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MINISTRY OF HEALTH GUIDELINES FOR THE MANAGEMENT OF COMMON PEDIATRIC DISEASES AND EMERGENCIES THE PEDIATRIC COUNCIL OF KUWAIT List of Contributors                                             Dr. Faisal El-Khuffash                                             Dr. Ghassan Al-Othman                                             Dr. Zeinat Hijazi                                             Dr. Yousif Habib                                             Dr. Lulu Abushaban                                             Dr. Khaled Al-Saeid                                             Dr. Mona Al-Khawari                                             Dr. Hassan Souri                                             Dr. Magdy H. Shafik                                             Dr. Eman Al-Enizi                                                                                                   Members of the Clinical Guidelines and Protocols Committee:         Dr. Kunle Adekile: Chairman and Editor                          Dr. Eiman Al-Enizi                          Dr. Hassan Souri                          Dr. Majda Homood                         Dr. Magdy H. Shafik                          Dr. Sameer Mady                 TABLE OF CONTENTS Cardiopulmonary Resuscitation Rehydration in Gastroenteritis Acute Exacerbation of Asthma Croup Status Epilepticus Hypertensive Emergencies Cardiac Arrythmias Acute Bacterial Meningitis Diabetic Ketoacidosis Shock Poisoning and Intoxication General Principles Iron Toxicity Acetaminophen Poisoning Salicylate Poisoning Phenothiazines Tricyclic antidepressants Beta Blockers Naphthalene Digoxin Caustics (Strong Acids and Alkalis) Hydrocarbons Organophosphorus Evaluation and Management of the Febrile Infant (<3months)   Cardiopulmonary Resuscitation (CPR)  Resuscitation team   Team l   Airway doc   Circulation doc   Medication nurse  Recording nurse components of CPR { Airway- Breathing- Circulation }  A: Airway Management A patent airway is demonstrated by: Smooth quiet airflow in and out of the patient A rising and falling of the chest with ventilation  Ensure patency of airways by: Removal of anatomical barriers (tongue) Removal of secretions and vomitus Removal of any foreign body  Patency of the airway may be maintained by one   methods: Head tilt = Infants < 1 yr: Sniffing position (mild extension of the neck) using a thin pillow or shoulderroll (towel folded to 1 inch thickness. Children: Mild extension of the neck. Jaw thrust = Small finger placed behind the angle of the jaw and the middle finger under  the mentum with lift-up action of the mandible to bring the lower incisors above or at thesame level with the upper incisors The aim of the above maneuvers is to lift up the tongue of the unconscious patientfrom the posterior pharynx.    B: Breathing Management Once airway control has been achieved, breathing is initiated. Many techniques  can be used but it is essential for the child’s chest to rise with inflation: Mouth-to-mouth ventilation can be done Bag mask ventilation (BMV) is preferable because of higher level of oxygen that can be administered Necessary equipment:  Oxygen source (non-rebreathing mask and reservoir is ideal).  Oropharyngeal or nasopharyngeal airway.  Self-inflating bag (Bag Mask resuscitator) and masks.  Laryngoscope handles and blades. Intubation medications (discussed below). Appropriate Equipment Size: Laryngoscope blades Age Size Preterm baby Miller (straight) 0 Fullterm baby Miller 1 1-12 months infant Miller 1 1-6 years child Miller 2/Macintosh 2 8 years and older Macintosh 3 or 4   Endotracheal Tube size: Age ETT - ID              Preterm <1250 g 2.5 mm             Preterm >1250 g 3.0 mm           Fullterm baby 3.5 m Formula for ETT size in child of 2years: ETT internal diameter (ID) in mm = Age (years) + 4 Depth of insertion of ETT from gum line in cm = 3 x ID (internal diameter) of the ETT.                        E.G. a 3.5 ETT would be inserted 10.5 cm from the gum line (3 x 3.5)                   Size of Oropharyngeal airway = distance form central incisors to the angle of the mandible) Size of Nasopharyngeal airway = distance form the tip of the nose to the tragus of the ear). Bag mask ventilation (BMV) of an apneic patient BMV is a very important maneuver that can sustain the life of the patient until  the airway is secured with an ETT. Choosing the correct mask size, maintaining  a proper seal of the mask on the face of the child and correct positioning of the  patient are essential for successful BMV BMV should be done from the head end of the bed where proper control of the airway is better achieved. Maintain patency of the airway Look for chest movement and listen for air entry continuously Mask should be held with left thumb and index finger. The mask’s superior rim should be over the nasal bridge and the lower rim should be in the cleft between the mentum and the lower lip. Use oral airway or nasopharyngeal airway to maintain patency of the airway if sniffing position or jaw thrust are difficult to achieve. These devices must be  used only in unconscious children It is preferable to have an assistant to do bagging while the doctor is  maintaining a seal using two hands. Until a nasogastric tube is passed to empty the stomach contents and deflate the  stomach of air, Sellick maneuver can be used to prevent regurgitation of stomach contents. This is done with pressure over the larynx and cricoid ring to occlude the esophagus. C. Circulation: Objectives: Maintain adequate circulating volume (fluid resuscitation). Provision of peripheral perfusion (chest compression, inotropic agents). Correct any dysrrhythmia (defibrillation/cardioversion/medications) Continuous assessment of the cardiovascular performance (central pulses  and cardiac rate and rhythm).                          Chest Compressions:                           Indications: Impalpable central pulses (infant = brachial artery,                               child = carotid or femoral artery).                    Newborns: Place the index and middle finger one finger breadth below the inter- mammary line with the other hand supporting the back  of the infant. Alternatively, use two thumbs on the anterior chest (same position as above) and the rest of fingers supporting the back Depth of compression = 1/3 the AP diameter of the chest.                Infants: Use similar maneuvers as above in      terms of  position of compressions. Depth of compressions = 1/ 3 the AP diameter of the chest. Rate of compressions = 1:5 (breath: compressions).                