Monthly Archives: August 2019

VIVA AID: MAO INHIBITORS AND OPIOIDS

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  • Some opioid analgesics are associated with a risk of serotonin syndrome in combination with MAOIs due to their serotonergic properties. Other combinations may result in opioid toxicity due to CYP450 enzyme inhibition by the MAOI.
  • Given the widespread availability of several suitable alternative drugs, the combination of dextromethorphan, methadone, pethidine, tramadol, fentanyl or tapentadol with an MAOI should usually be avoided, including in the 14 day period following the withdrawal of an irreversible MAOI.
  • Morphine, codeine, oxycodone and buprenorphine are alternative opioids for patients receiving MAOIs, though starting at a low dose and titrating cautiously against clinical response is advised. Blood pressure and the signs and symptoms of CNS and respiratory depression should be monitored closely.
  • The MAOI/pethidine interaction has two distinct forms: an excitatory and a depressive form. Pethidine must never be used in the presence of MAOIs because of the risk of a fatal excitatory interaction. Morphine does not cause this excitatory interaction, and is the drug of choice provided an allowance is made for possible potentiation of the depressive narcotic effect.

 

VIVA SCENE: C-SPINE X-RAY

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WHETHER TO DO C SPINE IMAGING IN TBI; CRITERIAS:

1. Screen Shot 2019-08-11 at 9.23.39 pm

2. Under the NEXUS guidelines, when an acute blunt force injury is present, a cervical spine is deemed to not need radiological imaging if all the following criteria are met:

  • There is no posterior midline cervical tenderness
  • There is no evidence of intoxication
  • The patient is alert and oriented to person, place, time, and event
  • There is no focal neurological deficit (see focal neurological signs)
  • There are no painful distracting injuries (e.g., long bone fracture)

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Lateral C-Spine Radiograph. (AABCDs)

A—Adequacy: An adequate film should include all seven cervical vertebrae and C7/T1 junction with optimum density so that the soft tissue shadow is visible clearly.

A—Alignment

a. Atlanto occipital alignment: The anterior and posterior margins of the foramen magnum should line up with the dens and the C1 spinolaminar line.

b. Vertebral alignment

Look for the following four lines (any incongruity= should be considered as evidence of ligamentous injury or occult fracture)

1. Anterior vertebral line—joining the anterior margin of vertebral bodies

2. Posterior vertebral line—joining the posterior margin of vertebral bodies

3. Spinolaminar line—joining the posterior margin of spinal canal

4. Spinous process/ Interspinous line—joining the tips of the spinous processes

B Bony Landmark: vertebral bodies, pedicles, laminae, and the facet joints are inspected

C Cartilagenous space: Predental space or the Atlanto-Dental Interval (ADI): which is the distance from dens to the body of C1. ADI should be < 3 mm in adults and < 5 mm in children. An increase in ADI depicts a fracture of the odontoid process or disruption of the transverse ligament

D—Disc space

Disc spaces should be roughly equal in height and symmetrical.

Loss of disc height can happen in degenerative diseases.

S—soft tissue

Prevertebral soft tissue space thickness can help in the diagnosis of retropharyngeal haemorrhage, which can be secondary to vertebral fractures. Maximum allowable distances :

Nasopharyngeal space (C1): 10 mm

Retropharyngeal space (C2–C4): 5–7 mm

Retrotracheal space (C5–C7): 14 mm in children and 22 mm in adults

VIVA SCENE IMAGING: CHEST X-RAY (CXR)

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  • Helpful MNEMONICS: ‘PRIP ABCDEFGHI’. Also in inspiratory films the level of the diaphragm is at the level of ribs 5/6 anteriorly and 8/10 posteriorly. (AR6PR10). 
  • Right heart border is formed predominantly by the right atrium along with the lower part of SVC, whilst the left border is formed by the aortic arch, pulmonary artery, left atrium, and ventricle. The right and left ventricle forms the inferior border. The right diaphragm is normally higher than the left due to the liver.
  • Areas where pathology is commonly missed: Apices (including behind the 1st rib and clavicle)—small pneumothoraces and masses. Hila—masses and lymph nodes; left hilum is 1–2 cm higher than right. Behind the heart—left lower lobar collapse and hiatus hernia. Below the diaphragm—free gas. Soft tissues—breast shadow or absence (look for lung and bone metastasis)
  • This is CXR of Mr Roy (Patient identity) done on 14/08/2019 (date of study)
  • Its an AP film (Projection)
  • Non rotated (Rotation)
  • Expiratory film (Inspiratory/Expiratory)
  • Adequately penetrated (Penetrated)
  • Trachea is central, no foreign bodies or other abnormalities (A– Airway)
  • On both sides, the bones and soft tissues appear normal; ribs, sternum, scapula, clavicle, spine, and humerus has no deposits or fractures (B-Bones and soft tissues)
  • The cardiac silhoutte is normal (C-Cardiac silhoutte)
  • There is no free air under the diaphragm. Bilateral costo- and cardio-phrenic angles are clear (D– Diaphragm and angles)
  • No effusions. Pleura is not visible (E-Effusion)
  • Both sides, the lung fields appear normal (F-Fields = lung fields)
  • Gastric bubble visible at left upper abdomen (G=Gastric bubble)
  • The hila and the mediastenum appears to be normal and not displaced. The CT ratio is less than 50% (H-Hila and mediastenum)
  • Endotracheal tube tip is seen 5 cms above the carina or T4/T5 interspace. NG tube passed down midline, past level of diaphragm, and deviates to left with tip seen in stomach. ECG leads and electrodes are noted (I=Insertions, Interventions: tubes and lines, chest drains, pacemakers, and metallic valves and artefacts)
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  • If an intrathoracic opacity is in anatomical contact with the heart border, then the opacity will obscure that border. If an intrathoracic opacity is in the posterior pleural cavity so not in direct anatomical contact with the heart border, this causes an overlap but not an obliteration of that border (Silhoutte sign)
  • When the alveoli no longer contain air and opacify, the air-filled bronchi passing through the alveoli may be visible as branching linear lucencies. (Air bronchogram)
  • Linear opacities measuring 1–6 cm extending from periphery to the hila caused by distension of anastomotic channels between peripheral and central lymphatics.(Kerley A lines)
  • Short horizontal lines, due to oedema of the interlobular septae, situated perpendicularly to the pleural surface at the lung base (Kerley B lines)
  • Reticular opacities at the lung base (Kerley C lines)
  • The mediastinal masses can be identified on the PA views but lateral films and/or CT scans are required to confirm further diagnosis
  • Anterior mediastenum: Anterior to trachea, Middle mediastenum: Anterior to heart, Posterior mediastenum: Posterior to heart
  • ANTERIOR MEDIASTENAL MASS: (4 T’s) Thymic tumour -Teratoma- Thyroid –  Terrible lymph nodes (LN) Ascending aortic aneurysm, MIDDLE MEDIASTENAL MASS (BAL) Bronchogenic cyst – Arch aneurysm- LNs, POSTERIOR MEDIASTENAL MASS: as expected it can be from Spine/Neurogenic; also hiatus hernia
  • Hilar mass: Most commonly TB/Sarcoidosis; also lymphoma
  • Collapse: Triangular opacity, Crowding of ribs, Mediastenal displacement, hyperinflation of other lobes
  • Consolidation: confluent ill defined opacity, bat wing distribution, no volume loss, air bronchogram
  • Effusion: Erect: obliteration of the costo- and cardio-phrenic angles and opacity with meniscus. Supine: graded haze giving a ground glass opacity
  • Emphysema: Decreased lung markings, flat diaphragm and hyperexpanded lung, Presence of bullae and peribronchial thickening, signs of cor pulmonale, right ventricular enlargement, pulmonary hypertension—enlargement of the central pulmonary arteries with oligaemic peripheral lung fields

