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Address for Correspondence
Anil Sachdev
Department o Pediatrics, Institute o Child HealthSir Ganga Ram Hospital, Rajindra Nagar, New Delhi-110 060
Email: [email protected] Website: www.piccindia.org
THE
INDIA
NACA
DEMYOFP
EDIAT
RIC
S
Message from the Secretary
The IntensivistNewsletterofIntensive Care ChapterIndian Academy of Pediatrics
Dear Colleagues,
Happy Diwali!
Currently, India, in particular Mumbai and Delhi, are having an outbreak o Dengue
Fever (DF) with several deaths being reported. An increasing number o cases
require close monitoring due to risk o complications. This outline reviews several
critical points in the basic evaluation and management o children having Dengue.
The World Health Organization denes Dengue Hemorrhagic Fever (DHF) when
Dengue illness is accompanied by positive tourniquet test, thrombocytopenia
(less than 100,000/mm3) and hem concentration hematocrit >20% above baseline
value.
DF is an acute illness characterized by ever, retro-orbital headache, severe myalgia,
and occasionally a rash, lasting rom 5 to 7 days. During seasonal periods o Dengue
in India (July to November), any inant or child presenting with ever and such other
symptoms should be evaluated or Dengue. These cases should be thoroughly
examined and closely ollowed with vital signs. Complete blood cell count (CBC)
and initial Dengue antibody titers should be taken. A small percentage o patients
with Dengue may progress to more severe orms o the disease, with hemorrhagic
maniestations and/or shock.
I would request all o you to report all cases to local authorities, so they may take
preventive measures. It also gives me great pleasure to inorm you that all the
preparations or the Annual conerence are complete. Dr. Santosh Soan and his team
are working hard to make Pediatric Intensive Care annual conerence a grand success.
I would request all o you to attend in large numbers.In Executive Board meeting to be held at Mangalore, on 17th Nov. 2012 we are
planning to pass a resolution to have a National CME, and 4 zonal CMEs, so we can
have more activities throughout year. I am very keen to host an Asian conerence or
International conerence o Pediatric Intensive Care. I would request all seniors to
guide us in this regard.
We must congratulate Dr Sunit Singhi who is a senior member o IAP-Pediatric
Intensive Care Chapter or completing 7 years as Asian representative in World
Federation o Pediatric Intensive and Critical Care Societies (WFIPICS)
I was really happy to see the last issue o the newsletter with some good new ideas.
You will agree with me that Dr. Anil Sachdev, the editor is doing a wonderul job.
Friends, please come orward and be an active member o the Intensive Care Chapter
and contribute in its growth and various activities especially Basic Pediatric CriticalCare Course. Only with your participation and support can we grow aster.
Yours truly,
Dr Kamlesh Shrivastava
Secretary
THE
INDIA
NACA
DEMYOFP
EDIAT
RIC
S
Conten
ts
Intensive Care Chapter
The IntensivistJuly-September, 2012
Editor
Anil Sachdev
Office Bearers
ChairpersonRajiv Uttam
Chairperson Elect
Santosh Soans
Secretary
Kamlesh Srivastava
Treasurer
Kundan Mittal
Immediate Past Chairperson
Nirmal Choraria
Executive Members
DP NakateKarunakara BP
Rashna Dass Hazarika
Sanjay Bana
Vikas Taneja
Message rom the Secretary ............................
Review Article
Adaptive Support Ventilation ............................
Hypertension in PICU..........................................
Journal Scan
Journal Scan ..........................................................
Case Report
An Unusual Case o Pneumonia
-----Lipoid pneumonia ......................................
Drug Review
Dexmedetomidine .............................................
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Nirmal ChorariaPast Chairman
Kundan MittalTreasurer
Anil SachdevEditor
Santosh T SoanChairman Elect
Rajiv UttamChairman Elect
Kamlesh SrivastavaSecretary
Intensive Care Chapter Indian Academy of Pediatrics 2012
Office BearersOffice Bearers
Karunakara [email protected]
Rashna Dass [email protected]
Vikas [email protected]
Sanjay [email protected]
Executive Members
AGM - Notice
Notice is hereby given or a General Body Meeting o IAP- Intensive Care Chapter to discuss various issues, as
stated under:
Venue : Dr. T MA PAI International Convention
Centre, Mangalore
Date : Saturday, 17th November, 2012
Time : 5.00 pm onwards
Agenda
1. Opening remark by Chairperson Dr. Rajeev Uttam.
2. To read and conrm the minutes o last AGM in 2011.
3. Business arising out o minutes
4. To adopt the annual report read by Secretary.
5. To adopt the audited account or year 2011- 2012 and present the budget proposal or the year 2012-2013.
6. To discuss about National CME and Zonal CMEs.
7. To decide about next annual conerence.
8. To decide about ormation o IAP Mahrashtra chapter.
9. Welcome new ocer bearers or year 2012.
10. Any other issue with the permission o chair.
Dr Kamlesh Shrivastava
Secretary
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Review Article
Adaptive Support VentilationRakesh Patel
Critical Care Fellow, Department o Pediatrics, Institute o Child Health, Sir Ganga Ram, Rajinder Nagar, New Delhi 110060
Introduction
Adaptive support ventilation (ASV) is a newly developed
closed loop dual control mode, using measured
dynamic compliance and time constant, with an
automated adjustment o tidal volume and respiratory
rate combined to meet the preset minute ventilation.
ASV is an advanced mode o ventilation, evolved rom
mandatory minute ventilation (MMV) implemented
with adaptive pressure control. This mode automatically
selects appropriate tidal volume (Vt) and requency ()or mandatory breaths and appropriate Vt or supported
breaths depending upon mechanics o respiration and
target minute ventilation (MV).
It was rst described by Laubscher et al in 1994 (1, 2)
and became commercially available in 1998 (Hamilton
Galileo ventilator, Hamilton Medical AG)
Mechanism
ASV is a pressure control mode and provides intermittent
mandatory breaths.
Adaptive support ventilation controls breaths in
optimal (adaptive) manner which helps minimizing the
mechanical work o breathing. The machine selects Vt
and requency or set percentage o MV set.
The ventilator calculates normal required MV based on
patients ideal weight (IBW) and estimated dead space.
The clinician sets target percentage o MV that the
ventilator will support: more than 100% MV i increased
requirement, and less than 100% MV while weaning. The
ventilator initially delivers test breaths (rst 5 breaths) in
which it measures the expiratory time constant (RCe) or
respiratory system and then uses it with estimated deadspace and normal MV to calculate breathing requency
and Vt. The underlying algorithm selects ventilatory
parameters in order to minimize work o breathing
(WOB) based on the principle that or each given level o
alveolar ventilation, there is a most eective combination
o Vt and respiratory rate while limiting peak inspiratory
pressures (PIP) (3-5).
The parameter RCe, obtained rom simplied analysis
o the expiratory fow-volume curve (6) is a measure o
the actual status o the passive respiratory mechanics o
the patient. A low RCe, typical o restrictive respiratory
disease i.e., sti lungs, results in the selection o a
ventilatory pattern with low TV and high . On the other
hand, a long RCe, typical o airway obstruction and/or
lung emphysema, results in the selection o a ventilatory
pattern with higher Vt and low . The parameter RCe
is also used to calculate the inspiratory time (Ti) o
mandatory breaths: Ti will be longer when RCe is short
(restrictive disease), and shorter when RCe is long
(obstructive disease), thus allowing a longer expiratory
time when exhalation is slower and intrinsic PEEP is more
likely to develop. The ventilator continuously monitors
the respiratory system mechanics and adjusts its settings
accordingly.
Depending on the patients spontaneous respiratory
rate, ASV can work as pressure controlled ventilation
(PCV), i there is no spontaneous breathing; as pressure
synchronize intermittent mandatory ventilation (SIMV),
when the patients respiratory rate is less than the target;
or as pressure support ventilation (PSV), i the patients
respiratory rate is greater than the target. ASV recognizes
spontaneous breathing and automatically switches
between mandatory pressure-controlled breaths and
spontaneous pressure-supported breaths in patients.