Older children: Place the heal of the hand over sternum above the xiphisternum below the sternum manubria. Depth of compression = 1/3 AP diameter of the chest.                                    Rate of compression = 1:5.                                  Note: regular check of the pulses is mandatory to confirm the               adequacy of                                    chest compressions. Basic formula for administration of drugs by infusion: 1µg /kg/min = [3 x weight (kg)] mg of the drug add to 50ml of solution Run at 1ml/hr. e.g. 5µg/kg/min = 5 x [3 x weight (kg)] mg in 50ml run at 1ml/hr 0.01µg/kg/min = 0.01 x [3 x weight (kg)] mg in 50ml run at 1ml/hr 0.03µg/kg/min = 0.03 x [3 x weight (kg)] mg in 50ml run at 1ml/hr Therefore if the baby’s weight is 5 kg:Infusion rate = 5 x [3 x 5]= 5 x 15 = 75 mg of the drug to be added to 50 ml of solution run at rate of 1 ml/h    D. Disability Continuous assessment of neurological status to assess the cerebral cortex (level ofconsciousness) and brain stem function (pupillary reaction to light). Use mnemonic AVPU (A = alert, V = response to verbal stimuli, P response to painful stimuli, U = unresponsive) or Glasgow coma scale (see appendix).        E. Exposure Ensure proper exposure of child for initial physicalassessment. Pay attention to exposed regions of the patient to avoid rapid heat loss (hypothermia could be  fatal in newborns and young infants).   ( up ) REHYDRATION IN GASTROENTERITIS PRINCIPLES: 1. In cases of shock or severe hypovolemia: 20 ml/kg body weight of Normal Saline (crystalloid) orplasma (colloid). Plasma can be replaced by 5% albumin: mix ONE portion of 20% albumin with THREE portions of normal saline, i.e. 5 mls albumin + 15 mls NS per kg. 1. Replace deficit: Estimate degree of dehydration Mild: <5% loss of body weight Moderate: 5-9% loss of body weight Severe: ³10% loss of body weight Volume: 50-100 ml/kg according to the degree of dehydration.Solution: A) Intravenous 0.45 N. saline in 5% dextrose (Na content75mmol/l). B) Oral WHO recommended oral rehydrating solution (Na content 90 mmol/l). Duration: 4-6 hours. 2. Maintenance provision: Volume: 3-10 kg: 100 ml/Kg. 11-20 kg: 1000 ml + 50/kg above 10 kg 21-30 kg: 1500 ml + 25/kg above 20 kg OR 1750 ml/m2 surface area. Solutions: a) Intravenous?0.25 N. Saline in 5 % glucose (Na content = mmol/l) b) Oral: Pedialyte 45 OR Mix one part WHO - ORS with one part of water. (Na content 45 mmol/l). c) Duration: Over the remaining 18-20 hours. Potassium: Add 20-30 mls of 4 % KCL to each 500 mls of rehydrating fluid (i.e. 10-15 mmols of K + per 500 mls). Do not exceed  30 mmols/l in the general ward.                         Sodium Bicarbonate: Should be avoided in the great majority of cases. Give if pH is below 7.15 or base excess is 15 or more or serum bicarbonate is less than 15 mmol/l. Give 0.5 mmol per kg to tide the patient over critical acidosis.        Example:              An infant weighing 10 kg with acute onset diarrhea                dehydration of more than a moderate degree (Hypovolemic)      (1 h) I.V. drip bottle 1: 200 mls Normal Saline (60 minutes)        .       Rate 100 mls/hour (8 h) I.V. drip bottle 3: 500 mls 0.25 N. Saline in 5% DW 30 mls 4% KCLRate 60 mls/hour (10 h) I.V. drip bottle 4: 500 mls 0.25 N. Saline in 5% DW. 30 mls 4% KCLRate 50 mls/hour Observe that bottles 1 and 2 provided 70 mls per kg as deficit replacement while bottles 3 and 4 provided 100/ mls  per kg as maintenance requirements. If there are ON-GOING LOSSES they should be  replaced with 0.45 NS. The volume ranges from 0-100 ml/kg (Clinical; check weight). APPENDIX A) Guidelines for Oral Rehydration: No shock or hypovolemia. Vomiting is NOT prominent. Child is NOT ill with aversion from fluids. Onset is NOT very stormy. Reliable home situation and access to medical care.                              Deficit: WHO-ORS (Na=90 mmol/l). 50-75 mls/kg over 6 hours. Give in small volumes every 5-15 minutes. Example: 10 kg infant. Deficit 500 mls. Approx. 100 mls/hour over five hours. Use household measures:                           1 tablespoon = 12-15 mls.                                    1 small coffee cup = 25-30 mls.    Or use a feeding bottle.                              Maintenance: Pedialyte 45 if a available (Na = 45 mmol/l)  Or dilute 1 part WHO-ORS with 1 part water. Milk can be given if desired. Breast-feeding should not be stopped. Administer the fluid in small volumes (considering sleeping times).                           B) Observations in more chronic cases: Sodium losses as not as severe as in acute cases. Shock or hypovolemia should be corrected as usual. Deficit correction should be slower i.e. over 6-8 hours. They are poorly tolerant to sodium overload. Avoid over-hydration. These children are poorly tolerant to volume overload. Early introduction of food (They need more calories than water). Investigate cause: malnutrition, malabsorption, disadvantageous home situation etc. ( up ) ACUTE EXACERBATION OF BRONCHIAL ASTHMA Initial management Assess severity: dyspnea, RR, HR, accessory muscles, cyanosis,  02 saturation, pulsus paradoxus and PEFR in children >5years (Table 1). Review regular and recent medications, especially steroids and theophylline. Nebulized salbutamol 0.03 ml/kg/dose + 2ml NS with 02 flow 6L/min to achieve 02 saturation ³ 95%. Assess after 20 min and may repeat same dose x 3 in one hour. Steroids if no immediate response, recently took steroids or severe attack. Sedation is contraindicated. Repeat assessment after one hour and manage according to response: A. GOOD RESPONSE (MILD EPISODE) PEFR > 80% predicted (if available) No wheeze or RD on examination. Response to salbutamol sustained for 4 hours Send Home. Continue salbutamol (nebulizer, nebuhaler, rotahaler) 4 hrly for 24-48 hr. B. INCOMPLETE RESPONSE (MODERATE EPISODE) PEFR >50-80% predicted or best O2 sat of 91-95% O/E moderate symptoms, accessory muscle use: Add oral prednisolone 1 mg/kg /day. Continue salbutamol nebulizer up to 3 times in second hr + Ipratopium bromide + 02 6L/min, then gradually space out. If response is sustained for 1 hr after last dose of salbutamol: Normal examination: PEFR >60%. No distress. 