Empiric antibiotics for general infection

Cite this article as:
Marc Anders. Empiric antibiotics for general infection, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3846
Age if meningitis excluded if meningitis is NOT excluded if Staphylococcus aureus suspected
< 3 months Amoxicillin 50 mg/kg q6hrGentamycin 7.5 mg/kg q24hr Amoxicillin 50 mg/kg q6hrGentamycin 7.5 mg/kg q24hr

Cefotaxime 50 mg/kg q6hr

Consider especially in infants aciclovir 20mg/kg q8hr

Amoxicillin 50 mg/kg q6hrCefotaxime 50 mg/kg q6hr

Vancomycin 15 mg/kg q6hr

Clindamycin 15 mg/kg q8hr

> 3 months Cefotaxime 50 mg/kg q6hrFlucloxacillin 50 mg/kg q4-6hr Cefotaxime 50 mg/kg q6hrFlucloxacillin 50 mg/kg q4-6hr Cefotaxime 50 mg/kg q6hrVancomycin 15 mg/kg q6hr

Clindamycin 15 mg/kg q8hr

any age group, if immuno-compromised Meropenem 20 mg/kg IV q8hrVancomycin 15 mg/kg q6hr

Gentamycin 7.5 mg/kg q24hr

if Meningitis is NOT excluded, and suspicion of severe Meningitis (gram stain), replace Flucloxacillin by Vancomycin 15 mg/kg q6hr to cover for Penicillin resistant Pneumococcus Meningitis 

Initial post-operative care and problems

Cite this article as:
Marc Anders. Initial post-operative care and problems, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3739

ABDOMINAL DISTENSION

Causes:

  • Air in stomach or bowel (usually from mask ventilation at induction of anaesthesia) or tension pneumothorax
  • Fuid in bowel or in peritoneal cavity (usually capillary leak, high RA pressure or PD fluid
  • Rarely fluid overload or peritoneal haematoma)
  • Exclude NEC, especially in neonates with parallel circulations or long cross-clamp time.

Investigation and management:

  • Examine chest and abdomen – percussion
  • Examine fluid drainage from PD catheter and chest drains (amount and redness; measure Hb)
  • Aspirate NG tube
  • Repeat CXR (compare with previous, air in stomach or bowel, pneumothorax)
  • Monitor abdominal girth
  • Check coagulation and platelets (correct if abnormal and bleeding)
  • Abdominal ultrasound if suspect retroperitoneal haemorrhage (femoral line)
  • If capillary leak is the problem, lasts up to 2 days (longer in neonates, after long operations, in sepsis and when the cardiac output is low); during this time, fluid restriction doesn’t prevent oedema or ascites, but only leads to hypovolaemia
  • Adjust ventilation if necessary to compensate for reduced abdominal compliance

ATELECTASIS

Causes:

  • Tracheal intubation
  • Thick secretions
  • Inadequate humidification (check humidifier tank and tubing temperatures)
  • Inadequate tracheal suction
  • Airway compression or collapse (e.g. malacia)
  • Paralysed hemidiaphragm while spontaneous ventilation

 

Signs:

  • Decreasing SaO2
  • Rising PaCO2
  • May be reduced ipsilateral chest movement, usually involves RUL and LLL.

 

Management:

  • Hand-ventilation
  • Instil normal saline (0.25-0.5 ml) into trachea before suction, physiotherapy, culture tracheal aspirate
  • X-ray screen diaphragm if clinical suspicion of paralysis
  • Bronchogram if other signs suggest malacia (hyperinflation, wheezing, prolonged expiration)

ATRIAL PRESSURE INCREASING

Examine patient

  • Check BP, heart rate, RAP, LAP
  • AV valve regurgitation: look for V wave in atrial trace (AV regurgitation or malposition of atrial catheter through AV valve)
  • Over-filling: in aortic or pulmonary stenosis, non-compliant ventricles cause atrial pressures to rise with small increases in volume. Treat by careful diuretics and/or GTN (filling pressures)
  • Tamponade: associated with tachycardia and falling BP and cardiac output. Notify surgeons and immediate echo, but do not delay chest opening if situation serious.
  • In infants, myocardial oedema without pericardial fluid can cause tamponade that may be immediately relieved by opening the chest.