The pressure level is then adapted to attain the target Vt
(within limits imposed by pressure alarms). Cycling-o
criteria is fow based in the case o assisted ventilation or
time based or mandatory inspiration.
The ventilator adjusts its breaths to avoid air trapping by
allowing enough time to exhale, to avoid hypoventilation
by delivering Vt greater than the dead space, and to
avoid volutrauma by avoiding large Vt Table 1).
The ventilator controls pressure or volume during
inspiration, but not simultaneously. It may switch rom
one control variable to another during a single breathor between breaths, which is designated as dual control.
Dual control is designed to assure patient-ventilator
synchrony by allowing as much fow as the patient
demands, while attempting to guarantee a minimum Vt.
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Table 1: Inherent advantages o adaptive support ventilation
Maintain at least pre-set minute ventilation
Take spontaneous breathing into account
Prevent tachypnea
Prevent Auto PEEP
Prevent excessive dead space ventilation
Fully ventilate in apnoea or low drive
Settings
The operator needs to add ollowing inputs into the machine:
Patient height( to calculate ideal body weight)
Gender
% of normal predicted MV goal
FiO2
PEEP
Figure 1: The ASV screen as implemented on GALILEO,
Hamilton. The ASV target graphic screen shows: mode; minute
ventilation%; PEEP; raction o inspiratory oxygen concentration;
minute volume curve target volume; saety boundary; actual
tidal volume/ respiratory requency combination; and theoptimal tidal volume/respiratory requency combination with
which the patient will be ventilated.
Clinical application
ASV is intended as a sole mode o ventilation rom initial
support to weaning.
Theoretically it oers:
automatic selection of ventilator settings
automatic adaptation to changing patient lung
mechanics less need for human manipulation of the machine
improves synchrony and automatic weaning
Clinical evidence
Automatically adjusted settings
In passive and paralysed patients, ASV selects dierent
combinations o tidal volume respiratory rate based
upon respiratory mechanics o the patient (8-10). While
in actively breathing patient no dierence was ound
in ventilator setting chosen by ASV or dierent clinical
scenario and lung physiology (8).
Patient ventilator interaction
Tassaux et al (11) conducted a crossover prospective
study comparing SIMV-PS with ASV in the early weaning
period o ten patients with acute respiratory ailure
o diverse causes. The results demonstrated that at a
similar level o MV, patients receiving ASV had a lowerlevel o respiratory drive (P0.1), lower WOB (based on
EMG respiratory muscle activity), and improved patient-
ventilator interactions, compared to SIMV-PS. Another
study also demonstrated improved patient ventilator
interaction in patients o respiratory ailure with ASV as
compared to SIMV-PS mode (12).
Duration o mechanical ventilation
Two trials suggest ASV may decrease time on mechanical
ventilation (13, 14).
Cassina et al (15) conducted a prospective observational
study o a cohort o 155 consecutive patients ater
ast-track cardiac surgery and confirmed the saety
aspects o ASV. One hundred thirty-our patients (86%)
were extubated within 6 hours. No reintubation due to
respiratory ailure was required. This ventilation mode
allowed rapid extubation in suitable patients and may
acilitate postoperative respiratory management.
Manual adjustments in ventilator
Petter et al (16) conducted a randomized controlled
trial compared ASV with standard protocol, ASV led to
ewer ventilatory adjustments but achieved similar postsurgical weaning outcomes.
Sulzer et al (14) reported reduced duration o tracheal
intubation, ewer arterial blood gas analysis and less
requent changes in ventilatory settings in post cardiac
surgery patients on ASV mode.
Weaning in chronic lung disease
ASV appropriately decreased ventilatory support in
patients with chronic respiratory ailure who tolerated
a conventional weaning trial, suggesting that ASV may
acilitate respiratory weaning (17).
Weaning o chronic obstructive pulmonary disease
patients with ASV compared to PSV does not decrease
overall length o mechanical ventilation, ICU stay and
mortality (18). However, in patients successully weaned,
the duration o weaning was signicantly shorter
with ASV. Hence, in patients with a more complicated
weaning, ASV might provide considerable benets and
also reduce sta workload, as it reduces manipulation
and time spent in adjusting the ventilator.
In a step-down centre or chronically ventilated patients,
Linton et al (19) conducted weaning trials using the ASV
mode and demonstrated the economy o automated
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weaning without the need or respiratory therapists or
continuous attendance by intensivists. Twenty seven
patients were placed on ASV at 90% o target minute
ventilation on arrival, and were reduced by 10% weekly
to 60% o target minute ventilation, i tolerated by the
patients. Twelve patients were successully weaned rom
the ventilator within 2 weeks to 2 months o admission
in the first twelve months ollowing establishment o the
acility.
Decrease work o breathing
ASV and work o breathing was analysed in 22 patients
with respiratory ailure. Patients were compared or WOB
in terms o PTP (Pressure time product) and P0.1 (airway
occlusion pressure at 0.1 second o inspiratory fow)
at various MV percentages. It was ound that minimal
PTP and P0.1 were ound at higher percentage (40%)
o ASV target. (ASV target was dened as appearance
o mandatory breaths at that percentage o MV). The
authors proposed an incremental % MV trial untilmandatory breaths appeared as a suitable approach
to dene the range that suciently reduce work o
breathing (20).
Other benefts
A notable nding in one study was the reduction in
apnoea and high-pressure alarms in the ASV group that
the authors suggested could potentially improve the
working environment o nurses (21).
In variety o lung disease
Belliato et al (22) tested ASV in patients with normal lungsand in those with restrictive lungs, in COPD patients and
in a physical lung model, with a normal level o and an
increased minute ventilation. In postoperative patients
with normal lungs, the ASV selected a ventilatory pattern
close to the physiological one. In COPD patients, the
ASV selected a high expiratory time pattern, and in
restrictive lungs, a reduced tidal volume pattern. In the
model, the selection was similar. In the hyperventilation
test, the ASV chose a balanced increase in both Vt and
respiratory rate. The authors explained that ASV would
select an adequate ventilatory pattern or a variety o
lung conditions.
Drawbacks
ASV delivers unsae respiratory rate- Vt combinations in
patients with acute ling injury(23).
Arnal et al(8) observed that almost 20% o acute lung
injury/acute respiratory distress patients could not be
ventilated with this mode due to an airway pressure o
more than 35 cmH2O, with an increased risk or ventilator
induced lung injury (24,25). In another study on cardiac
surgery patients, recently published by Dongelmans
et al (26) the Vt was more than 8 ml/kg in a substantial
number o patients, underlining a possible risk or
ventilator induced lung injury.
Though ASV provides minimum Vt, it cannot guarantee
a constant volume. One concern is that the ventilator
cannot distinguish between improved pulmonary
compliance and increased patient eort (27).
To explain, the underlying problem is that ASV is not
based on transpulmonary pressure (PL), and thusrespiratory mechanics. PL equals the dierence between
the alveolar pressure and the pleural pressure (Ppl), and
determines the degree o lung distension. In patients
with a very active drive (due to ever, pain, anxiety,
delirium or distress induced by underlying disease),
the Ppl becomes more negative and the PL increases,
while the Paw remains constant or decreased. The
ventilator could mistakenly consider this situation as
an improvement o the patients compliance, and thus
reduce the supportive pressure, leading to insucient
ventilation support. Weaning time would be prolonged
without adequate management.Overall, there are inconsistent ndings with ASV that
might be attributed to the dierent patient populations
studied. Moreover, in short-time ventilated postoperative
patients, a more advanced closed-loop controlled mode
might not necessarily prevail over conventional modes.
The underlying algorithms probably do not ully
apply to the individual patients and dynamic changes
o underlying condition. For instance, although a
substantial eort has been made in order to calculate
dead space, the resulting calculations remain estimates
not necessarily refecting the individual truth (28).
Majority o clinical studies o ASV have been conducted
in cardiothoracic patients, easibility o ASV in dierent
group o patients is yet to be studied extensively. The
eect o ASV on mortality has not yet been studied.