VIVA SCENE : NEONATE /OLDER CHILD Vs ADULT

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CVS:

  • Average HR is 120-180 bpm and SBP 50-90 mm of Hg at birth
  • Oxygen consumption is twice that of an adult 7 ml/kg/min. But because of a fixed stroke volume, increasing the HR is the only way to increase CO. Also neonatal myocardium consists of more non-contractile connective tissue.
  • Parasympathetic system is predominant; bradycardia can happen in response to hypoxia or tracheal suction. Asystole is the most common form of cardiac arrest and ventricular fibrillation is uncommon
  • Circulating volume approx 90 ml/kg @ birth (300-400 ml in an average neonate). Bleeding contributes proportionately a greater loss of total volume in a neonate, compared to an adult. Right ventricular mass equal to left ventricular mass until 6 months of age, resulting in right axis deviation on the ECG.
  • Transitional circulation: Before birth the SVR is low due to the low resistance placental circulation whereas the pulmonary resistance is high. At birth the SVR rapidly increases after clamping of the umbilical cord and PVR decreases following functional closure of foramen ovale (due to increased venous return to left atrium from pulmonary arteries) and ductus arteriosus (in response to increased PaO2 in blood). But this can be reversed back to the foetal state due to stimuli including hypoxia, heypecarbia and acidosis, leading to a perpetuating cycle of worsening hypoxia. This is known as transitional circulation or prsistent foetal circulation.

AIRWAY/ RESPIRATORY SYSTEM

  • Relatively larger head, short neck, large tongue and narrow nasal passages.
  • High anterior larynx (level C2/3 compared to C5/6 in the adult).
  • Large U-shaped floppy epiglottis.
  • Narrowest point of the larynx is at the level of the cricoid cartilage (in adults it is at the laryngeal inlet).
  • Trauma to the small airway can easily lead to oedema and airway obstruction. 1 mm oedema can narrow an infant’s airway by 60% (resistance ∝1/radius).
  • Equal angles of mainstem bronchi (in adults the right main bronchus is more vertical).
  • A compliant chestwall: FRC is less as the elastic recoil pulls the compliant chest wall inwards. Closing volume is larger than FRC until 6–8 years of age resulting in airway closure at end-expiration; this can be reduced by CPAP
  • Fatiguable respiratory and accessory muscles: The diaphragm has less % of fatigue resistant type I respiratory fibres. Raised abdominal pressure can splint the diaphragm precipitating respiratory failure. Diaphragmatic breathing > intercostal breathing. Diaphragmatic movement restricted by relatively large liver.
  • Horizontally aligned ribs prevent the bucket handle movement of the ribs during inspiration
  • Incompletely developed alveoli.Born with only 10% of the total number of alveoli as adults. Alveoli develop over first 8 years. Higher alveolar ventilation 100–150 mL/kg/min compared with 60 mL/kg/min in adult.
  • Inconsistant ventilatory response to hypercapnoea. Higher risk of apnoea
  • Sinusoidal respiratory pattern, no end-expiratory pause (inspiratory/expiratory ratio 1:1). Resting repiratory rate is high and increases further if respiratory compensation is required. Limited capability to increase the tidal volume
  • Obligate nasal breathers; nasal obstruction (e.g. choanal atresia, respiratory infection) can precipitate respiratory failure
  • MAC infant > neonate > adult

CNS

  • CNS development is incomplete at birth
  • Myelination starts before birth and continues throughout the first year
  • Spinal cord ends at L3 (L1 by age 2 years).
  • Unfused fontanelle and sutures makes it more compliant and can expand to some extent in response to raised ICP. ICP is less than the adult: 2-4 mm of Hg
  • Cerebral Blood Flow is less in the neonate than the adult and autoregulation operates at less SBPs
  • In premature infants autoregulation is absent and perfusion is pressure dependent
  • Blood brain barrier is more permeable and hence the neonate is more sensitive to sedatives
  • Neonate responds to pain with tachycardia, hypertension, grimaces etc

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TEMPERATURE REGULATION

  • Higher thermoneutral temperature (temperature below which an individual is unable to maintain core body temperature) 32 degree C for a term infant compared with 28 for an adult.