 

Management:

  • Re-calibrate transducers
  • Examine chest and abdomen
  • Check blood gas, electrolytes and lactate
  • Hand-ventilate and suction ETT
  • Check ECG rhythm
  • Obtain a CXR
  • Notify surgeons if tamponade suspected
  • Trial of vasodilators, diuretics and inotropes.

CARDIAC TAMPONADE

Signs:

  • Rising HR
  • Increasing lactate and metabolic acidosis
  • Falling BP with low pulse pressure and narrowing of systolic and diastolic BP
  • Both atrial pressures rise (especially RA)
  • Chest drainage may increase (if due to increased bleeding) or (usually) decrease (drainage blocked)
  • Heart sounds may be muffled
  • QRS complexes may be smaller
  • Milk drains (are they on adequate suction, are the drain reservoirs full)
  • If there is the slightest suspicion of tamponade, notify the surgeon (do not delay for investigations)

 

Management:

  • Obtain CXR (may show increase in heart size; more globular heart shape; increased distance from pacing wires or LA/PA lines to heart border)
  • Obtain echo
  • Check blood gases and clotting (PT, PTT, fibrinogen, platelets)
  • Milk the chest drains
  • Stop vasodilators
  • Give blood or saline 10 ml/kg
  • Maintain the coronary perfusion pressure using inotropes
  • Consider clotting factors or platelets; if ACT >100 sec, give protamine 0.5 mg/kg and re-check ACT
  • Consider aspirating LA or PA lines to check position of their tips (? in pericardial cavity); may need urgent chest opening to prevent further deterioration

CONVULSIONS

In a paralysed child, a seizure may consist only of increases in HR, BP, PA or atrial pressures or spontaneous variations in pupil size.

  • Review history: pre-op; intra-op and post-op events
  • Check blood glucose, gases and electrolytes (including Ca++ and Mg++)
  • Cease muscle relaxants
  • Check autonomic response to IV midazolam bolus
  • Neurological examination when muscle power returns
  • Consider consulting neurologist (is this a fit? prognosis? follow-up ?)
  • Monitor EEG during autonomic changes to confirm seizure present
  • Consider CT scan; load with phenobarbitone up to 30 mg/kg IV in 5-10mg/kg increments (beware hypotension)
  • Continue phenobarbitone if fits continue; avoid IV phenytoin (myocardial depressant) after cardiac surgery. Consider keppra 10 mg/kg IV

FEVER

All children become febrile after open heart surgery, and most become febrile after any thoracotomy. The fever appears as soon as the child re-warms after the operation, and lasts 24-48 hours. During this time, the child can still become septic, but the diagnosis of sepsis depends on other signs. A secondary increase in temperature (after the normal post-op fever has settled) means sepsis until proven otherwise (CRP, PCT, WCC, ITR).

High post-operative fever may be associated with marked tachycardia, and an increase in VO2 (11% increase in VO2 per 1oC increase in temperature).

Regular paracetamol (single dose 30 mg/kg post-op) to keep core temperature <37.5oC. If the temperature is >39oC despite paracetamol and the child is still paralysed, consider using cool peritoneal dialysis (1.5% solution at room temperature in 30 minutes cycles, each of 10 ml/kg) or surface cooling to normothermia, using a cooling blanket.


HAEMORRHAGE

Causes:

  • Thrombocytopenia
  • Poor platelet function
  • Dilution or consumption of clotting factors
  • Residual heparin (usually in the first 4 hours post-op)
  • Surgical problem

 

Signs:

  • Losses from chest drains remain bright red and increase in amount or fail to decrease normally
  • Tamponade
  • Hypoventilation and/or poor unilateral chest movement; increasing abdominal distension.

 

Investigation and management:

  • Notify surgeon early
  • Measure Hb of chest drain fluid
  • Repeat CXR if suspect tamponade or pneumothorax
  • Check ACT, TEG, coagulation and platelets
  • Give protamine 0.5 mg/kg IV and repeat ACT
  • Give platelets 10 ml/kg; give FFP 10 ml/kg if ACT, PT or APTT remain prolonged despite protamine; give cryoprecipitate if fibrinogen low; consider giving aprotinin if major bleeding persists despite the above
  • Urgent echo if tamponade is suspected
  • If aspirin stopped within 4 days of surgery, give DDAVP if post-op bleeding is a problem

HYPERTENSION

Common after repair of coarctation beyond the newborn period and after heart transplant. Other causes are pain, awareness, fits, full bladder, hypercarbia, vasoconstriction.