02 saturation >95%. Discharge home. Salbutamol neb 4 hrly. Continue steroids oral x 3-5 days. If response is still incomplete with any of the following: Hx high-risk patient. Mild-moderate symptoms PEFR 50-70% O2 sat not improving, go to © below C. POOR RESPONSE (SEVERE EPISODE) PEFR <50% predicted or personal best. Continue salbutamol neb hrly + ipratopium bromide neb (500mg/ml) 0.5 ml between 1-4 yr, 1 ml ³ 5 yrs + 2 ml NS in O2 6L/min. Monitor HR, O2, ABG & watch for CO2 retention IV fluids if patient is dehydrated or vomiting. Add IV hydrocortisone 5 mg/kg/dose 6 hrly. Assess after one hour. If 02 sat is improving, moderate symptoms, PEFR >50% but< 70% continue systemic steroids and continue salbutamol + ipratropium neb hrly then gradually space out When PEFR >70% and sustained on medication, discharge home on steroids, follow up and education If no improvement within 6 hours Admit to ICU. Continuous salbutamol neb 1 ml +3 ml NS with cardiac monitor. IV aminophylline 5 mg/kg/dose 6 hrly slowly Do not give IV if on oral theophylline. Check serum level, may give maintenance 0.7mg/kg/hour and monitor level. Intubation and ventilation ± IV salbutamol: Loading dose = 1mcg/kg/ min slowly over 10 min Maintenance = 0.2 mg/kg/ min increasing by 0.1mg/kg/min. (maximum 4 mg/kg/min) Watch out for hypokalemia (ventolin as well as steroids effect) The following patients are at high risk of asthma-related death and require special attention: Prior intubation for asthma Current use of systemic steroids or recent withdrawal from steroid Past history of syncope or hypoxic seizure due to asthma Prior admission to ICU for asthma Infants PaCO2 >6.5 kpa <10% improvement in PEFR Wide daily fluctuation in PEFR ( up ) CROUP (LARYNGO-TRACHEO-BRONCHITIS) Clinical syndrome characterized by a barking cough, hoarseness  and inspiratory stridor o Viral laryngo-tracheo-bronchitis (commonest o Spasmodic (as above except for being recurrent) o Bacterial (very rare) Management: Rule out epiglottitis (high fever, toxic look, drooling, muffled voice and cervical lymphadenopathy). If highly suspected: don’t look into throat, call anesthetist for immediate intubation, no blood work, no IV etc. Mild Croup Mist + home care Moderate and severe croup Immediate admission Keep child calm in quiet room with parent Oxygen via mask NO SEDATION as this will decrease respiratory drive and mask clinical signs of hypoxia such as agitation and anxiety. Dexamethasone 0.3-0.6 ml/1kg(oral, IM.IV), OR prednisolone 1 mg/kg oral OR single dose budesonide 2 mg + 2 cc normal saline nebulized. If better after one hour, just observe. If not responding or severe from outset give: Epinephrine 4 ml of 1:1000 preparation + 2 ml normal saline via nebulizer. Repeat dose after 30 min if necessary then space out. Repeat dose of steroids after 12 and 24 hours. Very rarely, intubation may be needed if there is: Progressive increase in stridor and exhaustion Distant breath sounds Progressive tachycardia and tachypnea Decreasing level of consciousness Important: Epinephrine may cause tachycardia, arrhythmias and rebound effect. Therefore, children on epinephrine: Should be on cardiac monitor and if heart rate exceeds 180/min hold epinephrine. Should be observed for at least 6 hours after last dose before discharge if they were not on steroids and for 2 hours if on steroids. Children given epinephrine in emergency room (casualty) SHOULD be admitted to the ward. ( up )   STATUS EPILEPTICUS Definition: An episode of continuous seizure (cerebral dysrrhythmia) or major convulsions lasting for >30 minutes with no recovery of consciousness between seizures. Etiology: Majority of children who present with status are not known to be epileptics 30 - 50% are complications of an acute CNS insult (e.g. meningitis, encephalitis, glucose/electrolyte disturbance), especially in young children. During the course of treatment, attempts should be made to look for a possible primary cause that needs specific management. During the seizure there is very high increase in cerebral blood flow to prevent brain asphyxia, therefore it is very important to monitor and maintain an adequate body circulation Management: A. Prevention of secondary hypoxia and stabilization of circulation: Clear airways by suction; insert an airway, keep on lateral prone position to prevent aspiration, decompress and empty stomach by nasogastric tube Give 100% O2 by face mask (3-5 l/min), assess vital functions (BP, RR, Pulse, Temp) Establish an IV line, collect blood samples (glucose, electrolytes, Ca, Mg, Phosph, PH, HCO3 ± anticonvulsant level) If hypoglycemic, give 2 ml/kg of 25% Dextrose If hypotensive with poor peripheral perfusion, correct with fluids (½ NS + 5DW). If IV access is difficult in hemodynamically unstable child with continuous seizure, give fluid and anticonvulsants through intra-osseous route. Evaluation for possible cause (history and examination) during stabilization and initial treatment B. Anti-convulsants If IV could not be established, give either Midazolam IM 0.2 mg/kg OR diazepam rectal 0.5 mg/kg as 1st choice OR paraldehyde IM 0.1 ml/kg If patient is shocked or cyanosed, with dilated pupils or has been convulsing for hours, go straight to Step VI of management Step I Diazepam I.V. 0.3 mg/kg (undiluted over 2 min) OR Lorazepam I.V. 0.1 mg/kg a. If seizure stops but patient does not recover consciousness Mannitol 1 g (=5 ml of 20%)/kg infused over 20 mins Adjust previous medication OR consider starting oral anticonvulsants and diagnostic work-up for possible underlying cause. b. If seizure does not stop or recurs after10-15 mins Repeat diazepam (or lorazepam) and to prevent further recurrence give: Phenytoin infusion, 10 mg/ml NS (under ECG monitor) Loading dose 15 mg/kg over 15-20 minsThen 10 mg/kg/24 hrs in divided doses (8-12 h) over next 24 hoursThen maintenance 5 mg/kg/day (q 12h)If patient already on regular phenytoin, give paraldehyde 0.1 ml/kg IM till phenytoin level known and then adjust dose according to blood level Adjust previous anti-epileptic medications or start oral anticonvulsants and diagnostic work-up for possible underlying cause. Step II. If seizure does not stop within 5-10 mins of 2nd dose of diazepam (or lorazepam) Start phenytoin I.V. 20 mg/kg over 20 mins (under ECG monitor) If already on phenytoin, give paraldehyde IM 0.1 ml/kg If still convulsing 10 mins after starting phenytoin, 3rd dose of diazepam may be given Consider pyridoxine (100mg I.V.) for child <2 years of ageContinuous monitoring of BP, Pulse, Resp and assessment of ?underlying cause At the end of phenytoin infusion start mannitol 20%, 5 ml/kg over 20 mins If there is response, continue maintenance phenytoin as in step IbIf no response go to step IV Step III Paraldehyde (if not given before) 0.1 ml/kg IM (if already given, or if no response after 5 mins, go to step V) Step IV (ICU care) Phenobarbitone, loading dose 20 mg/kg, I.V. slowly (over 10 min) Be prepared for ventilation ± intubation, monitor BP for hypotension If there’s response, continue maintenance phenobarb (12-24 h from loading) 5 mg/kg/day bid. If no response in 10-15 min, orseizure already lasted >60 min, go to V Step V Intubation + ventilation + muscle