  • Neonate loss heat very readily due to a high body surface area to weight ratio and absence of shivering in infants ❤ months
  • Produces heat by metabolism of brown fat (5-6% of body wt, stored around kidneys, scapula and mediastenum) by non shivering thermogenesis. Beta adrenergic mediated and contributes to significant amount of the O2 demand placed on the cardiorespiratory system. Ablated by beta blockade

RENAL SYSTEM

  • Immature at birth
  • Higher total body water (80%) at birth
  • Renal blood flow is 6% of cardiac output at birth rising to 18% of cardiac output at 1 month (compared with 20% in adult).
  • Reduced GFR, tubular function until 6–8 months of age
  • Reduced H+ ion excretion
  • Cannot tolerate both excessive water/ sodium load and dehydration (decresed ability to conserve water)
  • Fluids must be carefully balanced based on weight, insensible and observed fluid losses and maintenance requirements

HEPATIC SYSTEM

Low hepatic glycogen stores means hypoglycaemia occurs readily with prolonged fasting

DRUG ADMINISTRATION

  • TBW is increased: so the volume of distribution of water soluble drugs will increase and hence need an increase in the dose. e.g. Succinyl choline (1 mg/kg in adult but 2 mg/kg in the neonate)
  • Succinyl choline by acting on the SA node can produce arrhythmias and even asystole in the neonate
  • Though the neonate is more sensitive to nondepolarizing muscle relaxants, the higher ECF volume increases the required dose; so the final required dose remains unchanged
  • Immature hepatic and renal systems make the metabolism and excretion of the drugs slow. e.g. half life of morphine is increased due to the reduced ability to produce glucoronide conjugates
  • Circulating levels of albumin and alpha acid glycoprotein is less, increasing the free fraction and a pronounced effect

  • MAC is age related. MAC values for an infant are: • sevoflurane = 3.3% • isoflurane = 1.9% • desflurane = 9.4%.

VIVA SCENE: ALL IMPORTANT PAEDIATRIC CASES IN ONE PLACE

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1. PYLORIC STENOSIS (PROTOTYPE CASE; ANY OTHER CASE, MAKE THIS A TEMPLATE AND ADD SPECIFIC POINTS RELEVANT FOR THAT CONDITION)

Most common cause of intestinal obstruction in infancy

Due to hypertrophy of circular pyloric muscle

Presentation: 4-6 weeks of age

Persistent projectile vomiting

There is obstruction at the level of pylorus: so bicarbonate rich fluid from intestine cannot mix with gastric secretions

So the vomiting causes metabolic alkalosis and hypokalemia due to loss of acidic gastric juice alone
The large bicarbonate load is in excess of kidney’s absorptive capacity and the urine becomes alkaline initially
Later when the fluid and electrolyte loss result in dehydration, the renin angiotensin system is activated and result in aldosterone secretion which tries to preserve sodium at the expense of K and Cl ions

This result in production of paradoxical acidic urine and worsening of metabolic alkalosis and hypokalemia

An attempt to compensate it through hypoventilation is initiated; but it will be insufficient and also this will trigger the hypoxic drive!

Hypoglycemia, hemoconcentration, mild uremia and unconjugated hyperbilirubinemia may be seen.
ANAESTHETIC CONCERNS

Pyloric stenosis is not an emergency

The DYSELECTROLYTEMIA and ACID BASE IMBALANCE should be corrected before taking up for surgery.

Increased chance for regurgitation, altered physiology and anatomy, altered drug dosages, difficult venous access, anxious parents are other concerns

There should be an experienced paediatric anaesthesiologist for the conduct of anaesthesia
P.A.C. AND EVALUATION

LOCATION: Needs resuscitation in a paediatric ICU or ward

INVESTIGATIONS: CBC, Blood sugar, RFT, LFT, group and hold, serial ABGs to know the effectiveness of resuscitation and decide on the dose of K administration. 3 mmol/kg/24 hour potassium should be added to maintenance fluids

HISTORY: From the parent; vomiting frequency, amount of feeds taken, diarrhoea, frequency of wetting of the nappy, fever, altered sensorium

EXAM: ?Dry mucus membrane ?Dry eyes (5% dehydration) ?Sunken fontanelle ?cool peripheries ?oliguria(10%) ?Hypotension ?Tachycardia ?Altered Sensorium (10%) ?prolonged capillary refill time

Naso Gastric tube insertion and 4 hourly aspiration of residue

FLUID RESUSCITATION:

  • For fluid resuscitation : use glucose‑free crystalloids that contain sodium in the range 131–154 mmol/litre, with a bolus of 20 ml/kg over less than 10 minutes. PlasmaLyte, 0.9% Saline ad Ringer Lactate

MAINTENANCE FLUIDS:

  • Calculate routine maintenance IV fluid rates using the Holliday–Segar formula (4 ml/kg/hr for the first 10 kg of weight, 2 ml/kg/hr for the next 10 kg and 1 ml/kg/hr for the weight over 20 kg).
  • This solution would preferably be enriched with glucose 5% (50 ml glucose 50% in 500 ml fluid) in order to provide an adequate caloric supply as recommended (4 to 8 mg glucose/kg/min). In addition, the osmolarity of such a solution makes it possible to be administered on a peripheral venous access.
  • Intraoperative: also will assess for blood loss; the maximum speed of transfusion should be 10ml/kg/hour (if no cardiac failure). Estimated blood volume x ( Desired Hct – Current Hct / Hct of the RBC ) will give the volume of PRBC to be transfused. (N.B.: As a general guide in laparotomies 10 ml/kg/ hour would be needed to compensate for evaporative losses). FFP if needed: 10-15 ml/kg

TARGETS:

  • Normovolemia
  • 1-2 ml/kg/hr of urine OR at least 2 wet nappies
  • Chloride > 95 mmol/L
  • pH <7.5
  • Base excess <6 mmol/L or bicarbonate < 30 mmol/L

CONDUCT OF ANAESTHESIA

  • Ensure that the child is adequately resuscitated
  • Procedure may take 30-60 mins
  • Paediatric anaesthetist
  • Ensure the availability of drugs-equipments for anaesthesia induction, maintenance and resuscitation
  • Attach monitors: ECG, SpO2 and NIBP(AAGBI standards)
  • 4 quadrant aspiration via Ryles tube
  • Preoxygenation for 3 mins
  • Modified rapid sequence induction with cricoid pressure
  • Propofol, Fentanyl and succinyl choline/ rocuronium 1 mg/kg
  • Straight bladed laryngoscope. Insert an uncuffed ETT of size 3.5 mm ID; I will also keep size 3 and 4
  • Ensure proper placement: 5 point auscultation and checking capnography trace
  • Release cricoid pressure and secure the tube
  • Hand ventilate the child before connecting to a ventilator (ventilation guided by ETCO2 values)
  • Paediatric mode; Pressure Controlled Ventilation
  • O2, Air and sevoflurane maintenance
  • Can consider an epidural for intra and postoperative analgesia (C/I Sepsis, coagulopathy)
  • Local anesthetic can be infiltrated by the surgeon; Ropivacaine or levobupivacaine; dose < 2mg/kg
  • Paracetamol iv (child <10 kg–> 7.5 mg/kg 6 hourly; max 30 mg/kg/day) OR
  • Paracetamol suppository 30 mg/kg loading dose followed by 20 mg/kg 6-8 hourly: max 60 mg/kg/day; continue postoperatively
  • Fentanyl 1microgram/kg iv boluses hourly is less cumulative and more predictable than morphine
  • If well hydrated with good renal perfusion: NSAIDs Ibuprofen 3 mg/kg three times daily or diclofenac per rectal 1 mg/kg/dose suppositories
  • Monitor urine output
  • Antiemetics: ondansetron 0.15 mg/kg
  • Extubation in lateral position
  • Risk of post operative apnoea: SpO2 monitoring with apnoea alarm
  • Regular and PRN analgesics in postoperative period