  • Examine chest, abdomen, pupils and fontanelle
  • Check blood gases and glucose
  • Give a morphine bolus and reassess
  • Give a midazolam bolus and reassess
  • Start infusion of sodium-nitroprusside (SNP): start with 0.1 mcg/kg/min and increase gradually to 2-3 mcg/kg/min if required (beware of cyanide toxicity and methaemoglobinaemia, especially rising lactate)
  • In a child >1 year of age, if HR >100 and still hypertensive, give an IV beta blocker (esmolol) – cave: negative inotropic effect – or alpha blocker (phentolamine)
  • Convert to bolus drugs when stable (atenolol, phenoxybenzamine, captopril)
  • Avoid giving a calcium channel blocker plus a beta blocker

HYPOTENSION

Causes:

  • Hypovolaemia
  • Low cardiac output
  • Excessive peripheral vasodilatation in the face of inadequate or limited cardiac output; has the child received a bolus of vasodilator (intermittently blocked CVC, sudden increase in flow of other fluid through the same line as the vasodilator)
  • Anaphylaxis
  • Low-resistance pathway from the aorta (e.g. central shunt, MAPCAs, AV fistula)

 

Management:

  • Exclude all the causes of inadequate cardiac output
  • If hypotension is profound, raise the legs
  • Give a fluid bolus 10 ml/kg and repeat if necessary (monitor RAP/LAP, may need >10 mmHg in the early postoperative phase)
  • If MAP <25 mmHg in a neonate or <40 mmHg in an older child, start external cardiac massage. Notify the cardiac surgeon
  • Give adrenaline bolus: 0.1 ml/kg of 1:10.000; repeat if necessary and start an adrenaline infusion
  • If there is aorto-pulmonary runoff and a high saturation, reduce the FiO2 to 0.21, increase PaCO2 to 45-55 mmHg and Hb to 140

HYPOVENTILATION

Cardinal sign:

  • Rising PaCO2

 

Causes:

  • Drugs
  • Brain injury in theatre or post-operative
  • Tracheal secretions
  • Atelectasis
  • Pneumothorax
  • Pulmonary oedema or chest wall oedema
  • Large leak around ETT or in ventilator circuit
  • Changed ventilator settings
  • Gas in stomach or recently started PD
  • Muscle relaxant ceased (reduced chest wall compliance)

 

Signs:

  • Tachycardia and sweating
  • Falling saturation and rising PaCO2
  • Rising PA pressure
  • BP may rise (hypercarbia) or fall (impaired myocardial performance)

 

Management:

  • Examine chest and abdomen
  • Blood gas, hand-ventilate, listen to chest, suction ETT yourself
  • Obtain CXR
  • Check ETT and ventilator circuit for leaks
  • Check ventilator settings, increase ventilation or change ventilation mode if necessary
  • Aspirate NG tube
  • Drain ascites
  • Hand ventilate and suction with saline for atelectasis.

HYPOXAEMIA

Falling PaO2 or falling saturation.

Causes:

  • Any of the causes of hypoventilation
  • Right-to-left shunt: intracardiac or intrapulmonary
  • Parenchymal lung disease
  • Pulmonary oedema
  • Atelectasis
  • Pneumonia
  • Intrapulmonary haemorrhage

 

Investigation:

  • Is it real? If SpO2 falling, rapidly check the oximeter pulse wave, try the probe on yourself, change probe site
  • Take a blood gas sample immediately (noting the oximeter reading at the time) and monitor the patient closely for signs of cyanosis, hypotension and low cardiac output
  • Examine the chest. Manually ventilate and suction the trachea yourself
  • CXR
  • Investigate hypoventilation if PaCO2 raised. Take blood from LA and arterial lines and measure saturation to look for intracardiac right-to-left shunt
  • Bubble-contrast echocardiograph to locate intracardiac R-to-L shunt

PULMONARY HYPERTENSION

Usually occurs on a background of high pulmonary blood flow or left heart obstruction. Acute rises in PA pressure usually occur in response to hypoxia, hypercarbia, acidosis or handling but may also occur with transfusion of platelets or FFP or infusion of protamine. It can also occur without stimulus or warning.