Conclusions
The ASV mode is a newly developed dual control
ventilator mode, and has the advantages o lung
protection, the use o ewer medical personnel resources
and acility, the weaning o both acutely and chronically
ventilated patients. Despite the fexibility o this mode,a clear clinical evidence o superiority over conventional
modes remains to be demonstrated; moreover a caveat
or the risk o high tidal volume with increased risk or
ventilator induced lung injury in patients with acute
lung injury/ acute respiratory distress syndrome must be
careully considered. ASV and other dual-control adaptive
pressure control modes cannot distinguish improving
lung mechanics rom a deranged ventilatory demand,
which might lead to some patients being distressed or
prolonging the weaning process without recognition and
adequate management. Large randomized controlled
studies o the ASV are needed to clariy the role o ASV
in clinical practice.
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Reerences
1. Laubscher TP, Frutiger A, Fanconi S, et al. Automatic
selection o tidal volume, respiratory requency and
minute ventilation in intubated ICU patients as start
up procedure or closed-loop controlled ventilation.
Int J Clin Monit Comput 1994; 11:1930.
2. Laubscher TP, Heinrichs W, Weiler N, et al. An adaptive
lung ventilation controller. IEEE Trans Biomed Eng1994; 41:5159.
3. Otis AB. The work o breathing. Physiol Rev 1954;
34:449458.
4. Otis AB, Fenn WO, Rahn H. Mechanics o breathing in
man. J Appl Physiol 1950; 2:592607.
5. Mead J. The control o respiratory requency. Ann N Y
Acad Sci 1963; 109: 724729.
6. Brunner JX, Laubscher TP, Banner MJ, et al. A simple
method to measure total expiratory time constant
based on the passive expiratory fow volume curve.
Crit Care Med 1995; 23: 1117-1122.
7. Hamilton Medical AG. Adaptive Support VentilationUsers Guide. Switzerland: Hamilton Medical AG,
1999.
8. Arnal JM, Wysocki M, Naati C, et al. Automatic
selection o breathing pattern using adaptive
support ventilation. Intensive Care Med 2008; 34:75
81.
9. Campbell RS, Sinamban RP, Johannigman JA, et al.
Clinical evaluation o a new closed loop ventilation
mode: adaptive supportive ventilation (ASV). Crit
Care 1999; 3(S1):P83.
10. Belliato M, Palo A, Pasero D, et al. A. Evaluation o
adaptive support ventilation in paralysed patients
and in a physical lung model. Int J Arti Organs 2004;27:709716.
11. Tassaux D, Dalmas E, Gratadour P, et al. Patient
ventilator interactions during partial ventilatory
support: a preliminary study comparing the eects
o adaptive support ventilation with synchronized
intermittent mandatory ventilation plus inspiratory
pressure support. Crit Care Med 2002; 30:801807.
12. Forel JM, Roch A, Papazian L. Paralytics in critical
care: not always the bad guy. Curr Opin Crit Care
2009; 15:5966.
13. Gruber PC, Gomersall CD, Leung P, et al. Randomized
controlled trial comparing adaptive-supportventilation with pressure-regulated volume-
controlled ventilation with auto mode in weaning
patients ater cardiac surgery. Anesthesiology 2008;
109:8187.
14. Sulzer CF, Chiolero R, Chassot PG, et al. Adaptive
support ventilation or ast tracheal extubation ater
cardiac surgery: a randomized controlled study.
Anesthesiology 2001; 95:13391345.
15. Cassina T, Chiolero R, Mauri R, et al. Clinical experience
with adaptive support ventilation or ast-track
cardiac surgery. J Cardiothorac Vasc Anesth 2003; 17:
571-575.
16. Petter AH, Chiolro RL, Cassina T, et al. Automatic
respirator/weaning with adaptive support
ventilation: the eect on duration o endotracheal
intubation and patient management. Anesth Analg
2003; 97:17431750.
17. Linton DM, Potgieter PD, Davis S, et al. Automatic
weaning rom mechanical ventilation using an
adaptive lung ventilation controller. Chest 1994;
106:18431850
18. Kirakli C, Ozdemir I, Ucar ZZ, et al. Adaptive support
ventilation or aster weaning in COPD: a randomised
controlled trial. Eur Respir J 2011; 38:774780.
19. Linton DM, Renov G, Laair J, et al. Adaptive Support
Ventilation as the sole mode o ventilatory support
in chronically ventilated patients. Crit Care Resusc
2006; 8: 11-14.
20. Wu CP, Lin HI, Perng WC, et al. Correlation between
the % MinVol setting and work o breathing during
adaptive support ventilation in patients with
respiratory ailure. Respir Care 2010; 55:334341.
21. Petter A, Chiolero R, Cassina T, et al. Automaticrespirator weaning with adaptive support
ventilation: the eect on duration o endotracheal
intubation and patient management. Anesth Analg.
2003; 97: 17431750.
22. Belliato M, Palo A, Pasero D, et al. Evaluation o
adaptive support ventilation in paralysed patients
and in a physical lung model. Int J Arti Organs 2004;
27: 709-716.
23. Dongelmans DA, Paulus F, Veelo DP, et al. Adaptive
support ventilation may deliver unwanted
respiratory rate-tidal volume combinations in
patients with acute lung injury ventilated accordingto an open lung concept. Anesthesiology 2011;
114:11381143.
24. Ventilation with lower tidal volumes as compared
with traditional tidal volumes or acute lung injury
and the acute respiratory distress syndrome. The
Acute Respiratory Distress Syndrome Network. N
Engl J Med 2000; 342:1301 1308.
25. Ferguson ND, Frutos-Vivar F, Esteban A, et al. Airway
pressures, tidal volumes, and mortality in patients
with acute respiratory distress syndrome. Crit Care
Med 2005; 33:2130.
26. Dongelmans DA, Veelo DP, Bindels A, et al.
Determinants o tidal volumes with adaptive
support ventilation: a multicenter observational
study. Anesth Analg 2008; 107: 932937.
27. Branson RD, Chatburn RL. Controversies in the
critical care setting. Should adaptive pressure
control modes be utilized or virtually all patients
receiving mechanical ventilation? Respir Care 2007;
52: 478-485.
28. Brewer L, Orr J, Pace N. Anatomic dead space cannot
be predicted by body weight. Respir Care 2008;
53:885891.
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Review Article
Hypertension in PICUAshish Kumar Simalti
Critical Care Fellow, Department o Pediatrics, Institute o Child Health,
Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi 110060
A hypertensive emergency is a clinical diagnosis that is
appropriate when marked hypertension is associated
with acute target-organ damage; in this setting, lowering
o blood pressure (BP) is typically begun within hours
o diagnosis. For hypertensive urgency with no acute
target-organ damage, BP lowering may occur over hours
to days. The Fourth Report on the Diagnosis, Evaluation,
and Treatment o High Blood Pressure in Children and
Adolescents classied pediatric hypertension into various
stages (1) (Table 1). The Joint National Committee on
Detection, Evaluation, and Treatment o Hypertension,
JNC7, has labeled acute severe elevation o BP above
180/120mmHg (about 20mmHg above the Stage II
hypertension) as Hypertensive Crisis in adults (2). About
1% o all adults with a diagnosis o hypertension develop
hypertensive crisis, o which 76% are hypertensive
urgencies and 24% are hypertensive emergencies (3).
Similar data in children is not available (4). Although the
prevalence o primary hypertension has been increasing
at an alarming rate particularly in adolescents and
older children (5), the incidence o hypertensive crisis
is very uncommon in pediatric patients with primary
hypertension and its occurrence is more common inpediatric patients with secondary hypertension (6).
Etiology
The etiology o hypertension depends on patients age,
onset (acute versus chronic), and duration (intermittent/
episodic or persistent). For example, conditions like
coarctation o aorta, renal vein, or artery thrombosis
predominate in neonates. However, renal parenchymal
diseases, pregnancy, endocrine conditions, autoimmune
diseases, medications, and substance abuse are
important etiologies in older children and adolescents.Conditions like phaeochromocytoma can present
with episodic or sustained hypertension whereas
chronic glomerulonephritis has persistent/sustained
hypertension (Table 2). In adults, majority o the cases
o hypertensive crises are due to non adherence
to prescribed medication, drug overdose, sudden
withdrawal o antihypertensive medications, and so
orth. In comparison to adults, majority o pediatric
hypertensive crises are renal in origin (7).
