monitoring, and in termittent BP monitoring. Follow hourly output. Therapy In the acute setting, prior to transfer (if needed), treatment will be sup- portive , and directed towards any complicating metabolic acidosis or hy- poglycaemia. All protein intake and oral feeds should be discontinued until the diagnosis is con \201 rmed. In orde r to avoid catabolism give continuous glucose infusion (10 \200\22315%) during illness or p eriods of fasting. Supportive care \200 \200 The underlying or precipitating illness needs to be treated. Later on, as a means of preven tion against infection, ensure that immunizations are up to date. Acidosis \200 \200 \200 Correct and optimize ventilation and circulation. After this, bicarbonate replacement may b e needed. For more persistent problems, treat in specialist centers. Hypoglycaemia Use glucose 25% (2 \200\2234mL/kg/dose IV). 05_McClure_05.indd 103 11/15/2012 12:19:03 AM CHAPTER 5 Emergency and high dependency care 104 Other acid \200\223base problems Since respiratory derangements in acid \200\223base have a lready been discussed, we will restrict this section to metabolic acidosis (see b p.958). A n aci- dotic pH (<7.30), with low bicarbonate (<20mmol/L), suggests a primary metabolic aci dosis. In an emergency, an alkalotic pH (>7.50) with raised bicarbonate (>30mmol/L) is most usually seen when supportive ventila- tion has been started in a patient with chronic hype rcapnia. Differential diagnosis of metabolic acidosis Calculate the anion gap (AG) AG = [Na] \200\223 ([HCO3] + [Cl]) Normal AG = 10 \200\22312mmol/L Increased anion gap metabolic acidosis This is due to the production of exogenous acid. As an aide-m moire, think of \200\230a mudpile \200\231 \200 Alcohol or aspirin \200 Met hanol \200 Uraemia \200 DKA \200 Paraldehyde \200 Ingestion or inborn error \200 Lactate \200 Ethylene glycol Normal anion gap metabolic acidosis This is commonly due to loss of bicarbonate from the gu t or kidney, or impaired acid secretion by the kidney \200 \200 Diarrhea Type I (distal) renal tubular acidosis (RTA): inability to excrete hydrogen ion; u rine pH always high (>6.5); caused by a variety of medications or inherited; often associat ed with hypokalaemia and hypercalciuria Type proximal tubule: usually associated with other proximal tubular dysfunction such as phosphaturia or glycosuria (Fanconi syndrome) Type IV (hyperkalaemic) RTA \200\224inadequate aldosterone production or inability to respond to i t: seen in acute pyelonephritis or obstructive uropathy (proximal) II RTA: impaired reabsorption of bicarbonate from 05_McClure_05.indd 104 11/15/2012 12:19:03 AM OTHER ACID \200\223BASE PROBLEMS 105 Clinical assessment History A thorough history is important. You will need to identify any symptoms of fever, \202 ank pain, and vomiting (pyelonephritis), lethargy, or altered men tal state (metabolic disease or poisoning). Then ask speci \201 c questions about the gast rointestinal and renal tracts, and growth. Last there may be a signi \201 cant family hist ory of renal disease, kidney stones, or early infant death. Examination A full examination is needed. Assess: \200 \200 \200 \200 \200 Hydration. Growth. Respiratory state (compensation for metabolic acidosis). Abdomen. CNS. Investigations Until you know the diagnosis, the key tests are as follows. \200 FBC with differential, serum electrolytes with urea and Blood. creatinine, glucose, LFTs (t ransaminases), arterial or capillary blood gas, lactate, pyruvate, ketone, plasma amino aci ds, ammonia, carnitine, and drug screen. Urine: and drug screen. Imaging: urinalysis, ketones, reducing substances, organic and amino acids, renal US scan looking for nephrocalcinosis (type I RTA). Monitoring Ensure the ABCs. Then, the form and type of monitoring will be dictated by the p atient \200\231s condition. Start with continuous pulse oximetry and ECG monitoring, and in termittent BP monitoring. Follow hourly output. Therapy If the patient is dehydrated then this problem should be treated with oral or IV re placement. This alone may improve serum bicarbonate. However, for the speci \201 c metabol ic disorders: \200 \200 Increased Distal pp.382 \200\223385); RTA: correct serum bicarbonate and increase \202 ui ds Hyperkalaemic to improve sodium delivery to the distal tubule (this will enhance potassi um secretion). AG: identify cause and treat; or proximal RTA: bicarbonate supplementation (see also b Bicarbonate treatment If you are using bicarbonate then: \200 \200 3]) x weight (kg) x 0.5mmol; Estimate the de \201 cit = (20 \200\223 [HCO Replace over 24 \200\22348hr with oral suppl ements. 