relaxant (use short-acting agent e.g. vecuronium in repeated doses to monitor seizure when EEG monitoring not available Start midazolam 0.2 mg/kg I.V. bolus followed by infusion 0.05 mg/kg/h up to 1 mg/kg/h OR Induction of phenobarb coma with phenobarb 10 mg/kg ½ hrly till control (up to 120 mg/kg/day) OR Thiopentone 30 mg/kg over 1 hour, then infusion 5 mg/kg/h (increase up to 20 mg/kg/h when needed, titrating for best control). Gas anesthesia with isoflorane (0.5-3%) may be used (+phenobarb) to control seizure. Monitor: BP (support with dopamine if ¯BP), pH for acidosis, and BGA (keep CO2 £4.0 Kpa) Monitor for hypoglycemia, hypocalcemia, consumptive coagulopathy (PT, APTT) and hyperpyrexia Restrict fluid to 60% maintenance (unless ¯BP) and continue treatment for brain edema - mannitol (6h) ± dexamethasone (with it give cimetidine I.V.)After stabilization consider CT scan and work up for cause.Treat for meningitis if indicated           ( up )   HYPERTENSIVE EMERGENCIES Definition: situations in which life or organ threatening damage will occur if BP is not reduced immediately; usually associated with elevated BP >30% normal for age e.g.: Hypertensive encephalopathy (headache, obtudation, convulsion, coma) Hypertension associated with ARF, acute heart failure, pulmonary edema, stroke, head trauma or myocardial ischemia. Adrenergic crisis Dissecting aneurysm Malignant hypertension History: Take detailed history of hypertension, renal or other diseases, drug ingestion, regular medications and doses. Physical Examination: Assess mental status changes; look for signs of CHF, pulmonary edema, diminished lower extremities pulses, papilledema and focal neurologic deficit. Investigations: Complete blood count and blood smear for fragmented RBCs e.g in hemolytic uremic syndrome 2. Serum electrolytes and urea 3. Urine - routine and microscopy 4. Chest X-ray, ECG 5. 24 hour urine for catecholamines if pheochromocytoma is suspected) 6. CT brain if hypertensive encephalopathy is suspected Management: Alert ICU team if needed Start anti-hypertensives without delay Aim at 10-25% reduction in BP in the first hour of therapy Restrict fluid and salt intake except in cases with hypovolemia Choice of anti-hypertensives is decided according to the cause and the presence of complications as follows.  ( up )     CARDIAC ARRYTHMIAS A. Sinus tachycardia (ST): Differentiation from supra-ventricular tachycardia can be difficult especially if the baby comes to the casualty ill or shocked. Children with ST usually have an underlying cause: Sepsis® look for fever. Bleeding® measure blood pressure for hypotension. The heart rate: Usually ST is £ 200 beats/min but supraventricular tachycardia SVT is > 200/min In ST the rate varies with time (i.e. if the child is crying HR > 180 & if quiet HR < 180 but in SVT the rate is usually fixed. Treatment: Look for underlying cause (sepsis, shock, bleeding) and treat it. B. Supra-ventricular tachycardia (SVT) Commonest type is re-entry tachycardia; other forms like nodal, atrial tachycardia, atrial flutter and atrial fibrillation are less common in children. Signs & Symptoms If SVT duration < 24 hours then the baby is irritable, vomiting, poor feeding but older child will present with chest pain, palpitation. If SVT > 24-48 h duration ,signs of heart failure develop ® hypotension, shock. Treatment If signs of shock, hypotension: Start I.V. line Put ECG monitor. Take S. electrolytes Arrange to shift to ICU Synchronized D.C. shock 0.25-0.5 J/kg should be done while anesthetist is available for intubation if necessary. (Note: Do not perform the procedure without ECG monitoring) If the patient is stable: Vagal maneuvers: Older child®ask to do Valsalva maneuver. Baby®Diving reflex using ice bag. (Note: It is also advisable to perform this while the patient is attached to ECG monitor). Drugs Adenosine: 0.1mg/kg I.V. fast injection; if no response within few seconds then repeat at 5-10 minute interval with increasing doses (0.2mg/kg-0.4mg/kg; Max 12 mg/dose) Verapamil: (This is contra-indicated under the age of 1 year). 0.1 mg/kg by slow I.V. infusion. Digoxin: can be given by rapid digitalization 40 mcg/kg divided as 20 mcg/kg first dose followed by 10 mcg/kg after 8 and16 hours respectively. Propranolol: I.V. dose 0.05-0.1 mg/kg (max of 2 mg) slowly. This must be given with caution because of the risk of hypotension. C. Ventricular tachycardia (VT) Less common in Pediatric age group. Seen mainly in children post-cardiac surgery or those with myocardial dysfunction secondary to acute myocarditis. The basic rule is that broad complex tachycardia is a VT unless a conduction delay or pre-excitation pattern is identified on the resting ECG. Treatment: (see Appendix 1) The child should be in ICU: Fix I.V. line. Take blood gases, S. electrolytes. Cardioversion if the patient is unstable (1 Joule/Kg) Start lidocaine 1 mg/kg I.V. bolus. This may be repeated every 5 minutes to a total of 3 doses if required. A lidocaine drip 2mg/kg/hour can be started later. Alternatively procainamide 15 mg/kg or propranolol 0.1 mg/kg I.V. slowly. D. Sinus bradycardia: (see Appendix 2) Reflects hypervagotonia. Can occur secondary to head injury, airway instrumentation, vomiting or strong stimulus. It can occur in patients with hypothyroidism. Postoperative cardiac patients with sinus node dysfunction. No treatment is required unless severe bradycardia; then pace maker is inserted. E. Complete heart block: Can be congenital in babies whose mothers have SLE. Associated with some forms of congenital heart disease (e.g. corrected transposition). Acquired complete heart block is usually secondary to heart surgery. Treatment: If the heart rate is <45/min or the patient is symptomatic then pace maker is required. ( up ) ACUTE BACTERIAL MENINGITIS Etiology: Neonates: Gp B streptococcus, E. coli (Kl strain), Listeria monocytogenes 1-3 mths: E. coli, H. influenza, Gp B streptococcus, Listeria Monocytogenes 3 mths-5yrs: H. influenza, N. meningitis. S. pneumoniae >5 yrs: S. pneumoniae, N. meningitis Investigations: CSF: Bacterial: 100-10000 W.B.C. (PMNcells), ­ protein ¯ glucose, +ve C.S.F culture. Viral: 10-500 W.B.C, Mononuclear cells, ­ or normal protein, normal glucose WITHOLD L.P.: if there is increased intracranial tension, cardiorespiratory compromise, infection at L.P. site, bleeding diathesis, shock. C.T. scan: If there is focal neurological deficit, papilledema or prolonged impaired consciousness Blood culture & Gram stain: +ve in bacterial meningitis C.B.C. & E.S.R Serum electrolytes: Na, K, (Mg & Ca if associated with seizures) Rapid diagnostic bacterial antigen test: Latex agglutination - most sensitive