Table 1: Denitions o normal and elevated blood pressure in
children
Normal blood pressure Systolic and diastolic blood
pressure below 90th centile
Pre-hypertension Systolic or diastolic blood pressure
above the 90th centile (or 120/80
mmHg), but below the 95th centile
Stage I hypertension Systolic or diastolic blood pressure
higher than or equal to the 95th
centile, but lower than the 99th
centile plus 5 mm Hg
Stage II hypertension Systolic or diastolic BP higher than
or equal to the 99th centile plus 5
mm Hg
Table 2: Causes o hypertension in children
Renal
Glomerulonephritis, Acute tubular necrosis, Pyelonephritis,
Hydronephrosis, Hemolytic-Uremic syndrome, Obstructive
uropathy, Congenital dysplastic kidneys, Multicystic kidneys,
Polycystic kidney disease, Renal artery stenosis, Renal vein
thrombosis, Wilms tumor, Diabetic nephropathy
Cardiovascular systemCoarctation o aorta, Takayasus arteritis, Moyamoya disease
Endocrine system
Cushings syndrome, Hyperthyroidism, Hyperparathyroidism,
Congenital adrenal hyperplasia Pheochromocytoma
Central nervous system
Raised intracranial pressure, Brain tumors, Intracranial
hemorrhage, Autonomic dysunction Neuroblastoma,
Encephalitis
Autoimmune disorders
Systemic lupus erythematosus, Polyarteritis nodosa,
Rheumatoid arthritis, Goodpastures disease Wegeners
Disease, Mixed connective tissue disorders
Medications, toxins, substance abuse
Corticosteroids, Tacrolimus, Cyclosporine, Erythropoietin,
Amphetamines, Oral contraceptives Anabolic steroids,
Phencyclidine, Vitamin D intoxication, Cocaine, Alcohol,
Smoking, Lead, thallium, mercury toxicity
Miscellaneous
Pain, Hypervolemia, Obesity, Umbilical artery cauterization,
Intrauterine growth retardation, Pregnancy, Hypercalcemia,
Drug withdrawal like opiates, blockers, Clonidine
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Pathophysiology and Pathogenesis
Blood pressure is a product o cardiac output and
systemic vascular resistance (SVR). Cardiac output is a
product o heart rate and stroke volume. In turn, stroke
volume is determined by preload, contractility, and ater-
load/SVR(8). The pathogenesis o hypertensive crisis is
multiactorial and actors that have been implicated
in the pathogenesis include fuid overload, sympatheticover activity, renin-angiotensin-aldosterone system
activation, oxidative stress, endothelial dysunction, and
infammation. There is a complex interaction between
all these actors and all or some actors occurring
simultaneously may be involved in the pathogenesis o
hypertensive crisis (6).
Autoregulation
Autoregulation is the ability o blood vessels to dilate or
constrict to maintain normal perusion. In normotensive
individuals, normal arteries can maintain relatively
normal fow rates over a wide range o mean arterialpressures, usually 60 to 150 mm Hg. Chronic elevations
o BP cause compensatory unctional and structural
changes in the arterial walls and shit the auto-regulatory
curve (pressure vs fow) to the right. This allows
hypertensive patients to maintain normal perusion and
to avoid excessive blood fow at higher levels o BP. When
the BP increases above the auto-regulatory threshold,
tissue damage occurs. The primary abnormality in
patients with hypertensive emergencies is altered auto-
regulatory capacity, particularly in the cerebral and
renal beds, which can deteriorate into rank arteritis and
ischemia. An understanding o autoregulation is criticalor therapy because the sudden lowering o BP into a
range that would otherwise be considered normal may
reduce it below the auto-regulatory capacity o the
hypertensive circulation and lead to inadequate tissue
perusion, ischemia, and/or inarction (9). Sensorineural
hearing is known to have occurred due to rapid reduction
o blood pressure (10).
Evaluation
Hypertensive emergency needs immediate attention.
The initial assessment should be directed towardsidentication o aected end organs and possible
causes. History taking and examination should be brie
and relevant (Table3). The diagnostic workup must be
individualized according to the history and physical
examination ndings (Table 4). Complicated diagnostic
tests and transport o patient to other departments or
evaluation should not be done until BP is adequately
controlled (11).
Table 3: Clinical eatures where hypertensive emergency must
be suspected (11)
Symptoms Signs
Headache Short stature, pedal edema, pallor
Dizziness Tachycardia, increased sweating, fushing
Excessive crying Moon ace, obesity
Epistaxis Absent or delayed emoral pulses,
Failure to thrive Abdominal bruit
Joint pain Retinal changes
Convulsions Neurological decit
Hemiplegia Personality changes
Altered sensorium
Visual disturbance
Table 4: Diagnostic workup in hypertensive emergency (11)
General Specic
Hemogram Ultrasound abdomen
Urine microscopic and routine Intravenous pyelography
Renal Function Test Echocardiography
Chest X-ray CT Scan
ECG Plasma Renin
Serum Electrolytes Urinary 17 ketosteroids
Vinyl mandellic acid
Serum catecholamines levels
Pharmacologic management hypertensive
emergency in PICU
When choosing pharmacological therapy, ast-
acting, intravenous, easily titratable antihypertensive
medications are generally used. According to Fourth
Report on the Diagnosis, Evaluation, and Treatment o
High Blood Pressure in Children and Adolescent, the
primary aim o antihypertensive treatment is to reduce
the blood pressure to
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9
decrease both aterload and preload. Advantageous
properties o this medication, and benet o its use,
are its short duration o action o 1 to 2 minutes and
its hal-lie o 3 to 4 minutes. This property also makes
the drug easy to titrate. However, abrupt cessation o
the inusion results in a rapid increase in blood pressure
(14). Because o its quick onset o action, invasive arterial
blood pressure monitoring is recommended. Sodium
nitroprusside increases intracranial pressure, which
would be disadvantageous in patients with hypertensive
encephalopathy or cerebrovascular accident. Sodium
nitroprusside may also lead to cyanide poisoning. It
contains 44% cyanide by weight that is released non-
enzymatically rom the parent drug and the amount
released is dependent on the dose. Inusions at rates o
greater than 4 g/kg/ min or 2 to 3 hours have led to
cyanide levels within the toxic range. This medication is
recommended or use only in patients who have normal
renal and hepatic unction and when other intravenous
antihypertensive medications are not available. I
higher inusions o sodium nitroprusside are needed,an inusion o thiosulate should be used to prevent the
accumulation o cyanide.
Labetalol
It is an intravenous non-selective -blocker that also
possesses 1-blocking eects and is commonly used
to treat hypertensive emergencies. It produces its
antihypertensive eect by decreasing the heart rate and
lowering systemic vascular resistance. This medication
can be given as an intravenous bolus or as a continuous
inusion. The hypotensive eects o labetalol begin within
2 to 5 minutes ater an intravenous bolus and peak at 5 to15 minutes. The eects can last or 2 to 4 hours. Because
this medication does not have pure -blocking eects,
the patients cardiac output is maintained. Labetalol
does reduce peripheral vascular resistance because o
its -blocking eects, and it does not reduce peripheral
blood fow (15). Clinicians should be aware o the possible
adverse eects associated with labetalol, especially
the development o sinoatrial/atrioventricular nodal
dysunction, such as heart block. Extra consideration
must also be taken or patients with a history o asthma,
because o the possible development o bronchospasm
due to the nonselective -receptor blockade.
Esmolol
Esmolol, an intravenous, cardio-selective -blocker,
has a rapid onset and a short duration o action, which
make titration easy. This medication lowers BP through a
decrease the rate and contractility o the heart through
the blockade o 1 receptors. Esmolol is given as an
initial 0.5 to 1.0 mg/kg intravenous loading dose over
1 minute and is ollowed by a continuous inusion. It is
an ideal agent or situations where the cardiac output,
heart rate, and blood pressure are increased, especially
when a patient is experiencing acute pulmonary edema,
diastolic dysunction, acute aortic dissection, and acute
postoperative hypertension. Caution should be used
when this medication is given to patients with asthma.