OTHER INTRAOPERATIVE CONCERNS

  • Strategies to avoid excessive heat loss, optimal analgesia and depth of anaesthesia, optimal fluid therapy
  • Constant monitoring of heart rate, oxygen saturation,EtCO2, blood pressure, body temperature, urine output
  • Check blood sugar to avoid hypoglycemia
  • To prevent hypothermia: Increase the ambient temperature of the OR prior to and during the surgery, body warmer, bubble wraps and plastic drapes to cover the body, cover the head, warm the iv fluids, HME to reduce heat loss from the respiratory system

PAIN EVALUATION IN PAEDIATRICS

  • Evaluated with the support of the parents
  • Using a combination of physiological and behavioural markers in neonates and infants
  • e.g. facial expression, sleeplessness, cry, body movements, posture, increased clinginess, loss of appetite, screaming, reluctance to move, CVS & RS changes
  • Neonate and Infant: Neonatal Pain Agitation and Sedation Score (N-PASS), Neonatal and Infant Pain Scale (NIPS), Face, Legs, Activity Cry and Consolatility scale (FLACC), Objective Pain Score
  • Pre-school and school children can be evaluated by scales like Faces scale ( Happy to crying faces
  • Adolescents: Visual Analogue Scale

POSTOPERATIVE CARE

  • In a high dependency unit or Paediatric Intensive Care unit
  • Will watch for respiratory depression and respiratory compromise, ?shock, pain levels, surgical complications, signs of loss of blood volume
  • Send sample for full blood count and serum electrolytes
  • Continue IV fluids

2.INTUSSUSCEPTION

  • Small bowel telescoping; most common cause of intestinal obstruction in first year of life; other diseases like Meckel’s diverticulum, lymphoma etc can present as intussuception.
  • HISTORY:Present with paroxysmal abdominal pain- child may hold legs to abdomen and red currant jelly like stools. Vomiting and dehydration can cause shock. Abdominal distension can compromise respiration. Infection, infarction,bleeding, perforation, Sepsis-shock etc also can occur.
  • EXAMINATION:Abdomen-guarding. Sausage shaped mass on the right side.
  • INVESTIGATION: Abdominal Ultra sound. X ray abdomen: ?obstruction ?perforation. Air enema can be therapeutic also but contraindicated if having perforation or peritonitis or if in shock.
  • If in shock–> resuscitate and take for laparotomy. A
  • ny repiratory compromise due to distension–> consider the need for mechanical ventilation

3.OESOPHAGEAL ATRESIA (OA) & TRACHEO OESOPHAGEAL FISTULA (TOF)

  • Defective embryonic development of oesophagus and trachea
  • Mostcommon types are 1. isolated OA with distal TOF 2. isolated OA and 3. isolated TOF
  • PAC: ask for SYMPTOMS: Repeated episodes of coughing,chocking and cyanosis worsened by feeding, resitance to pass a nasogastric tube; evaluate for associated congenital anomalies- VACTERL: Vertebral Anal Cardiac Tracheo Esophageal Renal Limb anomalies; problems of prematurity- lung disease, retinal problems, impaired glucose regulation
  • OPTIMISATION: The ligation of a TEF is urgent, but not emergent, except in the setting of respiratory insufficiency severe enough to require ventilatory support. Use IV fluids with glucose to avoid hypoglycemia and to achieve euvolemia. Use specialised suction called Replogle suction to clear the upper part of the oesophagus. Avoiding feeding. Upright positioning of the infant to minimize gastroesophageal reflux. Administration of antibiotic therapy to treat sepsis or aspiration pneumonia. Uncomplicated surgery can be done within 24 hours of birth, to reduce the chance of aspiration of pooled secretions.
  • ANAESTHESIA TECHNIQUE (See above) Specific points for TOF: Under monitoring with pulseoximeter, suction the upper pouch–>Preoxygenation with 100 % O2; avoid vigorous bag and mask ventilation; else the air will pass via TOF into stomach causing distension and splinting of the diaphragm–> An awake technique with titration of small doses of fentanyl (0.2 to 0.5 mcg/kg) allows intubation of the trachea without excessive hemodynamic stimulation or depression. OR an inhalational anesthetic with or without muscle relaxation and with cautious, gentle positive pressure ventilation as needed (Ref: Smith’s anaesthesia for infants & children 8/e) –> place ETT–> allow child to breath spontaneously–>examine airway with a rigid bronchoscope and establish the exact anatomy–> replace and position ETT in a way to occlude the TOF–> once the ETT is placed in the correct position, NMBA can be given. Consider IBP and central venous access based on individual case. Child usually in Right lateral position; take care to maintain the iv access safely.

4.CONGENITAL DIAPHRAGMATIC HERNIA (CDH)

  • Repair is not an emergency procedure. Usually delayed for 24-48 hours for the pulmonary resistance to come down. Baby should be resuscitated first. Delivery should take place as close to term as possible to achieve maximum lung maturity. ABG, Chest x-ray and Echo shold be done. Do an oroogastric suction to clear the part of the bowel in the chest. Intubatin and ventilation should aim to reduce barotrauma with smaller tidal volumes and permissive hypercapnea.