High risk patients:

  • Keep well sedated & paralysed for first 4-8 hours. Fentanyl 1-2 mcg/kg pre suction and handling
  • Minimise handling
  • Aim for PaCO2 30-35, PaO2 120 mmHg, pH >7.4
  • Dobutamine plus milrinone is a good combination for systemic cardiac output and pulmonary vasodilation
  • Start NO (10 ppm) if increasing PA pressure causes tachycardia, hypotension, desaturation and signs of poor cardiac output or if mean PA pressure > half mean systemic BP
  • In patients without a PA line, pulmonary hypertension may be indicated by acute desaturation, decreased lung compliance, wheeze and hypotension.

ETT SUCTION

Tracheal stimulation can cause severe increases in PA pressure.

When suction is considered necessary, pre-medicate with fentanyl (1-2 mcg/kg) to ablate airway responsiveness. Suction the ETT cautiously and quickly.


SEPSIS

Increase in temperature (infection); decrease in cardiac output; increase in pulmonary artery pressure; warm skin, bounding pulses and reduced aortic diastolic pressure; oliguria; decline in conscious state; increasing lactate and metabolic acidosis; unexplained increase or decrease in blood glucose; increased CRP or PCT; decreased platelet count.

 

Investigation:

  • Examine the child for evidence that sepsis is present and for a septic focus: wound, lungs, cannulation sites (including signs of caval thrombosis), meningitis, endocarditis (new murmurs, skin infarcts, fundi, splenomegaly, urinalysis), ears, paranasal sinuses (especially with prolonged nasal intubation), bones, joints, urinary tract
  • Repeat FBE and CRP
  • Blood cultures: percutaneous, arterial line and central venous cannula. Do not culture arterial line tip
  • Consider formal non-bronchoscopic bronchoalveolar lavage if there are lung opacities on chest x-ray
  • Culture drain fluid. Culture any pus and send a pus smear on a microscope slide for Gram stain. Culture urine from suprapubic aspirate or catheter (not from a bag specimen)
  • Think of fungal sepsis: examine skin, mouth, larynx, fundi
  • Arrange ultrasound examination of kidneys.

 

Management:

  • Consider antibiotics (choice depends on probable organism: flucloxacillin (or vancomycin) plus gentamicin usually appropriate when the organism is unknown; monitor drug levels carefully; add oral nystatin).
  • Review culture results and CRP daily. Cease antibiotics after 48 hours if culture results remain negative and clinical evidence of sepsis gone.
  • Otherwise, continue antibiotics for 5 days (longer for severe and intractable infections such as mediastinitis and endocarditis)

SWEATING

Causes:

  • Pain, awareness, high PaCO2 (inadequate alveolar ventilation), hypovolaemia, low cardiac output, hypoglycaemia, heart failure, drug withdrawal.

Assessment:

  • Examine child (hydration, vein status, response to voice, passive movement and tracheal suction; other signs of sympathetic stimulation (such as pupils)
  • Review chart (change in pressures, HR, respiratory rate, temperature and ventilation)

 

Management:

  • Hand-ventilate and suction trachea
  • Check gas and glucose
  • Trial of fluid bolus 5-10 ml/kg
  • Trial of morphine bolus 50 mcg/kg, repeat if necessary
  • Try IV midazolam

TACHYCARDIA

An important sign that something is wrong.

You must identify the cause: arrhythmia, low cardiac output, pulmonary hypertensive crisis, hypoventilation or hypoxaemia, hypoglycaemia, central (fits, fever, pain or full bladder), drugs (pancuronium or inotropes), anatomy (e.g. small LV).

Examine the child: chest, abdomen, pupils, fontanelle.

Check the heart pressures, temp, urine output, ECG, atrial electrogram.

Check blood gases and electrolytes and glucose.

Echo.


TACHYPNOEA

If the respiratory rate rises progressively, a cause must be found.

Causes:

  • Pain or other distress
  • Restrictive lung disease (pulmonary oedema, atelectasis, pulmonary haemorrhage, pneumonia)
  • Pneumothorax or pleural effusion
  • Fever; sepsis
  • Metabolic acidosis
  • Pulmonary hypertension
  • Neuromuscular weakness (residual relaxants or other cause)

 

Investigation:

  • Examine (chest, abdomen, pupils, muscle power, autonomic signs of distress, response to voice, passive limb movement and tracheal suction)
  • Review chart (PA and LA pressure, BP, temperature, urine output)
  • Blood gas; hand-ventilate and personally suction trachea
  • Repeat CXR
  • CRP; platelet count; culture blood, urine, tracheal aspirate and drain fluid

 

Management:

  • Consider trial bolus of morphine or midazolam
  • Observe pattern of ventilation (shallow tachypnoea versus hyperpnoea; coordination with the ventilator)
  • Increase ventilation (mandatory rate or support pressure) if muscle weakness present

VENTILATOR DEPENDENCE

A high pCO2 may be appropriate if there is metabolic alkalosis caused by hypochloraemia from diuretic use.