The American College o Cardiology and the American
Heart Association also concluded that esmolol may be
contraindicated in patients with decompensated heart
ailure and bradycardia (16).
Nitroglycerin
Intravenously administered nitroglycerin is a potent
vasodilator, and when used in high doses, arterial tone
is also aected (17). It reduces BP by reducing both
aterload and preload. These eects are undesirable in
patients with compromised renal and cerebral perusion.
It has an onset o action o 1 to 5 minutes and duration
o action o 5 to 10 minutes ater the continuous
inusion is discontinued. Although nitroglycerin has
pharmacokinetic properties similar to those o sodium
nitroprusside, it is not considered a rst-line agent orthe treatment o hypertensive emergencies, primarily
because o its side eects o refex tachycardia and
tachyphylaxis. Nitroglycerine is not as ecacious as
sodium nitroprusside. However, it may be used as
an adjunctive agent or hypertensive emergencies
associated with myocardial ischemia or pulmonary
edema.
Nicardipine
It is an intravenous dihydropyridine-derivative calcium
channel blocker and produces its antihypertensive eects
by vasodilation o coronary vasculature and relaxationo smooth muscle. This medication has high vascular
selectivity and strong cerebral and coronary vasodilatory
activity. It has an onset o action o 5 to 15 minutes and
duration o action o 4 to 6 hours while hal lie is 1 hour.
Due to these actors titration o dosage is more dicult.
The dosing o this medication is independent o weight,
which can be useul in most hypertensive emergencies,
especially in high adrenergic states (18).
Fenoldopam
It is a unique agent among the intravenous
antihypertensive medications. It is a dopamine D1-receptor agonist that was approved in 1997 or
hypertensive emergencies. This medication causes
peripheral vasodilation by acting upon peripheral
dopamine type 1 receptors. Fenoldopam also activates
dopaminergic receptors on the proximal and distal
tubules o the kidney, thereby inhibiting sodium
reabsorption, resulting in diuresis and natriuresis. It has
an onset o action o 5 minutes and duration o eect o
30 to 60 minutes. This medication improves creatinine
clearance, urine fow rates, and sodium excretion in
patients with and without normal kidney unction (19).
It is recommended in cases o acute pulmonary edema,
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10
diastolic dysunction, hypertensive encephalopathy,
acute renal ailure, and microangiopathic anemia. This
drug may cause hypersensitive reaction due to the
presence o sodium metabisulphate in the solution.
This medication should also be avoided in patients with
increased intraocular hypertension and glaucoma (20).
ClevidipineThe newest intravenous antihypertensive agent
approved or hypertensive emergencies is clevidipine.
This medication is a third-generation dihydropyridine
calcium channel blocker that inhibits L-type calcium
channels in a voltage-dependent manner. The BP
lowering is dose dependent and rapid, with a short
hal lie o 1 to 2 minutes, a quick onset o action o 2
to 4 minutes and a short duration o action o 5 to 15
minutes. These properties make this medication easy to
titrate. Clevidipine lowers systemic vascular resistance
and does not aect the venous capacitance vessels
or cardiac lling pressures. When compared withsodium nitroprusside, it has greater eects on arterial
vasodilatation and ewer eects on venodilatation (21).
Although studies have not been conducted in patients
with hepatic or renal impairment, the metabolism and
elimination o clevidipine should not be aected by
impairment o these organs.
Types o hypertensive emergencies
The type o ongoing acute target-organ damage makes
a great deal o dierence in the way a patient with a
very elevated BP should be evaluated and treated.These are most easily arranged by the organ system
being damaged: aorta, cardiac, hemorrhagic, obstetric,
catecholamine excess states, renal, or neurologic. Because
there is, in general, little overlap across these areas, it is
easiest to consider each separately. The recommended
process o care includes brie ocused neurologic and
cardiovascular examinations; direct ophthalmoscopy;
and an electrocardiogram, urinalysis, and blood testing
or renal unction (eg, serum creatinine). Comparison
o a patients current results with previous ndings will
allow an appropriate decision to be made about how
acute the observed target-organ damage is. Although
let ventricular hypertrophy has been detected more
commonly in patients with a hypertensive crisis
than in control subjects with echocardiography, an
electrocardiogram is both quicker to obtain and interpret
and less expensive (9, 22). The specic level o BP is not
a necessary or sucient condition or the diagnosis o a
hypertensive emergency. Young patients with previously
normal BPs can occasionally have acute target-organ
damage caused by an elevated BP like in the setting
o acute glomerulonephritis, at the same time many
patients with chronic, but poorly treated, hypertension
present with much higher BPs and yet have no acute
target organ damage and need not be immediately
treated in a hospital with antihypertensive drugs (23).
Renal hypertensive emergency
Normal renal autoregulation enables the kidney to
maintain a constant renal blood fow and glomerular
ltration rate or mean arterial pressures between 80
and 160 mm Hg (24). Many patients who present withhypertensive emergencies have microscopic hematuria
or acutely worsened renal unction; gross hematuria
is less common but should trigger urologic evaluation
ater BP reduction has been achieved. A urinalysis and
measurement o serum creatinine should be perormed
initially in the assessment o all patients with a very
high BP, and the latter can be compared with values
in the recent medical record to establish whether the
deterioration in renal unction is acute. During treatment
or hypertensive emergencies, many patients with
acute-on-chronic renal excretory dysunction display a
temporary increase in serum creatinine, even when BP islowered careully and correctly. Optimal drug therapy or
hypertensive emergencies with renal signs or symptoms
is controversial. Although nitroprusside is the drug with
the lowest acquisition cost and longest track record, many
physicians avor the dopamine-1 agonist, enoldopam
mesylate, which not only avoids potential cyanide and
thiocyanate toxicity during prolonged inusions or
high doses o nitroprusside, but also has some acute
benecial eects in the kidney like natriuresis, diuresis,
and creatinine clearance (19).
Neurologic hypertensive emergency
In patients with a very high BP and neurologic
abnormalities (including altered mental status),a
thorough examination o the optic undi by direct
ophthalmoscopy is essential. Patients with papilledema
or new hemorrhages or exudates have hypertensive
emergencies and oten maniest some degree o
hypertensive encephalopathy. A thorough initial
neurologic examination is also important to document
the extent and severity o ocal neurologic deects that
could change during treatment and then be attributed
to an overaggressive lowering o BP or an acute stroke,
either o which would change therapy. The most dicult
o these is hypertensive encephalopathy, typically a
diagnosis o exclusion (25). Hemorrhagic and thrombotic
strokes are usually diagnosed by demonstrating ocal
neurologic decits and a corroborating computed
axial tomographic or magnetic resonance imaging
scan o the head. Hypertension associated with head
trauma (Cushings refex) usually has the characteristic
history and corroborating physical ndings, but the
BP goal is controversial. The management o each o
these neurologic conditions is somewhat dierent.
Sodium nitroprusside is still the drug typically chosen
or encephalopathy and can be used in other conditions.
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Nimodipine has both antihypertensive and anti-ischemic
eects and has improved long-term outcomes in
subarachnoid hemorrhage but not in ischemic stroke.
The BP goal during treatment also depends on the
presenting diagnosis: BP lowering is warranted and
therapeutic in hypertensive encephalopathy
Cardiac hypertensive emergencyPulmonary edema is one common presentation o
hypertensive emergencies that directly involve the
heart. Most patients present with dyspnea, anxiety,
and/or chest pain, and are hypertensive at presentation,
sometimes severely so. Lowering BP is probably a
useul modality in this circumstance because it reduces
myocardial oxygen demand. The usual order o inusion
includes urosemide and then enalapril (which improves
hemodynamic outcomes ater pulmonary edema
(26), ollowed by nitroprusside i needed. Intravenous
nicardipine has been most commonly used ater cardiac
surgery. Like all vasodilators, all these drugs cause refextachycardia, but their coronary arterial dilator eects
typically oset the increased cardiac oxygen demand.