5.EXOMPHALOS & GASTROSCHISIS

  • Due to failure of the migation of the gut into the abdominal cavity during fetal development, there is a herniation of the abdominal contents with a covering sac through a midline defect in the abdominal wall and other congenital anomalies may accompany. Whereas gastroschisis is an isolated anomaly where the gastric contents without any covering sac herniates through a defect in the abdominal wall but not in the midline.
  • There is chance of infection and extensive loss of heat and moisture from the exposed bowel; so it should initially be covered with a non porous material and extreme priority shoud be given for the eveluating the fluid loss and replacement and also for establishing normothermia
  • Primary closure or if respiratory compromise is not allowing it, a staged closure may be necessary

6. INGUINAL HERNIA / REGIONAL TECHNIQUES

  • Mask or IV induction with general anesthesia (with or without endotracheal intubation); spinal anesthesia as a primary anesthetic; caudal anesthesia or analgesia. Muscle relaxation is not necessary but may be a valuable adjunct for decreasing anesthetic requirements and providing optimal surgical conditions.

  • Equipment: Low compression volume anesthesia breathing circuit (circle absorption system vs. Mapleson D ). Monitoring: Standard noninvasive monitoring

  • Maintenance: 1. Inhalation agent plus local infiltration or ilioinguinal-iliohypogastric block on the surgical field OR maintenance caudal analgesia, allow the avoidance of opiates. Neuromuscular blockade with nondepolarizing agent, if chosen. 2. Volume support with judicious amounts of crystalloids.(See 1.) Blood loss is minimal.

  • Emergence and Perioperative Care: 1. Vigilance regarding perioperative abnormalities of control of breathing: periodic breathing/apnea; laryngospasm/bronchospasm; bradycardia; hypoglycemia; continuously monitor with a pulseoximeter. 2. Pain management. (See:1)

Regional anaesthesia:

  • SPINAL ANAESTHESIA: For neonates and infants, a 1 inch 22-gauge spinal needle is inserted at the L4-5 interspace. 0.5 to 0.6 mg/kg of either isobaric or hyperbaric bupivacaine will provide an average of 80 minutes of surgical analgesia for infants and young children who are less than 5 kg in weight. For infants or toddlers 5 to 15 kg, the dosage of hyperbaric bupivacaine or tetracaine is 0.4 mg/kg, and for children weighing more than 15 kg, the dosage of bupivacaine or tetracaine is 0.3 mg/kg . Isobaric ropivacaine has been studied in children for spinal anesthesia at a dosage of 0.5 mg/kg up to 20 mg.
  • CAUDAL BLOCK: The recommended concentration of bupivacaine for a singleshot caudal is 0.125% to 0.25%. An epinephrine dosage of 2.5 mcg/mL, or a concentration of 1:400,000 may be used as an additive for central blocks. Epinephrine will serve as a marker for intravascular injection and decrease systemic absorption of local anesthetic. Additionally, epinephrine may prolong the duration of a regional block. Preservative Free Ketamine, fentanyl, clonidine etc also can also be used as additives. See table: Smith 8/eScreen Shot 2019-08-25 at 11.48.27 am
  • ILIOINGUINAL /ILIOHYPOGASTRIC BLOCK: Can be given after induction, but before the incision; a blunt 22 or 25 gauge needle is inserted 1 cm superior and 1 cm medial to the anterosuperior iliac spine; the needle is initially directed posterolaterally to contact the inner superficial lip of the ileum, then withdrawn while injecting local anesthetic during needle movement. Once skin is reached, the needle is redirected toward the inguinal ligament (ensuring that the needle does not enter the ligament) and local anesthetic is injected after a pop is felt. Can perform under US guidance too. Can use 0.25 mL/kg of 0.5% levobupivacaine or 0.5% ropivacaine at 3 mg/kg. (Ref: Smith’s anaesthesia for infants & children 8/e)
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VIVA AID: INTRAVENOUS FLUIDS IN PAEDIATRIC POPULATION; SALIENT POINTS FROM VARIOUS GUIDELINES

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NICE 2015 GUIDELINES

  • For fluid resuscitation in children and young people: use glucose‑free crystalloids that contain sodium in the range 131–154 mmol/litre, with a bolus of 20 ml/kg over less than 10 minutes. Take into account pre‑existing conditions like cardiac disease or kidney disease, as smaller fluid volumes may be needed.
  • For term neonates who need IV fluid resuscitation: use glucose‑free crystalloids that contain sodium in the range 131–154 mmol/litre, with a bolus of 10–20 ml/kg over less than 10 minutes.
  • Do not use tetrastarch for fluid resuscitation.
  • Calculate routine maintenance IV fluid rates for children and young people using the Holliday–Segar formula (100 ml/kg/day for the first 10 kg of weight, 50 ml/kg/day for the next 10 kg and 20 ml/kg/day for the weight over 20 kg). Be aware that over a 24‑hour period, males rarely need more than 2500 ml and females rarely need more than 2000 ml of fluids.
  • Calculate routine maintenance IV fluid rates for term neonates according to their age, using the following as a guide:
  • From birth to day 1: 50–60 ml/kg/day.
  • Day 2: 70–80 ml/kg/day.
  • Day 3: 80–100 ml/kg/day.
  • Day 4: 100–120 ml/kg/day.
  • Days 5–28: 120–150 ml/kg/day.
  • IV fluids for routine maintenance in children and young people: initially use isotonic crystalloids that contain sodium in the range 131–154 mmol/litre.
  • Measure plasma electrolyte concentrations and blood glucose when starting IV fluids for routine maintenance (except before most elective surgery), and at least every 24 hours thereafter.
  • Base any subsequent IV fluid prescriptions on the plasma electrolyte concentrations and blood glucose measurements.
  • If term neonates need IV fluids for routine maintenance: initially use isotonic crystalloids that contain sodium in the range 131–154 mmol/litre with 5–10% glucose
  • If there is a risk of water retention associated with non‑osmotic antidiuretic hormone (ADH) secretion, consider either:
    • restricting fluids to 50–80% of routine maintenance needs or
    • reducing fluids, calculated on the basis of insensible losses within the range 300–400 ml/m2/24 hours plus urinary output.