in C.S.F DNA hybridization & PCR test - For tuberculosis MANAGEMENT START empirical antimicrobial treatment: <3 mths of age: Ampicillin (200 mg/kg/day)+ Cefotaxime (200mg/kg/day qid, I.V.) >3 mths of age: Cefotaxime (200mg/kg/day) or Ceftriaxone (100 mg/kg/day). *N.B.: When S. pneumoniae is suspected (from Gram stain), consider adding vancomycin. COMMENCE Specific therapy - Based on L.P. & blood culture results when available. Negative cultures R/O bacterial meningitis except in suppressed meningitis Dexamethasone: I.V. 0.15 mg/kg/dose qid for 2-4 days (1st dose before antibiotics) SUPPORTIVE CARE: Daily Weight chart, Input and Output chart. Record vital signs every l5min until stable & then every hour for next 24hrs. Urine specific gravity (SIADH). Serum Na, Mg, K, Cl. Neurological examination: Fundus & Audiometric test Daily measurement of head circumference Fluid restriction - N.P.O. for 24hrs (fluid 2/3 maintenance). Maintain intravascular volume. Anticonvulsants - If seizures - phenobarbitone. Assisted ventilation - If respiratory failure. CHEMOPROPHYLAXIS: Inform preventive medicine doctor.                                                            ( up ) DIABETIC KETOACIDOSIS Definition: Hyperglycemia (Blood Glucose>11 mmol/L) pH <7.3 and /or bicarbonate <15 mmol/L and Heavy glycosuria and ketonuria and who are 5% or more dehydrated ± vomiting ± drowsy. Emergency assessment Confirm the diagnosis History of polyuria, polydypsia, weight loss, vomiting and abdominal pain Biochemical confirmation, BG, pH, ketonuria, glycosuria Clinical assessment Assessment of Conscious level Severity of Dehydration: 3% just detectable, reduced skin turgor 5% dry mucous membranes 10% capillary return 3 seconds or more, sunken eyes 10% + shock, poor peripheral pulses Signs of Shock and poor perfusion. Evidence of Acidosis-- hyperventilation. Immediate investigation Weigh the child Capillary BG Venous BG, bicarbonate, electrolyte and urea Capillaries, venous or arterial blood gases. Clinical and laboratory monitoring Careful, frequent clinical and laboratory monitoring to detect warning signs of complications is of paramount importance. Hourly pulse rate, respiratory rate, BP Hourly or more frequent neurological observations Flow sheets: metabolic, fluid intake and output, fluid type and rate of insulin. Hourly capillary BG (cross-check every 2 or 4 h against venous glucose. Venous bicarbonate & electrolytes every 2 hours after start of therapy then 4 hourly until acidosis reversed. Check for K+ hourly if abnormal (<3 or >6) and EEG monitoring is recommended. Test each urine specimen for glucose and ketones. Treatment during the first 24-48 hours in hospital: ICU care if severe metabolic derangement (PH<7.1, hyperventilation, in shock, depressed level of consciousness, persistent vomiting, and in young children (<5 years). Resuscitation In shock with poor peripheral pulses, or coma Oxygen (100%) by face mask Normal saline 0.9% 10ml/kg over 20-60 minutes (should be repeated if peripheral pulses remain poor). Vomiting/impaired consciousness-insert nasogastric tube to drain stomach Fluids Calculate total amount of fluid = deficit + 48h maintenance. Replace this volume evenly over 48 h as normal saline 0.9% initially Subtract the resuscitation dose from the deficit. Maximum volume of fluids: 4000 ml/M2/d Total free water deficit: Infant Children Mild: 5% = 50 cc/kg 3% = 30 cc/kg Moderate: 10% = 100 cc/kg 6% = 60cc/kg Severe: 15% = 150 cc/kg 9% = 90 cc/kg Maintenance fluid requirements for the 48 hours: 200 cc/kg for the first 10 kg BW + 100 cc/kg for the next 10 kg BW + 40 cc/kg for the rest of BW When BG falls to 12-15 mmol/l add Dextrose, the most recommended saline 0.45 % with 5% glucose Oral fluid in severe dehydration and acidosis allow sips of cool water if no vomiting Sodium & osmolality: Corrected Na for glucose: measured Na + 2 ´ (BG-5.5) 5.5 A fall in serum sodium has been noted as one of the few laboratory correlates of impending cerebral edema If serum sodium falls below 135 mmol/l, reassess the fluid replacement calculations, consider increasing the concentration of sodium chloride and observe with vigilance. Initial serum sodium>150 mmol/l might prompt even slower rehydration rate than 48 hours. Serum osmolality should not be lowered by more than 2-3 mOsm/kg/hour. Serum osmolality (mOsm)=2 ´ (Na+K) + BG (mmol) Potassium: Patient not passing urine: add no K+ K+ >6.0 mmol/L add no K+ 5.0-6.0 mmol/L add 20 mmol/L (20 ml/pint) 3.5-5 mmol/L add 40 mmol/L (40 ml/pint) <3.5 mmol/L add 60 mmol/L (60ml/pint) Consider central venous line to give K+ >60mmol/L maximum safe rate of K supplement 0.5 mmol/kg/hour (2, 4) Oral/nasogastric KCl boluses (0.5-1 mmol/kg BW) may also be administered (3). Bicarbonate: There is no evidence that Bicarbonate is either necessary or safe in DKA. It should NOT be used in the initial resuscitation, but may be considered for treatment of impaired cardiac contractility in persistent severe shock. (If it is considered proceed with caution giving 1-2mmol/kg bicarbonate over 60minutes) Insulin Insulin should not be started until shock has been successfully reversed by emergency resuscitation and saline/potassium rehydration regimen has begun. Recommended dose of insulin 0.1unit/kg per hour by separate drip infusion (0.05u/kg/hour for younger patients). No initial bolus of insulin A solution of soluble insulin 5 units/kg in 250 ml Normal saline (infusion rate 5ml/h to deliver 0.1u/kg/h of insulin) The rate of insulin infusion is adjusted to maintain a fall of 5 mmol/L/h (the rate of fall in first 2 hours may exceed this due to rehydration and volume expansion). When BG falls to 12-15mmol/l change to Dextrose-Saline infusion (as above) to maintain BG in the desired range of 8-12mmol/l If BG rises above 15mmol/l, increase the insulin infusion by 25% If BG falls to <8mmol/l or falls too rapidly, increase the concentration of Dextrose to 10%(or more) with added saline Do not stop insulin infusion or decrease below 0.05 units/kg per h What to do in persistent acidosis? Persistent acidosis is likely to be caused by inadequate resuscitation, inadequate insulin effect or sepsis. In presence of ongoing acidosis (with normalization of blood glucose) the amount of glucose should be adjusted in the infusion to maintain BG between 8-12 mmol/L, by adding 7.5% or 10% dextrose and to continue insulin infusion at rate of 0.1u/kg/h. Reduce insulin dose only after acidosis has been corrected. 7.5% D: add 25ml of 50% D to 500 ml 5% dextrose. 