Obstetric hypertensive emergencies
In pregnant adolescents, hypertensive emergencies
are dened dierently rom those in non pregnant
women. Normally, BP declines during the rst trimester
o pregnancy; as a result, hypertensive emergencies (and
preeclampsia) are typically diagnosed at much lower
levels o BP than in non pregnant women. Because o the
risks o eclampsia to mothers and etuses, obstetricians
are much more vigilant about elevated BP readingsthan other physicians. Many o the usual drugs used
or hypertension are contraindicated in pregnancy.
Nitroprusside is metabolized to cyanide, which is
especially toxic to etuses. Angiotensin-converting
enzyme inhibitors and angiotensin II receptor blockers
are contraindicated in the second and third trimesters o
pregnancy because o nephrotoxic and other potentially
adverse (and even atal) eects in etuses. Magnesium
sulate, methyldopa, and hydralazine are the drugs
commonly used, with oral niedipine or -blockers being
add-on drugs (27). Intravenous enoldopam is currently
being studied in pregnancy but does not yet have FDA
approval or this indication. No matter which drug is
chosen, delivery o an inant typically lowers the new
mothers BP and is oten hastened by the obstetrician in
preeclampsia or eclampsia.
Hypertensive emergency caused by catecholamine
excess
True hypertensive emergencies due to an excess ocatecholamines can be caused by pheochromocytoma
(or other chroman tumor), monoamine oxidase
(MAO) inhibitor crisis, and intoxication with cocaine
or other drugs o abuse. Patients with catecholamine
excess states caused by severe burns can be given
a beta-blocker (alone), which has other benecial
eects on both metabolism and outcomes.(28)
Treatment o hypertensive emergencies caused by
pheochromocytoma or cocaine toxicity usually begins
with an intravenous ala-blocker (phentolamine), and
the beta-blocker is added thereater only i necessary.(9)
Aortic Dissection
Aortic dissection is rare in children and is managed
dierently rom other hypertensive emergencies
because o its very high short term risk or patients and
both the lower target BP (systolic BP 120 mm Hg or
adults and 50th centile or children) and the short time
recommended or its achievement (
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12
Esmolol 125500 g/
kg/min
Beta-blocker 1020
min
Bradycardia, hypotension,
bronchospasm, skin necrosis
ater extravasation, Raynauds
phenomenon, congestive
cardiac ailure, cocaine toxicity
Labetalol 0.253 mg/kg/
hr IV
Combined alpha and
beta blocker
Up to 4
hrs
Bradycardia, hypotension,
atrioventricular conduction
disturbances, headache,
asthma, nasal congestion
Hydralazine 0.10.6 mg/kg/
dose every 46
hrs IV
Direct vasodilatation
o arterioles
14 hrs Palpitations, fushing,
tachycardia, ever, rash,
headache, arthralgia, SLE-
like syndrome, positive ANA,
peripheral neuropathy
Fenoldopam 0.81.2 g/kg/
min IV
Dopamine D1
receptor agonist
1 hr Tachycardia, hypotension,
fushing, headache,
hypokalemia, nasal
congestion
Clevidipine 0.5-3.5 mcg/kg/min IV L-type calciumchannel blocker up to 15minutes Headache, nausea, vomiting,hypotension Patients with lipiddisorders and egg
and soy protein
allergies
Phentolamine 0.050.1 mg/
kg/dose IV
(max 5mg per
dose)
-adrenergic blocker 1530
min
Tachycardia, palpitations,
hypotension, fushing,
headache, nasal congestion,
exacerbation o peptic ulcer
Enalapril 510 mcg/kg/
dose q 824
hrs IV
Angiotensin
converting enzyme
inhibitor
46 hrs Hypotension, hyperkalemia,
oliguria, rash, angioedema,
agranulocytosis, neutropenia,
cough, atal hepatic necrosis
(rare)
Supra-renal aortic
stenosis and B/L
renal stenosis; most
valuable in neonatal
hypertension
Niedipine 0.10.25 mg/kg/dose q 46
hrs (max 10
mg/dose) oral
Calcium channelblocker
48 hrs Flushing, hypotension,tachycardia, palpitations,
syncope, peripheral edema,
headache, thrombocytopenia,
rash, urticaria, elevated liver
enzymes
Clonidine 0.05-0.1 mg/
dose orally
Central -agonist 68 hrs Bradycardia, hypotension,
rebound hypertension with
abrupt withdrawal, sedation,
dry mouth,
Avoid sudden
discontinuation
Minoxidil 0.1-0.2 mg/kg/
day (max 5mg/
day) orally
Hyperpolarization o
K+channels resulting
in smooth muscle
relaxation
Up to 24
hrs
Tachycardia, fuid retention,
rash, headache, weight
gain, pulmonary edema,
Stevens-Johnson syndrome,
photosensitivity, pericardial
eusion
Losartan Dose or < 6
years is not
established.
Children >6
years 0.7 mg/kg
once daily (max
dose 100 mg/
day) orally
Angiotensin II
receptor blocker
24 hrs Hypotension, chest pain,
hyperkalemia, azotemia,
headache, ever, syncope,
diarrhea, fu-like illness
Suprarenal aortic
stenosis and B/L
renal stenosis
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13
Reerences
1. Falkner B, Daniels S. Summary o the ourth report
on the diagnosis, evaluation, and treatment o
high blood pressure in children and adolescents.
Hypertension 2004; 44: 387388.
2. Jones D W, Hall J E. Seventh report o the joint national
committee on prevention, detection, evaluation,
and treatment o high blood pressure and evidencerom new hypertension trials. Hypertension 2004;
43: 13.
3. Zampaglione B, Pascale C, Marchisio M, et al.
Hypertensive urgencies and emergencies:
prevalence and clinical presentation. Hypertension
1996; 27: 144147.
4. Kearney P M, Whelton M, Reynolds K, et al. Global
burden o hypertension: analysis o Worldwide data.
Lancet 2005; 365: 217223.
5. Soro J M, Lai D, Turner J, et al. Overweight, ethnicity,
and the prevalence o hypertension in school-aged
children. Pediatrics 2004; 113: 475482.6. Singh D, Akingbola O, Yosypiv I, et al. Emergency
management o hypertension in children Int J
Nephrol 2012 :doi:10,1155/2012/420247
7. Deal J E, Barratt T M, Dillon M J. Management o
hypertensive emergencies. Arch Dis Child1992; 67:
10891092.
8. Singh M,. Mensah G A,Bakris G. Pathogenesis and
clinical physiology o hypertension. Cardiol Clin
2010; 28: 545559.
9. Elliott W J. Clinical Features in the Management
o Selected Hypertensive Emergencies. Prog
Cardiovasc Dis 2006; 48: 316-325.
10. Chao TK. Sudden sensorineural hearing loss ater
rapid reduction o blood pressure in malignant
hypertension. Ann Otol Rhinol Laryngol 2004;
113:73-75.
11. Singhi SC, Kohli V. Management o hypertensive
emergencies. Indian Pediatr 1992; 29: 1181-1186.
12. Daniels S R. Summary o the ourth report on the
diagnosis, evaluation, and treatment o high blood
pressure in children and adolescents. Hypertension
2004; 44:387388.
13. Benson JE, Gerlach JT, Dasta JF. National survey o
acute hypertensive management. Crit Care Shock
2008; 11: 154166.14. Varon J, Marik PE. The diagnosis and management
o hypertensive crises. Chest 2000; 118: 214227.
15. Pearce CJ, Wallin JD. Labetalol and other agents that
block both alpha- and beta-adrenergic receptors.
Cleve Clin J Med 1994; 61: 5969.
16. Hunt SA, Abraham WT, Chin M H, et al. ACC/AHA
2005 guideline update or the diagnosis and
management o chronic heart ailure in the adult:
a report o the American College o Cardiology/
American Heart Association Task Force on Practice
Guidelines. Circulation 2005;112: 154235.