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EUROPEAN CONSENSUS 2011 FOR INTRAOPERATIVE FLUID THERAPY

An appropriate solution for intraoperative infusion in children should have an osmolarity and sodium content close to the physiologic range in order to avoid hyponatraemia, an addition of 1–2.5% glucose in order to avoid hypoglycaemia, lipolysis or hyperglycaemia and should also include metabolic anions (i.e. acetate, lactate or malate) as bicarbonate precursors to avoid acid–base balance disturbances (i.e. hyperchloraemic acidosis). The intraoperative infusion of isotonic solutions containing 1–2.5% glucose in children is considered well established use in Europe

BELGIAN PERIOPERATIVE FLUID RECOMMENDATIONS 2012

For children undergoing uncomplicated day-case surgery or minor surgery and those expected to remain nil-by-mouth for at least 24 hours after surgery or undergoing major surgery, a full volume maintenance fluid should be administered during the intraoperative period and immediate post-operative period, as this is associated both with a reduced incidence of postoperative nausea and vomiting particularly in those children receiving opioids, and with a significantly reduced postoperative increase in ADH concentration. The latter presumed to be a result of correction of hypovolemia. 

During the first postoperative day, decreased volumes of the maintenance fluid consisting of an isotonic solution at two-thirds or 70% of the calculated maintenance rate is recommended, provided the child is normovolemic.

This solution would preferably be enriched with glucose 5% (50 ml glucose 50% in 500 ml fluid) in order to provide an adequate caloric supply as recommended (4 to 8 mg glucose/kg/min). In addition, the osmolarity of such a solution makes it possible to be administered on a peripheral venous access.

Recognizing that fluids used to replace ongoing losses should reflect the electrolyte composition of fluid lost, NaCl 0.9% has been considered as appropriate in most cases. Isotonic fluids including colloids are to be used as a bolus in the event of hypovolemia.

Consider iv. fluids as medications.

Administer isotonic fluids (saline 0.9%, Plasmalyte®, Hartmann® or colloids) as a bolus in the event of hypovolemia.

Monitoring plasma electrolytes and glucose concentrations regularly i.e. once daily or more if clinically indicated (documented plasma [Na] < 135 mmol/L)

AMERICAN ACADEMY OF PAEDIATRICS 2018

The American Academy of Pediatrics recommends that patients 28 days to 18 years of age requiring maintenance IVFs should receive isotonic solutions with appropriate potassium chloride and dextrose because they significantly decrease the risk of developing hyponatremia. (For the purposes of this guideline, isotonic solutions have a sodium concentration similar to PlasmaLyte, or 0.9% NaCl)

APA CONSENSUS GUIDELINE ON PERIOPERATIVE FLUID MANAGEMENT IN CHILDREN 2007/ 2010 REVIEW

EXECUTIVE SUMMARY

1. Children can safely be allowed clear fluids 2 hours before surgery without increasing the risk of aspiration.

2. Food should normally be withheld for 6 hours prior to surgery in children aged 6 months or older.

3. In children under 6 months of age it is probably safe to allow a breast milk feed up to 4 hours before surgery

4. Dehydration without signs of hypovolaemia should be corrected slowly.

5. Hypovolaemia should be corrected rapidly to maintain cardiac output and organ perfusion.

6. In the child, a fall in blood pressure is a late sign of hypovolaemia.

7. Maintenance fluid requirements should be calculated using the formula of Holliday and Segar

8. A fluid management plan for any child should address 3 key issues

i. any fluid deficit which is present

ii. maintenance fluid requirements

iii. any losses due to surgery e.g. blood loss, 3rd space losses

9. During surgery all of these requirements should be managed by giving isotonic fluid in all children over 1 month of age

10. The majority of children over 1 month of age will maintain a normal blood sugar if given non-dextrose containing fluid during surgery

11. Children at risk of hypoglycaemia if non-dextrose containing fluid is given are those on parenteral nutrition or a dextrose containing solution prior to theatre, children of low body weight (<3rd centile) or having surgery of more than 3 hours duration and children having extensive regional anaesthesia. These children at risk should be given dextrose containing solutions or have their blood glucose monitored during surgery.

12. Blood loss during surgery should be replaced initially with crystalloid or colloid, and then with blood once the haematocrit has fallen to 25%. Children with cyanotic congenital heart disease and neonates may need a higher haematocrit to maintain oxygenation.

13. Fluid therapy should be monitored by daily electrolyte estimation, use of a fluid input/output chart and daily weighing if feasible.

14. Acute dilutional hyponatraemia is a medical emergency and should be managed in PICU.

VIVA SCENE: Neuroanaesthesia- Management of Traumatic Brain Injury and other questions

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TBI MANAGEMENT (Based on BTF 4e Guidelines)

  • Principal of management of head injury is to prevent secondary brain injury due to hypoxia, hyper/hypocarbia, hypovolaemia, hypotension, and increased ICP.
  • Primary survey and management of other life-threatening injury (tension pneumothorax, cardiac tamponade, airway obstruction, etc.) assessment with GCS
  • Continuous high-flow O2 for all potential TBI cases
  • Airway repositioning maneuvers if needed
  • Evaluate the GCS. GCS<8, increased risk of aspiration, concern for hypoxemia and hypercarbia, need for hyperventilation: all such concerns when present are addressed with intubation and mechanical ventilation.
  • C-Spine imaging based on NEXUS or Canadian C Spine rule criteria (see below)
  • Obtain large bore IV’s and/or central venous access for patients requiring vasoactive drugs. For surgical procedures:
  • ASA monitors along with direct intra-arterial pressure monitoring (zeroed at the level of the head to facilitate assessment of cerebral perfusion pressure [CPP]) and bladder catheterization are established. Avoid hypotension due to induction drugs and surges in BP during intubation and pinning using slow drug administration and vasoactive drugs.
  • All attempts at intubation should include in-line neck stabilization. Anesthetic drugs that allow for rapid control of the airway while avoiding an increase in intracranial pressure (ICP) and providing hemodynamic stability are preferred. For rapid sequence intubation, succinylcholine or rocuronium may be used.
  • Choice of drugs must be tailored to each individual patient. IV anesthetics are cerebral vasoconstrictors whereas volatile agents increase cerebral blood flow (CBF) above 1 MAC

  • Lidocaine in doses of 1.5 mg/kg may inhibit the adverse effects of laryngoscopy decreasing ICP, CMR, and CBF with minimal hemodynamic effects