 

Causes:

Respiratory depression.

Drugs or encephalopathy. Irregular, shallow breaths; high PaCO2; sleepy; may be other evidence of encephalopathy (e.g. fits); often prolonged or high-dose morphine or midazolam infusion; wait (days) for sedatives to be excreted. Neurological examination; check fontanelle; cerebral ultrasound (insensitive) ± CT scan (wait several days)

Phrenic nerve palsy. Unilateral or (rarely) bilateral; often transient (weeks); no ipsilateral inspiratory movement of abdomen. Diagnosis: ultrasound and / or X-ray image intensifier (screening) – both give false negatives. Plication should be considered early in a small infant with unilateral palsy who has failed extubation, and after a week of failed attempts in an older child (especially in palliative repair).

 

Neuromuscular weakness. Residual muscle relaxants; previous period of poor cardiac output; impaired liver or kidney function; oedema or ascites fluid store relaxant drugs; prolonged or high dose relaxants (especially if doses given before child moves). Diagnosis: train of four. Management: Wait until movement returns (can lift legs off bed) before giving neostigmine-atropine; don’t rely on neostigmine-atropine to reverse a profoundly paralysed child; ICU myopathy (prolonged IPPV + relaxants ± steroids ± sepsis; severely ill with normal train of 4); EMG and consult neurologists if suspected; pressure support ventilation + good nutrition + wait (avoid steroids and muscle relaxants).

Pleural effusion. If drainage required (after discussion), send fluid for culture, cell count, triglycerides. Triglyceride >1.1 mmol/L (if fed) and cells >1000/μL with lymphocytes >80% suggests chylothorax; echo and ultrasound (exclude SVC obstruction), change to monogen, or stop feeds and give TPN (77% respond at a mean of 12 days, 45 days if MCT given); if no response by 14 days, consider trial of octreotide 5 mcg/kg/hr IV (see chylothorax)

Tracheobronchomalacia. Wheeze, prolonged expiration, and active use of expiratory muscles; gas trapping clinically and on CXR; bronchogram and/or bronchoscopy; use high CPAP (10-15 cmH2O); wean CPAP using deep sedation (morphine ± chloral ± diazepam ± chlorpromazine); anticipate days to weeks of repeated attempts to wean.

Residual cardiac abnormality. Left-to-right shunt; obstruction in left heart or pulmonary veins; left-sided AV valve dysfunction; hypoplastic LV; PA stenosis or distortion in BCPS or Fontan patients. Cardiac catheter ± re-operation.


References:

[1] Pediatr Cardiol. 2013 Feb;34(2):341-7. McDonald ET AL: Impact of 22q11.2 deletion on the postoperative course of children after cardiac surgery


All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Diabetes Insipidus

Cite this article as:
Tessa Davis. Diabetes Insipidus, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3030

A 5-year-old girl is on the ward following resection of a craniopharyngioma.  The nurses call you because her urine output has increased dramatically over the last few hours.  You check her sodium and it’s 150.

Is your brain hurting just thinking about it?

 

Bottom Line

  • Suspect diabetes insipidus if there is polyuria, polydipsia in the presence of a high serum Na and low urinary Na
  • Manage with vasopressin and appropriate hydration
  • Watch for hyponatraemia following the commencement of treatment
  • This can be a life-long condition and ease of management will depend on whether the patient has an intact thirst centre

 

What is DI?

In diabetes insipidus, the body produces no (or very little) anti-diuretic hormone.  This means that the patient cannot concentrate the urine and ends up with dehydration and electrolyte imbalance.

 

What causes it?

ADH is a hormone that regulated fluids and sodium retention.

In cranial DI the pituitary does not properly signal for the release of ADH when needed (i.e. when dehydrated) and so there is no ADH to instigate fluid retention.  Due to dehydration, the body then tries to retain sodium.