17. Bussman WD, Kenedi P, von Mengden HJ, et al.
Comparison o nitroglycerin with niedipine
in patients with hypertensive crisis or severe
hypertension. Clin Invest 1993; 70: 10851088.
18. Marik PE, Varon J. Hypertensive crises challenges
and management. Chest 2007; 131: 19491962
19. Oparil S, Aronson S, Deeb GM, et al. Fenoldopam:
a new parenteral antihypertensiveconsensus
roundtable on the management o perioperative
hypertension and hypertensive crises. Am J
Hypertens 1999; 12: 653664.
20. Shusterman NH, Elliot WJ, White WB. Fenoldopam,
but not nitroprusside, improves renal unction in
severely hypertensive patients with impaired renal
unction. Am J Med. 1993; 95:161168.
21. Kieler-Jensen N, Jolin-Mellgard A, Nordlander M.et
al. Coronary and systemic hemodynamic eects oclevidipine, an ultra-short-acting calcium antagonist,
or treatment o hypertension ater coronary artery
surgery. Acta Anaesthesiol Scand 2000; 44: 186194.
22. Nadar S, Beevers DG, Lip GY. Echocardiographic
changes in patients with malignant phase
hypertension:The West Birmingham Malignant
Hypertension Register. J Hum Hypertens 2005;19:
69-75.
23. Phillips RA, Greenblatt J, Krako LR. Hypertensive
emergencies. Prog Cardiovasc Dis 2002; 45:33- 48,
24. Aggarwal M, Khan I A. Hypertensive Crisis:
Hypertensive emergencies and urgencies. CardiolClin 2006; 24: 135146.
25. Vaughan CJ, Delanty N. Hypertensive emergencies.
Lancet 2000; 356:411-417.
26. Annane D, Bellissant E, Pussard E, et al. Placebo
controlled, randomized, double-blind study o
intravenous enalapril ecacy and saety in acute
cardiogenic pulmonary edema. Circulation 1996;
94:1316-1324,
27. Vermillion ST, Scardo JA, Newman RB, et a l. A
randomized, double-blind trial o oral niedipine and
intravenous labetalol in hypertensive emergencies
o pregnancy. Am J Obstet Gynecol 1999; 181: 858-
861,
28. Herndon DN, Hart DW, Wol SE, et al: Reversal o
catabolism by beta-blockade ater severe burns. N
Engl J Med 2001; 345: 1223-1229.
29. Ouriel K. Descending thoracic aortic dissection:
Clinical aspects and anatomic correlations. Semin
Vasc Surg 2002;15: 83-88.
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14
Adherence to PALS Sepsis Guidelines and
Hospital Length o Stay
Paul R, Neuman MI, Monuteaux MC, et al.
Pediatrics 2012; 130:e273e280
Objectives: Few studies have evaluated sepsis guideline
adherence in a tertiary pediatric emergency department
setting. Authors sought to evaluate (1) adherence to 2006
Pediatric Advanced Lie Support guidelines or severe
sepsis and septic shock (SS), (2) barriers to adherence,
and (3) hospital length o stay (LOS) contingent on
guideline adherence.
Methods:Prospective cohort study o children presenting
to a large urban academic pediatric emergency
department with SS. Adherence to 5 algorithmic time-
specic goals was reviewed: early recognition o SS,
obtaining vascular access, administering intravenous
fuids, delivery o vasopressors or fuid reractory shock,
and antibiotic administration. Adherence to each time-
dened goal and adherence to all 5 components as a
bundle were reviewed. A detailed electronic medical
record analysis evaluated adherence barriers. The
association between guideline adherence and hospital
LOS was evaluated by using multivariate negative
binomial regression.
Results: A total o 126 patients had severe sepsis
(14%) or septic shock (86%). The median age was 9
years (interquartile range, 316). There was a 37% and
35% adherence rate to fuid and inotrope guidelines,
respectively. Nineteen percent adhered to the
5-component bundle. Patients who received 60 mL/
kg o intravenous fuids within 60 minutes had a 57%
shorter hospital LOS (P = .039) than children who did not.
Complete bundle adherence resulted in a 57% shorter
hospital LOS (P = .009).
Conclusions: Overall adherence to Pediatric Advanced
Lie Support sepsis guidelines was low; however,
when patients were managed within the guidelines
recommendations, patients had signicantly shorter
duration o hospitalization.
Journal Scan
Journal ScanSheikh Minhas
Fellow Pediatric Critical Care, Department o Pediatrics, Institute o Child Health, Sir Ganga Ram Hospital, Rajinder
Nagar, New Delhi 110060
Procalcitonin useulness or the initiation o
antibiotic treatment in intensive care unit
patients
Layios N, Lambermont B, Canivet JL, et al.
Crit Care Med 2012; 40: 23042309
Objectives: To test the useulness o procalcitonin
serum level or the reduction o antibiotic consumption
in intensive care unit patients.
Design: Single-center, prospective, randomized controlledstudy.
Setting: Five intensive care units rom a tertiary teaching
hospital.
Patients: All consecutive adult patients hospitalized or >48
hrs in the intensive care unit during a 9-month period.
Interventions: Procalcitonin serum level was obtained
or all consecutive patients suspected o developing
inection either on admission or during intensive care
unit stay. The use o antibiotics was more or less strongly
discouraged or recommended according to the Muller
classication. Patients were randomized into two groups:one using the procalcitonin results (procalcitonin
group) and one being blinded to the procalcitonin
results (control group). The primary end point was the
reduction o antibiotic use expressed as a proportion
o treatment days and o daily dened dose per 100
intensive care unit days using a procalcitonin-guided
approach. Secondary end points included: a posteriori
assessment o the accuracy o the inectious diagnosis
when using procalcitonin in the intensive care unit and
o the diagnostic concordance between the intensive
care unit physician and the inectious-disease specialist.
Measurements and Main Results: There were 258patients in the procalcitonin group and 251 patients
in the control group. A signicantly higher amount o
withheld treatment was observed in the procalcitonin
group o patients classied by the intensive care unit
clinicians as having possible inection. This, however, did
not result in a reduction o antibiotic consumption. The
treatment days represented 62.6 34.4% and 57.7
34.4% o the intensive care unit stays in the procalcitonin
and control groups, respectively (p = .11). According to
the inectious-disease specialist, 33.8% o the cases in
which no inection was conrmed, had a procalcitonin
value >1g/L and 14.9% o the cases with conrmed
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inection had procalcitonin levels
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aeration changes during or ater a recruitment maneuver
(RM) in ventilated patients with acute lung injury (ALI).
However, there are no published data on the lung
aeration changes during or ater a RM in ventilated
pediatric patients with ALI.
Objective: To describe CT-scan lung aeration changes
and gas exchange ater lung recruitment in pediatric
ALI and assess the saety o transporting patients in theacute phase o ALI to the CT-scanner.
Methods: Authors present a case series completed in a
subset o six patients enrolled in the previously published
study o ecacy and saety o lung recruitment in
pediatric patients with ALI.
Intervention: RM using incremental positive end-
expiratory pressure.
Results: There was a variable increase in aerated and
poorly aerated lung ater the RM ranging rom 3% to 72%
(median 20%; interquartile range 6, 47; P = 0.03) (Fig 1). All
patients had improvement in the ratio o partial pressureo arterial oxygen over raction o inspired oxygen (PaO2/
FiO2) ater the RM (median 14%; interquartile range: 8,
72; P = 0.03). There was a decrease in the partial pressure
o arterial carbon dioxide (PaCO2) in our o six subjects
ater the RM (median --5%; interquartile range: --9, 2;
P = 0.5). One subject had transient hypercapnia (41%
increase in PaCO2) during the RM and this correlated
with the smallest increase (3%) in aerated and poorly
aerated lung. All patients tolerated the RM without
hemodynamic compromise, barotrauma, hypoxemia, or
dysrhythmias.