  • Careful positioning to avoid impedance to venous drainage due to extreme neck rotation or tilt. Avoid ties around the neck for endotracheal tube fixation
  • Avoid increases in intrathoracic pressure (obstructed endotracheal tubes, bronchospasm).
  • Maintain SBP at ≥ 110 mmHg  for patients 15 to 49 or over 70 years and at ≥ 100 mmHg for patients 50 to 69years old. The recommended target CPP value is between 60 and 70 mmHg
  • Isotonic crystalloid is the preferred fluid..A single SBP measurement < 90 mmHg will initiate intravenous (IV) fluid resuscitation with an initial bolus of 1 L of NS/RL in adults and adolescents and 20 ml/kg in older children followed by maintenance rates to keep SBP ≥ 90 mmHg
  • Also hypovolemia resulting from extracranial hemorrhage should be ruled out
  • Maintain ETCO2 between 35 and 45 mmHg (4.5-6 kPa). Avoid hyperventilation, especially in the first 12 hours. If you are going to hyperventilate the patient, use jugular venous saturation monitoring to ensure the brain is getting enough oxygen
  • ABGs to titrate the ventilation and manage the fluids and electrolytes administration and to decide on postoperative ventilation if needed
  • Avoid hypo and hyperglycemia
  • Anaesthetic technique should allow a smooth and rapid recovery and prompt neurological assessment. Again avoid bucking over the endotracheal tube. Labetalol can be used to control sympathetic surges during extubation
  • Continuous monitoring to avoid hypovolemia, hypotension, hypercarbia, hypoxia, hypoglycemia and dyselectrolytemias post extubation
  • Adequate perioperative analgesia is important to prevent further raise in ICP due to pain. Analgesic options: Paracetamol, opioids like fentanyl, scalp block
  • Discuss with the neurosurgeon regarding expected neurological recovery and modify the decision for extubation accordingly

  • Propofol may be used for ICP control. High dose barbiturates are recommended to control ICP refractory to maximum standard surgical and medical treatments while ensuring hemodynamic stability

  • Drain CSF for the first 12 hours for patients with a GCS of less than 6. Continuous drainage is better than intermittent

  • ICP Monitoring is Indicated if GCS is 3-8 and an abnormal CT OR Indicated if GCS is 3-8, there is a normal CT, and any two of the following

    • Age over 40
    • Motor posturing
    • Hypotension (SBP under 90 mmHg)
  • GCS < 8 with ICP > 22 mmHg require intervention

  • Decompressive craniectomy has been used but has not been found to improve outcome

  • Use routine protocol to prevent VAP; no need for prophylactic antibiotics
  • “Stable” TBI should have TED stockings and heparin or clexane
  • Osmotherapy may be used in herniating patients.

  • Treatment with anticonvulsants within 7 days of injury

  • Glucose-containing fluids should be avoided and blood sugar monitored to maintain levels between 4–8 mmol/L.

  • INDICATIONS FOR CT SCAN: GCS < 13 on presentation • Suspected open or depressed skull fracture • Signs of basal skull fracture (haemotympanum, CSF leak from ear or nose, battle’s sign, panda eyes) • Focal neurological signs. Also: More than one episode of vomiting following head injury • History of loss of consciousness following injury or more than 30 minutes of retrograde amnesia of events immediately prior to injury • Mechanism of injury (e.g. cyclist or pedestrian struck by motor vehicle, occupant ejected from a motor vehicle)
  • INDICATIONS FOR INTUBATION: GCS < 8 in adult and < 9 in paediatric patients • Seizure after trauma • Airway obstruction, airway injury • Severe facial injury (Le Fort fracture, mandible fracture) • Inability to maintain oxygenation/ventilation (PaO2 < 9 kPa on air or < 13 kPa with oxygen, PaCo2 < 4 kPa or > 6 kPa) • To facilitate transfer of patient to tertiary centre • Alcohol or other drug intoxication plus signs of head injury (Remember Brain–>Face–>Airway–>Lung–>Stomach!)

SHALL WE DO A C-SPINE IMAGING?

  1. Under the NEXUS guidelines, when an acute blunt force injury is present, a cervical spine is deemed to not need radiological imaging if all the following criteria are met:
  • There is no posterior midline cervical tenderness
  • There is no evidence of intoxication
  • The patient is alert and oriented to person, place, time, and event
  • There is no focal neurological deficit (see focal neurological signs)
  • There are no painful distracting injuries (e.g., long bone fracture)

2. CANADIAN C-SPINE RULE

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MANAGEMENT OF SDH: SPECIFIC POINTS

  • Subdural hematomas are the most common focal intracranial lesion

  • They have the highest mortality rate of all lesions , which is likely due to the associated brain injury and decrease in cerebral blood flow that accompany these lesions. Outcome worsens as the amount of midline shift exceeds the thickness of the hematoma

  • The hematoma is located between the brain and the dura and has a crescent shape. It is usually caused by tearing of the bridging veins connecting the cerebral cortex and dural sinuses

  • The management of these lesions is immediate surgical decompression, which has been shown to improve outcome

MANAGEMENT OF EDH: SPECIFIC POINTS

  • They generally have a better prognosis than subdural hematomas with the main determinant of outcome being preoperative neurologic status

  • Epidural hematomas are biconvex and are located between the dura and skull

  • The usual etiology is a torn middle meningeal artery, but the blood may also come from a skull fracture or bridging veins.

  • The classic presentation includes a lucid interval followed by neurologic deterioration and coma

  • Treatment is prompt surgical decompression when the following criteria are met: more than 30 mL for supratentorial and more than 10 mL for infratentorial hematomas, thickness of more than 15 mm, midline shift of more than 5 mm, or the presence of other intracranial lesions

  • Expectant management with close observation is acceptable for small lesions.

  • Since the brain parenchyma is usually not injured, the prognosis is excellent if the hematoma is rapidly decompressed

 

VIVA SCENE: GASTRIC ULCER BLEED AND OTHER QUESTIONS

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STRESS ULCER RISK FACTORS

Stress ulceration in intensive care patients is relatively common (approaching 90% by day 3 with no prophylaxis), although the incidence of clinically important GI bleeding is less than 2%. There are six major risk factors: 1.Respiratory failure requiring ventilation for >48 hours 2.Coagulopathy 3.Sepsis 4.Hypotension 5.Hepatic failure 6.Renal failure

STRESS ULCER PATHOPHYSIOLOGY

  • Impaired mucosal blood flow 2.Mucosal ischemia 3.Reduced mucus production 4.Reduced mucosal Prostaglandin production 5.increased gastrin production 6.acid-base abnormalities 7.reflux of bile.