10% D: add 50ml of 50% D to 500 ml 5% dextrose. Transition to SC insulin injections Oral fluids should only be introduced when substantial clinical improvement has occurred [mild acidosis (bicarbonate >15mmol/l) & ketosis may still present] When oral fluids are tolerated IV fluid should be reduced Half an hour before the meal, administer 0.25 u/kg short-acting insulin subcutaneously, and gradually discontinue the insulin infusion over the next hour. S.C. insulin must be administered at least every 6 hours, unless intermediate insulin is used. Dose: 0.1-0.25 u/kg/6hours. Never omit insulin entirely during six-hour management in a known diabetic. Cerebral Edema Occurs in the first 24 h after starting rehydration when the general condition of the child might seems to be improving Monitor at regular interval to detect any changes consistent with cerebral edema. Warning signs/symptoms: Headache & slowing of heart rate Change in neurological status (restlessness, irritability, increased drowsiness, incontinence) specific neurological signs (e.g. cranial N palsies) Rising BP, decreased O2 saturation Convulsions, papilledema, respiratory arrest are late signs. Management Exclude hypoglycemia If warning signs occur (see above) give immediate IV Mannitol 1g/kg over 20 minutes (i.e. 5ml/kg 20% solution) Halve rehydration infusion rate until situation is improved Nurse with child’s head elevated Move to intensive care unit Alert anesthetic and senior pediatric staff Consider continuation of Mannitol infusion 0.25g/kg/hour to prevent rebound increase in intracranial pressure (or repeat bolus every 4-6hours); max of 6 doses Cranial imaging should only be considered after child has been stabilized. Intracranial events other than edema may occur e.g. hemorrhage, thrombosis, infarction   Management of children with mild acidosis If venous bicarbonate level >15mmol/l and/or pH >7.3andIf no vomiting and oral hydration can be maintained and If there are no signs of dehydration Give subcutaneous insulin, rapid-acting insulin (regular), Dose: 0.1-0.25u/kg at least every 6 hours (3-4 hours if needed) Monitoring of BG, bicarbonate and electrolyte every 6 hours If there is no improvement (worsening of acidosis) treat with IV fluid therapy and IV insulin  ( up )   SHOCK Definition: Circulatory dysfunction resulting in the failure to provide sufficient nutrients and oxygen to satisfy the needs of tissues. Classification: 1. Hypovolemic shock 2. Distributive shock 3. Cardiogenic shock 4. Septic shock Stages: Compensated: Homeostatic mechanisms are functioning to maintain essential organ perfusion. Decompensated: Circulatory compensation fails because of ischemia, endothelial injury, and elaboration of toxic materials. Irreversible: Irreversible functional loss in essential organs indicates that death is imminent. Hypovolemic Shock Results from decreased intravascular volume and decreased venous return. Etiology: Dehydration: gastroenteritis, heat stroke,diabetes insipidus, diabetic ketoacidosis Burns Hemorrhage 2. Distributive Shock Abnormalities in vasomotor tone with maldistribution of a normal circulating volume. Peripheral pooling and vascular shunting lead to a state of relative hypovolemia. Etiology: AnaphylaxisNeurologic injury: (e.g.) head injury, spinal shockSeptic shock Drugs: (e.g.) barbiturates and anti- hypertensives 3. Cardiogenic shock Cardiac pump failure Etiology: Congenital heart disease Ischemic heart disease: (e.g. Kawasaki disease) Traumatic Infectious cardiomyopathies Drug toxicity Hypoglycemia 4. Septic shock Deficient intravascular volume, maldistribution of intravascular volume and impaired myocardial function. Clinical features: Cold sweaty extremities with low surface temperature. Decreased capillary filling: Capillary refill that takes >5 seconds is abnormal (firmly compress soft tissue or nail bed for 5 seconds). Pallor with peripheral cyanosis Physical findings of dehydration especially in hypovolemic shock Oliguria Altered mental status Acidosis Tachycardia Hypotension (a late sign of shock) Investigations: Serum electrolytes Complete blood count (CBC) Serum ionized calcium (hypocalcemia occurs frequently in shock) Arterial blood gas analysis Septic work up in suspected septic shock Monitoring of a child in shock: Vital signs Color Level of consciousness Continuous ECG monitoring Pulse oximetry Blood gases & blood glucose Intake-output fluid chart (Urine output < ml/kg/h indicates renal hypoperfusion) Treatment: Transfer the shocked child to the ICU. Treat underlying cause: Correct hypoxemia: keep oxygen saturation 95-100%. Give enough oxygen. Incubator care and mechanical ventilation, if required. Correct acid-base disturbances: A base deficit > 8 mmol/L in acute shock should be corrected. Repeated slow boluses of sodium bicarbonate 1-2 mmol/kg can be used. Correct hypoglycemia Intravascular volume expansion: Normal saline 10-20 ml/kg over 10 minutes, can be repeated as necessary (up to 3 times) Steroids: Not indicated in shock, except when it is secondary to adrenal failure (e.g. in Waterhouse-Friderichsen syndrome after meningococcal or H. influenzae infection). Monitor PT, APTT, platelet count & FDP. Use vitamin K, fresh frozen plasma and platelet transfusion to correct coagulopathies Antacids or H2-receptor blockers such as cimetidine or ranitidine can prevent gastrointestinal blood loss from acute gastritis. Renal support: early with volume augmentation and diuretics such as furosemide. Also low dose dopamine may prevent acute renal failure. Acute renal failure may require peritoneal or hemodialysis. Cardiac contractility Augmentation: Dopamine & dobutamine                                         Anaphylaxis                                         Etiology: Drugs: Penicillin, local anesthetics, contrast media for radiological investigations Desensitization injections. Blood transfusion Food allergy: milk, egg, shellfish, nuts. Insect stings. Clinical picture: Early: Sensation of warmth, itching especially in axilla and groin. Feeling of anxiety and panic. Progressive: Erythematous or urticarial rash. Edema of the face, neck, soft tissue. Severe: Bronchospasm Laryngeal edema, dyspnea, stridor, aphonia, drooling Hypotension (shock) Arrythmias, cardiac arrest Management: Admit to hospital and observe for at least 12 hours Stop administration of causal agent Place the patient in recumbent position and elevate the lower limbs. Adrenaline: 0.1 ml/kg of 1: 10000 solution I.V slowly (over 10 minutes) or I.M This may be repeated at 5 minute intervals. Oxygen by mask. Mechanical ventilation may be required. I.V. volume expander. Give colloid or crystalloid solution. Give repeated boluses of 10 ml /kg until the blood pressure is restored. Bronchodilator therapy: Salbutamol continuous nebulized (0.5%) or IV bolus (5µg/kg) or IV