Cranial DI causes include: surgery (trans-sphenoidal); traumatic brain injury; idiopathic; autoimmune; tumours (suprasellar, lung, breast, lymphoma, leukaemia); hypoxic brain injury; brain stem death; profound hyponatraemia; radiotherapy; drugs – amiodarone, lithium; inflammatory conditions – sickle cell, sarcoid, Wegener’s, histiocytosis X; infections – TB, abscess, encephalitis, meningitis; vascular disease – CVA, SAH, Sheehan’s syndrome.

In nephrogenic DI, ADH is being produced but the kidneys are not responding to it.   This is a different condition and will not be dealt with in this post.

How can I recognise it?

The symptoms of DI can include polyuria, polydipsia and dehydration or weight loss.

In some patients, the thirst centre is not intact and so they will no have symptoms of polydipsia.

 

Biochemical abnormalities

  • Urine output >4ml/kg/hr for 2 hours
  • Serum Na>145
  • Osmolality: serum >295 mOsmol/kg H2O And urine <450 mOsmol/kg H2O
  • Weight loss of >5%

Additional studies such as plasma ADH, urine specific gravity and a water deprivation test can assist with diagnosis. Urine specific gravity is a particularly handy test as it can be done there and then without going to the lab.

 

  • Water deprivation test

  • This test aims to check if the kidneys can concentrate urine in the presence of ADH
  • The patient is fluid deprived for 8 hours or until 5% of body weight is lost
  • Measure plasma osmolality every 4 hours. and urine volume and osmolality every 2 hours.
  • After the 8 hours, the patient is given IM vasopressin unless there is a clear indication of DI prior to this
  • urine and serum osmolality are checked over the following 4 hours
  • In cranial DI the urine osmolality will initially be low (<300 mmol/kg) and after vasopressin it will rise to >800
  • In nephrogenic DI giving the vasopressin will not make any difference to the osmolality

 

What is the treatment?

Management in ICU

If the patient has a high serum Na, high urine output and low urine osmolality in the post-op period, treatment should be considered (usually in discussion with the endocrine team).

Treatment is based around a combination of rehydration and vasopressin.

Vasopressin can be given IN, orally or IV.

The aim is to keep the Na at 135-140.  If the Na>150 the amount of vasopressin should be increased.

The other aim is to maintain hydration and a normal urine output (target 2-3 mls/kg/hr).

Be careful of hyponatraemia from over-treatment and also of bringing the sodium down too fast (this can cause cerebral oedema).

If the Na<135 then either stop the vasopressin or give some hypertonic saline.  Consider fluid restriction or frusemide if the Na continues to fall and is <130.  These patients can have seizures due to hyponatraemia post commencement of vasopressin if it’s not tightly monitored.

 

Calculating sodium replacement

(Target sodium – current sodium) x 0.6 x weight = mmol Na required to reach target

 

Sodium content of fluids

[wpsm_comparison_table id=”9″ class=”center-table-align”]

Ongoing DI management

Daily serum electrolytes and osmolality, and daily urine osmolality are required until stable.

Make sure sodium is above 145 mmol/L prior to administration of vasopressin.

Should have 1-2 hrs of diuresis (greater than 4ml/kg/hour) prior to administration of next dose to avoid hyponatraemia.

Patients should be weighed daily and keep a strict fluid balance chart.

 

What is cerebral salt wasting (CSW)?

This is rare but can occur following cranial surgery.

It causes polyuria and dehydration but with high urinary sodium (i.e. hyponatraemic dehydration).

The urine:serum osmolality ratio will be greater than 1.

CSW is managed with fluid replacement and salt replacement of urinary sodium losses (as guided by the serum sodium).

What’s the prognosis?

DI can be transient or permanent.

Pratheesh et al (2013) did a retrospective analysis of 102 children who were status post removal of craniopharyngioma (and compared them to adults)

  • DI was more common post-op in children than adults (80% v 63%)
  • Triphasic response (fluctuating serum sodium levels) was more common in children
  • Children had a higher incidence of permanent DI (55.6%)

 

Selected references

Diabetes insipidus, Royal Children’s Hospital (Melbourne)

Diabetes insipidus, Medscape

Pratheesh R, Swallow DM, Rajaratnam S, Jacob KS, Chacko G, Joseph M, et al. Incidence, predictors and early post-operative course of diabetes insipidus in paediatric craniopharygioma: a comparison with adults. Childs Nerv Syst. 2013;29(6):941-9.

How to do the water deprivation test