TYPES OF ULCERS

Curling’s ulcers associated with extensive burns

Cushing’s ulcers associated with intracranial pathology and gastric acid hypersecretion

STRESS ULCER MANAGEMENT

  • Optimal oxygen delivery to gastric mucosa, avoid hypotension
  • Enteral feeding
  • Proton pump inhibitors, H2 antagonists: by increasing the pH of gastric contents, there is an increased risk of bacterial colonisation and subsequent nosocomial pneumonia.
  • Sucralfate: Aluminium salt of sulphated sucrose and is given in a dose of 1g by NG tube, 6-hourly. It forms a paste at low pH, which preferentially binds to areas of peptic ulceration, thereby providing a physical barrier to the effects of acid. Some investigators have demonstrated a reduction in the rate of nosocomial pneumonias in patients treated with sulcralfate.

MANAGEMENT OF GI BLEED

ECG, NIBP and SpO2 monitoring

Get two wide bore IV access and start RL or NS upto 2 Ls

Support airway: evaluate for the need for airway protection; high volume effective suction must, reduce induction agents dose in hypovolemia

Invasive arterial and central venous pressure monitoring may be necessary in massive bleeds, intubated patients and those with co-morbidities

Insert a Foley for measurement of I/O.

Look for evidence of shock due to severe bleeding: tachycardia,hypotension, ongoing bleed, no response to 2L of crystalloids, HR>90, SBP<100

Rule out hemoptysis and epistaxis

H/O Peptic ulcer disease, NSAID use, alcholism, cirrhosis, coagulation disorders

Order CBC, PT, PTT, BUN, Creatinine, Glucose, Na,K, LFT Cross match 4–6 units of blood as needed

Upright lateral CXR or lateral decubitus abdominal X-rays

Blood should be given promptly if there is persistent haemodynamic instability despite
2 L of crystalloid or colloid, if the initial haemoglobin level is <7 mg/dL, if there is a significant risk of re-bleeding and in those patients with co-morbidities making them unable to tolerate periods of anaemia

Correct coagulopathy

Arrange for endoscopy: both diagnostic / therapeutic

Consider use of vasopressin or octreotide IV, i.v. PPIs.

NSAID INDUCED GASTRIC ULCERS

NSAIDs reduce circulating prostaglandins that are essential in maintaining gastric mucosal integrity. The more an NSAID blocks COX 1, the greater is its tendency to cause peptic ulceration and promote bleeding. Selective COX 2 inhibitors cause less bleeding and fewer ulcers than other NSAIDs

NSAID INDUCED RENAL FAILURE

NSAIDs reduce afferent arteriolar blood flow by antagonizing vasodilatory prostaglandins in patients with in patients with risk factors. In this situation, glomerular filtration rate (GFR) drops leading to AKI.

RISK FACTORS: pre-existing renal dysfunction, diabetics, elderly patients, dehydration, decompensated cirrhosis, CHF and patients on ARBs/ACE inhibitors. The mechanism involves reduced levels of prostacyclin, which are required to maintain renal perfusion.

NSAIDs can result in Acute kidney injury (AKI) resulting in the abrupt loss of kidney function, leading to the retention of waste products, electrolyte disturbances, and volume status changes

NSAIDs can also result in Acute interstitial nephritis (AIN) is a renal lesion characterized by a rapid deterioration in kidney function with inflammation and edema of the renal interstitium

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RIFLE Classification for AKI

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THIS PATIENT REQUIRES BLOOD TRANSFUSION: ABO INCOMPATIBILITY; WHAT’S IT?

Blood groups result from the different antigens expressed on RBCs. ABO and Rh systems are the most important out of the 29 groups. Early in life persons develop antibodies in plasma against non-self antigens.

ANTIGEN IN RBC

ANTIBODY IN PLASMA

Group A has A antigen

Group A has antibody to group B

Group B has B antigen

Group B has antibodies to group A

Group O has no antigen

Group O has antibody to group A and group B

Group AB has A and B antigens

Group AB individuals do not have antibody to group A or B.

So the blood group AB are ideal recipients, as their plasma doesn’t contain any antibody that can agglutinate the donor blood. In the same way blood group O are ideal donors, as once the antibody containing plasma is removed, it contains no antigens to agglutinate with the antibodies in donor’s blood.

RBC

1 Group O individuals can receive blood from group O donors only ( as the antibodies against A or B in their plasma will react with any A or B antigens which enter the circulation)

2 Group A individuals can receive blood from group A and O donors

3 Group B individuals can receive blood from group B and O donors

4 Group AB individuals can receive blood from AB donors, and also from group A, B and O donors ( as their plasma don’t have any antibodies against any antigens)

PLASMA

In plasma transfusion, group AB plasma can be given to a patient of any ABO group because it contains neither anti-A nor anti-B antibody. Group A plasma (with anti-B) can be given to group O and A patients. Group B plasma to group O and B patients only. Group O plasma (anti-A + anti-B) can be given to group O patients only.

PLATELETS

The Platelet Concentrates transfused must be ABO-identical, or at least ABO-compatible, in order to give a good yield (In an emergency, ABO non-identical units can be used, although the improvement seen in platelet count post-transfusion may be less.) Group O PC can be used for patients with blood groups A, B, and AB ONLY IF, they are resuspended in additive/preservative solutions, or if negative for high titre anti-A/A,B. Rh-negative patients, in particular women of childbearing age, should receive, if possible, RhD-negative PC

Rh BLOOD GROUP

Is the second most important group system. Out of the existing C,D and E antigens, D is the most antigenic one. Anti D antibodies are not normally found in the blood of Rh negative individuals; instead they develop it only when itcomes into contact with Rh positive blood during child birth or inappropriate transfusion. In case of subsequent transfusins or pregnancies with Rh positive blood- this can cause rapid destruction of RhD positive red cells (Hemolytic disease of the newborn in subsequent pregnancies; to prevent this sensitization we should give Rhesus imunoglobulin= Anti-D prophylaxis- to the Rh negative mother who gave birth to an Rh positive baby). FFP does not need to be Rh-compatible. Anti-D prophylaxis is not necessary in Rh D-negative recipients of Rh D-positive FFP.

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