infusion (1-10µg/kg/min) Aminophylline: 6 mg/kg IV over 10 minutes followed by infusion 0.9 mg/kg/hour. Relief of the upper airway obstruction: mild to moderate edema may respond to inhalation of nebulized 1% adrenaline, but intubation may be needed. Additional measures: -I.V hydrocortisone 5 mg/kg or dexamethazone 0.1-0.3 mg/kg. -I.V chlorpheniramine (Piriton) 0.25/kg (maximum 10 mg)                          ( up )   POISONING AND INTOXICATION Poisoning results from the complex interaction of the agent, the child and the family environment. The peak incidence is at age of 2 years. Among toddlers, most poisonings are accidental and usually involve household products or single drugs. Adolescent ingestion, on the other hand, may involve multiple drugs often in a suicide attempt. Typically, toddlers are asymptomatic at presentation because of the small amount, non-toxic nature of the ingestant and early seeking of medical help. Poisoning however should be considered in any well patient presenting with an acute change in mental status such as lethargy, agitation, delirium, seizures or coma. General rules: Assess patient’s respiratory effort, ensure patent air ways, suction of any secretions and, if necessary, intubate the patient. Secure large I.V. line Check vital signs (pulse, b.p., temp. pupillary size and reaction). Attach cardiac monitor, pulse oximeter and obtain ECG. Give a bolus of 20 mlof NS if there are signs of hypoperfusion (poor capillary refill, pallor, and cool extremities). Insert urine catheter in unconscious patient and collect urine sample for routine examination and toxicological screening. Even with a clear history of overdose or ingestion, perform full neurological examination to R/O possibility of occult head injury. Collect investigations: CBC, BGA, LFT, RBS, electrolytes, urine and blood for toxicological screening. In suspected eye exposure: · Remove contact lenses, if any. · Remove any solid material gently with cotton swab. · Irrigate with NS for at least 30 min. · Alkali corneal burn is an emergency; call an ophthalmologist. Remove contaminated clothes, wash skin and hair with soap and water for at least 30 min. Prevent or minimize absorption of the ingestant by orogastric lavage with a large-bore tube in patients who arrived soon after a life-threatening ingestion. If sensorium is depressed, protect airway and intubate if necessary before lavage. Use aliquots of 50 ml. NS. Corrosive and non-toxic ingestions are contraindications to gastric lavage. Most health authorities no longer recommend syrup of ipecac. Activated charcoal is now recommended as the sole intervention for almost all overdoses. Remove contaminated clothes, wash skinand hair with soap and water for at least 30 min. Prevent or minimize absorption of the ingestant by orogastric lavage with a large-bore tube in patients who arrived soon after a life-threatening ingestion. If sensorium is depressed, protect airway and intubate if necessary before lavage. Use aliquots of 50 ml. NS. Corrosive and non-toxic ingestions are contraindications to gastric lavage. Most health authorities no longer recommend syrup of ipecac . Activated charcoal is now recommended as the sole  intervention for almost all overdoses. There is no contraindication for its use but the following agents are not effectively absorbed by it: iron and heavy metal poisoning, alcohol, organophosphorus compounds,  hydrocarbons, caustics and corrosives. Whole bowel irrigation through rapid administration of polyethylene glycol (GoLYTELY) 40ml/kg/hr PO/NGT,  max. 2 L/hr. (the end point is a clear rectal fluid) is useful in substances not absorbed by charcoal such as iron and slow-release medications. Ileus, intestinal obstruction, perforation and GI hemorrhage are contraindications. Iron Toxicity Iron toxicity occurs when the peak plasma level exceeds 400 mcg/dl. Ingestion of 20mg/kg of elemental iron are of concern however all ingestion should be considered potentially dangerous.Elemental iron in ferrous gluconate is 12%, in ferrous fumarate is 33% and in ferrous sulfate is 20%. Stages of toxicity: Stage 1: (½ - 12 hr) nausea, vomiting, abdominal pain,diarrhea, shock, seizures and coma may occur. Stage 2: (8-36hr) a latent period with false improvement of symptoms. Observe closely. Stage 3: (12- 48hr) hepatic failure with hypoglycemia, metabolic acidosis, bleeding, shock, coma, convulsion and death. Stage 4: (4-8 wk) late complication with pyloric stenosis. INVESTIGATIONS: CBC, urea and electrolyte, LFT.Collect serum iron on admission and 4 hours after ingestion. X-ray abdomen to visualize iron tablets. MANAGEMENT: General supportive measures. Avoid use of activated charcoal (iron not adsorbed toit). Avoid oral use of sod. bicarb, phosphate, or oral desferoxamine (DFO), as all are ineffective and may be harmful. Start chelation therapy with DFO if serum iron is more  than 300mg/dl (50 mmol/l) in symptomatic patient or with history of significant ingestion. Give 15mg/kg/hr of DFO in D5% IV (max.6 gm/day), the classic “vin rose” urine color changes may be a clue  for significant ingestion but its absence does not rule out this possibility. Stop chelation after urine is no more “vin rose” or patient is asymptomatic. Acetaminophen (Paracetamol) Poisoning Often seen in children above 6 year and adolescent.  Overdose result in toxic liver damage. Stages of toxicity: Phase I (1-24h): non-specific symptoms as anorexia,  nausea, vomiting and abdominal pain. Phase II (24-72 h): latent period there may be RUQ pain and elevated liver enzymes. Phase III (3-4 days): sequelae of hepatic failure with jaundice, coagulopathy, encephalopathy, coma and possible death. Phase IV (7-8 days): in survivors with resolution of all symptoms. NB. Disturbed mental state is not usual on first day, if present  suspect other coinciding drug ingestion. Management: Gastric lavage and activated charcoal (up to 6 hrs. after ingestion) Obtain blood acetaminophen level, correlate it with the time of ingestion and plot it on the nomogram. Give N-acetylcysteine (NAC) if the level is in the  toxic range (most effective if given within 8-10 hrs.  after ingestion, but it should be given up to 36 hrs. after ingestion). i. I.V. dose: 150mg/kg in 200ml D5% over 60 min. then 50mg/kg in 500ml D5% over 4 hrs. Then 100 mg/kg in 1000 ml D5% over next 16 hrs. i. If allergic reaction develops give antihistaminics iii. Oral dose: give 20% of NAC diluted 1:4 in carbonated beverage as a loading dose of 140 mg/kg, then 70mg/kg q4 hrs. for 17 doses. - NB. Oral preparations are not for IV use.  