05_McClure_05.indd 105 11/15/2012 12:19:03 AM CHAPTER 5 Emergency and high dependency care 106 Further reading BSPED-recommended DKA Management Guidelines (2009). Available at: M www.bsp ed.org.uk/ professional/guidelines/docs/DKAGuideline.pdf Wolfsdorf J, Craig ME, Daneman D, et al. (2007) ISPAD Clinical Practice Consensus Guideline s 2006 \200\2232007. Pediat Diabet 8: 28 \200\22343. For the evidence base to the DKA manag ement guidelines, see the 2007 ISPAD guidelines. Available at: M http://www.ispad.org/FileC enter/10-Wolfsdorf_ Ped_Diab_2007,8.28 \200\22343.pdf 05_McClure_05.indd 106 11/15/2012 12:19:03 AM 107 Chapter 6 Neonatology Newborn life support 108 Perinatal de \201 nitions 110 Small for gestational age 111 Large for gestational Conventional positive pressure ventilation 162 High frequency oscillatory ventilation 164 Bronchopulmonary dysplasia 166 age 112 Prematurity 114 Birth at the limit of viability 116 Outcome following prematurity 117 Basic obstetrics 118 Obstetric problems 120 Maternal disorders causing neonatal disease 124 Circulatory adaptation at birth 168 Patent ductus arteriosus 169 CNS malformations 170 Hypoxic \200\223ischaemic encephalopathy 172 Cerebral hemorrhage and ischaemia 176 Birth trauma 126 Non-speci \201 cally ill neonate 128 Necrotizing enterocolitis 178 Neonatal infection 180 Transplacental (congenital Neonatal jaundice 130 Hypoglycaemia 132 Neonatal seizures 134 The \202 oppy infant 136 Hy drops foetalis 138 Routine care of the newborn 140 Milk feeding 142 Routine neonatal infection) 182 Prevention of neonatal infection 184 Neonatal abstinence syndrome 186 Inborn errors of metabolism 187 Retinopathy of prematurity 188 examination 144 Metabolic bone disease 190 Orofacial clefts 191 Neonatal hematology 192 Rh disease (rhesus haemolytic Normal variations and minor abnormalities 146 Newborn \202 uid and electrolyte balance 148 disease) 194 Respiratory distress syndrome 150 Acute respiratory diseases 152 Bilirubin encephalopathy (kernicterus) 195 Neonatal dermatology 196 Perinatal death 198 Neonatal X-rays 156 Neonatal respiratory support 160 06_McClure_06.indd 107 11/14/2012 11:22:39 PM CHAPTER 6 Neonatology 108 Newborn life support All who attend deliveries should be pro \201 cient in newborn resusci tation, ideally taught on a recognized course (newborn life support (NLS) or equivalent). T he algorithm on b p.109 demonstrates a general approach to resuscitation (see Fig. 6.1). Pr eterm infants require special consideration (b p.114). Before birth \200 \200 Check equipment. Ask about: Gestation? Fetal distress? Meconium? At birth \200 For uncompromised babies, a delay in cord clamping of at least one minute is recommended. T here is insuf \201 cient evidence to recommend a delay in babies who require resuscitation . Meconium \200 Vigorous infants born through meconium stained liquor do NOT require airway suctioning eith er on the perineum or the resuscitaire. Pale, \202 oppy, poor respiration, or bradycardia ? Inspect oropharynx and perform suction if required. If appropriate expertise is available , tracheal intubation and suction may be useful in non-vigorous babies. If expertise not av ailable, or if attempted intubation is prolonged or unsuccessful, start mask ventilation, p articularly if there is persistent bradycardia. Lung in \202 ation \200 \200 \200 In \202 ation breaths are given initially, use air (21% O 3s each breath, 7 30cmH Once the chest is moving, ventilation breaths (shorter and gentler) are given at a rate of 30 \200 \22340/min if required. 2). 20 (term infants) \200\224give in sets of 5. Airway maneuvers \200 \200 \200 \200 Jaw thrust (2 person technique very useful). Direct inspection of oropharynx and airway suc tion. Guedel airway. Intubation (if competent). Chest compressions \200 \200 \200 7100/min, using two thumbs technique. Rate 3 chest compressions per lung in \202 ation (3: 1 ratio). Re-assess infant after each 30secs (15 cycles). Drugs \200 Give through umbilical venous catheter (UVC) or IO (high dose endotracheal tube (ETT) adren aline can be considered). Remember, drugs are B.A.D. ( Bicarbonate/Adrenaline/Dextrose 10%). 06_McClure_06.indd 108 11/14/2012 11:22:39 PM NEWBORN LIFE SUPPORT 109 Dry the baby Remove any wet towels and cover Start the clock or note the time Birth AT 30 s Assess (tone), breathing and heart rate ALL If gasping or not breathing: Open the airway Give 5 inflation breaths Consider SpO2 monitor ing STAGES 60 s Re-assess If no increase in heart rate look for chest movement ASK: Acceptable* pre-ductal SpO2 2 min 60% 70% 3 min 80% 4 min 85% 5 min 90% 10 min If chest not moving: Recheck head position Consider 2-person airway control and other airwa y maneuvers Repeat inflation breaths consider SpO2 monitoring Look for a response If no increase in heart rate look for chest movement DO When the chest is moving: If heart rate is not detectable or slow (<60/min) Start chest com pressions 3 compressions to each breath YOU NEED Reassess heart rate every 30s If heart rate is not detectable or slow (<60/min) consider ve nous access and drugs HELP? Fig. 6.1 Newborn life support. SpO2 values are 25th centile for term infants. Reproduced wi th kind permission of Resuscitation Council (UK) 2010. 06_McClure_06.indd 109 11/14/2012 11:22:39 PM CHAPTER 6 Neonatology 110 Perinatal de \201 nitions See also b p.10. Gestational age (post-menstrual age) Age measur ed from the \201 rst day of the last menstrual period before conception and expressed in com- plete weeks or days. Chronological/postnatal age Time elapsed from birth.