Follow the patient with LFT, urea, electrolytes, RBS. Salicylate Poisoning Toxicity is declining because of alternative use of  other antipyretics. Toxicity occurs usually because of accidental ingestion of methyl salicylate solution (7gm./5ml). The minimum acute toxic dose is 150mg/kg. Salicylate delays gastric evacuation so it prolongs the time of absorption. Clinical picture: Mild poisoning causes abdominal pain vomiting and tachypnea. With moderate toxicity, severe tachypnea occurs with fever, lethargy, dehydration, metabolic acidosis and hypo or hyperglycemia. Sever poisoning lead to coma, seizures, oliguria, pulmonary edema, hemorrhage and death. Diagnosis and management: General supportive cares Gastric wash and activated charcoal. Obtain serum salicylate level at presentation and 6 hrs after ingestion and plot level on a standard nomogram. Collect blood for ABG, electrolytes, sugar, PT, and CBC. Ensure adequate urine output by boluses of 20ml/kg of fluids (at least 1ml/kg/hr of urine) After ensuring adequate urine output, alkalinize urine by infusing a solution of D5% with 44mEq/L of sodium  bicarbonate and 30-60 mEq/L of KCl at twice the maintenance  rate. The aim is a urine output of 3ml/kg/h with a urine pH of >7.5. Keep serum potassium level in higher normal range (both bicarb. and tachypnea lower potassium level). Treat fever by sponges. Give vit K if PT is more than 2 sec than control ndications for dialysis: Salicylate level over 100mg/dl. Severe acidosis, oliguria or anuria Pulmonary edema. Intractable seizures. Indications for dialysis: Salicylate level over 100mg/dl. Severe acidosis, oliguria or anuria Pulmonary edema. Intractable seizures. Phenothiazines Chlorpromazine, prochlorperazine, and thioridazine. Widely used as antiemetic and tranquilizer Extra pyramidal manifestation is the most common reaction (tort Collis, opisthotonus, difficult speech, facial grimacing and oculogyric crisis) Other symptoms include hypotension, dry mouth, urine  retention, blurred vision, depressed sensorium, and tachycardia.) Onset of symptoms may be delayed up to 24 hrs after ingestion. Management: Supportive care. Activated charcoal (if less than 4 hrs.) Give: Diphenhydramine 2mg/kg (up to 50mg IV or IM) Benz atropine mesylate (Cogent in) 0.5-1mg for toddlers, 1-2 mg for adolescent (IV or IM slowly). Both are diagnostic and therapeutic for the extra pyramidal symptoms. Treat seizures with Valium and an IV loading dose of phenytoin. Tricyclic Antidepressants Imipramine (tofranil), amitriptyline (tryptizol) and doxepin are the commonly available preparations. They have a direct myocardial (quinidine-like) depression and anticholinergic (atropine-like) activity. Clinical Features: Depressed level of consciousness, seizures, delirium,  lethargy and coma Anticholinergic (atropine-like) effects can occur Cardiovascular manifestations include tachycardia,  ventricular arrythmia and hypotension Management: General supportive care (ICU care may be necessary  in severe cases) Activated charcoal. Continuous ECG monitoring Hypertension is transient; usually needs no treatment For hypotension, give 20 ml/kg normal saline Give IV valium and loading dose of phenytoin for seizures Treat life-threatening ventricular arrthymias with lidocaine or phenytoin Supraventricular arrthymias need no treatment Beta Blockers Widely used for the treatment of hypertension, angina,  arrythmia, migraine headaches and various other conditions. Life-threatening poisoning can occur especially after propranolol ingestion. Clinical Features: Most common findings are bradycardia (sinus, AV,  nodal or ventricular) ECG abnormalities include wide QRS and BB block, ventricular arrythmia, hypotension and hyperkalemia CNS manifestations occur especially with propranolol and include depressed sensorium, delirium, coma and convulsions. Bronchospasm can occur especially in patients with asthma Others include hypoglycemia (watch blood sugar),  hyperkalemia and hypotension Management General supportive care o Continuous ECG and blood pressure monitoring o Obtain blood electrolytes and glucose level o Correct hypotension with a bolus of normal saline IV § Give isoprotrenol if no response Treat hypoglycemia with 1 ml/kg D50% Correct significant hypokalemia Treat seizures with valium Naphthalene (Mothball) Can cause severe hemolysis in patients with G6PD deficiency. Most cases are asymptomatic. Hemolysis can occur up to 1-2 days after ingestion (with pallor,  jaundice, oliguria). nvestigations: CBC and retics. G6PD screening Management: Activated charcoal. May require packed RBCs transfusion if hemolysis is severe DIGOXI Manifestations: Anorexia, nausea, vomiting occur early followed by headache, disorientation, somnolence. Cardiac findings include bradycardia with AV block and prolonged P-R interval. Any form of cardiac arrhythmia can occur. Massive overdose leads to severe hyperkalemia, ventricular fibrillation, ventricular tachycardia, coma and seizure. Toxicity increases with hypokalemia, hypercalcemia, hypomagnesemia. Investigations : Collect serum digoxin level. Obtain an ECG, determine P-R interval. Serum electrolytes Management: Basic measures including activated charcoal (even several hours after ingestion) Continuous ECG monitoring. Treat clinically significant arrhythmia: Bradycardia due to AV OR SA block → atropine 0.01mg/kg IV  (Max. 0.5 mg) Ventricular arrhythmia →phenytoin (2 mg/kg IV slowly over 20 min). Repeat every 5 min. until arrhythmia stopped or max. of 15-20 mg/kg. Lidocaine can a1so be used, 1mg IV bolus then 20-50 ug/kg/min continuous infusion. Treat hyperkalemia aggressively. a. Mild (5-6 mEq/L) →sod. bicarb. b. Moderate (6-8mEq/L)→glucose and insulin infusion c. Severe (≥ 8mEq/L)→ Kayxalate enema Use Fab antibodies (digoxin antibodies or dig bind) in case of uncontrolled arrhythmia or sever hyperkalemia unresponsive to treatment. (one vial = 40 mg, each can bind 0.6 mg digoxin ) number of vials to given = body load (IV over 30 min.)   NB. - Give as bolus if cardiac arrest is imminent nmol/L = ng/mL digoxin level. Caustics (Strong Acids and Alkalis) Acids: toilet bowl and drain cleaners, battery fluid, metal cleaner and industrial acids. Alkalis: ammonia, oven and drain cleaners, dishwasher detergents. Patient with significant exposure usually critically ill and develops symptoms early. Absence of oral burns does not mean absence of serious esophageal injury. Caustics in liquid form are more commonly associated with esophageal burns. Clinical picture : Any or all of the following may be present: Oropharyngeal and/or abdominal pains Drooling Vomiting Retrosternal burning Stridor Dyspnea Perioral burns Diagnosis and management: General supportive measures. Determine the substance and time of ingestion.