Figure 1: CT scan o two patients taken beore and ater
recruitment maneuver (RM)
Pre RM Post RM Pre RM Post RM
Conclusions: Lung recruitment results in improvedlung aeration as detected by lung tomography. This is
accompanied by improvements in oxygenation and
ventilation. However, the clinical signicance o these
ndings is uncertain. Transporting patients in early ALI to
the CT-scanner seems sae and easible.
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Case Report
An Unusual Case o Pneumonia -----Lipoid pneumoniaPreeti Anand
Fellow, Pediatric Critical Care, Department o Pediatrics, Institute o Child Health, Sir Ganga Ram Hospital, Rajinder
Nagar, New Delhi 110060
Exogenous lipoid pneumonia is pneumonitis resulting
rom the aspiration or inhalation o a atty substance
(1). We report a case o a child with history o ingestion
o baby oil presenting as acute respiratory distress
syndrome (ARDS).
Case report
10-month emale inant, presented with complaints o
accidental ingestion o 15 ml o baby oil one month priorto admission. She developed cough and one episode
o vomiting ater ingestion. She was noticed to have
ever the next day which was mild to moderate grade,
responding to antipyretics, not associated with chills and
rigors. Fever was associated with tachypnea, dry cough
and decreased oral intake. She was treated with oral
antibiotics ollowing, which the ever subsided but the
tachypnea persisted. As the symptoms persisted she was
given a trial o oral steroids and nebulization. The chest
x-ray done outside showed diuse bilateral haziness (Fig
1). She was reerred to our institution with progressively
increasing ever and respiratory distress.
Figure 1: Chest X ray done one month ater ingestion
On admission to our hospital, the inant was ound to
be irritable but alert. She had tachypnea (60/min) and
tachycardia (160/min) with blood pressure o 60/40 mm
o Hg and SpO2
88% in room air and 90% on oxygen by
non-rebreathing mask. The child had nasal faring and
subcostal and suprasternal retractions and auscultation
o the chest revealed diuse crackles. There were no
cardiac murmurs, hepatosplenomegaly and neurological
decits.
Arterial blood gas at admission showed compensated
respiratory alkalosis with metabolic acidosis with
hypoxemia (pH-7.44, PaCO2
26.9, PaO2
52.4, HCO3
17.9, lactate 0.83). Chest x- ray showed bilateral non-
homogenous opacities (Fig 2).
Figure 2: Chest X Ray on admission to our center
In view o the increased work o breathing with
borderline PaO2, BIPAP with non-invasive ventilator was
initiated but child did not tolerate and became agitated
and desaturated. So she was intubated and started on
mechanical ventilation on pressure regulated volume
control mode (PRVC) with FiO2
1.0, PEEP at 8 cm H2O
increased upto 12 cm H2O, tidal volume 7 ml/kg, rate
25/min and inspiratory time o 33%. Serial blood gases
showed respiratory acidosis with worsening PaO2/FiO
2
ratio o < 100mmHg (pH-7.11, PaCO2
66.1mmHg, PaO2
81.5mmHg, HCO3 20.6mmol/L, lactate 0.57mmol/L).
The ventilation rate increased to 35/min, tidal volumeincreased to 11ml/kg achieving PIP o 35 cm H2O and
PEEP to 12 cm H2O. In view o the high peak pressures,
progressive respiratory acidosis and worsening
oxygenation on conventional ventilation necessitated
shiting to high requency oscillatory ventilation (HFOV;
Sensormedics 3100A). Endotracheal aspirates sent on
admission or lipid-laden macrophages was positive
while the gram stain and culture were negative.
The initial HFOV settings were FiO2
1.0, amplitude o 53
cm H2O, requency o 9 Hz and MAP 27 cm H
2O. The ABG
showed improvement pH-7.298, PaCO2
33.9mmHg, PaO2
82.2mmHg, HCO3 16.2mmol/L, lactate 1.18mmol/L. The
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FiO2
was gradually decreased to 0.6, amplitude decreased
to 44 cm H2O, requency o 9.0 Hz and MAP 26 cm o H
2O.
On the above settings the SpO2
improved to 98% and
the heart rate settled at 132/min and the ABG status was
pH-7.213, PaCO2
54.2mmHg, HCO3
21.3mmol/L, PaO2
104.1mmHg, lactate 0.83mmol/L. The HFOV amplitude
was increased to 50 cm H2O, FiO
2decreased to 0.5 and
MAP was decreased to 23 cm H2
O. Gradually the settings
were decreased and she was shited to conventional
ventilation on day 4 o admission to SIMV +PS (volume
control) mode with FiO2
0.6, PEEP at 8 cm H2O, PS 12 cm,
rate 20/min, tidal volume o 8ml/kg and inspiratory time
o 33%.
In view o the hemodynamic instability the child
was given fuid boluses at 20ml/Kg and later started
on inotrope support- dopamine at 10mcg/kg/min,
which was later tapered and discontinued on day 2 o
admission ater which she remained hemodynamically
stable. The IV antibiotics were continued or 14 days
and later discontinued ater repeat sepsis screen came
negative. Initial investigations showed total leucocyte
count 18800/mm3 with C- reactive protein o 6 mg/L and
sterile blood culture.
Flexible bronchoscopy with large volume lavage
(with 50 ml saline) was done on day 7 o admission.
Bronchoscopy showed whitish mucoid secretions all
over the tracheobronchial tree (Fig3).
Figure 3: Flexible bronchoscopy showing mucoid secretion in
segmental bronchus
Pale white colored (milky) broncho-alveolar lavage
was obtained and sent or investigations and camepositive or lipid-laden macrophages however the
cultures were sterile. The ventilator requirements
increased marginally ater the procedure. She was
started on methylprednisolone at 2mg/kg/day, which
was discontinued ater 7 days. CECT scan o chest
showed extensive diuse ground glass appearance,
which was consistent with lipoid pneumonia (Fig 4).
Repeat bronchoscopic broncho-alveolar lavage urther
helped decrease the ventilator settings and the child
was successully extubated on day 11 o admission to
our center. This child was electively started on BIPAP
intermittently or 4 hours with 2 hours o rest period
during which child was oxygenated with simple mask
to maintain SpO2
above 90%. Nasogastric eeding was
started on day 4 o admission and an attempt was made
to provide proteins and calories through enteral route.
During her stay in the hospital child had undergone
repeated broncho-alveolar lavages with 75-80 ml o
saline on weekly basis. To avoid post lavage hypoxemia
and increased work o breathing, only one lung lavage
was done at a time. Child was started with azathioprine
(2.5mg/kg) once a day and prednisolone 2mg/kg on
alternate day on day 20 o admission. At the time o
writing o this report, inant is on BIPAP (IPAP 10 cmH2O,
EPAP 5 cmH2O) or 4 hrs with 2 hrs o simple mask
oxygenation at 4-5L/min fow rate. She has gained only
700 gms o weight in 4 months inspite o high calorie
eed and has developed clubbing o all ngers during
her stay in the hospital and there is no radiological
improvement in the serial chest radiographs. We could
not give suractant due to nancial reasons.
Figure 4: CECT o the chest diuse ground appearance with
consolidation o right lower lobe
Lipoid pneumonia- Review o literature
Lipoid pneumonia (LP) is the result o a oreign body-
type reaction to the presence o lipid material within the
lung parenchyma. Lipoid pneumonia is an uncommon
entity and an autopsy series reported a requency o only
1.02.5% (2).
LP can be endogenous or exogenous based on the
source o lipids. Endogenous lipid pneumonia results
rom accumulation o lipids within the intra-alveolar
macrophages in the setting o bronchial obstruction,chronic pulmonary inection, pulmonary alveolar
proteinosis, or at storage diseases (3,4). The aspiration or
inhalation o exogenous lipids like mineral oil (present in
Johnson baby oil), animal ats and vegetable oils, lead to
exogenous lipoid pneumonia.
Exogenous lipoid pneumonia
Exogenous lipoid pneumonia was rst described by
Laughlen (3,5) in 1925, when he reported the presence
o oil droplets in the lung during the autopsies o three
children and one adult who had received mineral oil
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nose drops or oral laxatives during lie (5). In 1929, Quinn
and Meyer illustrated how aspiration o the oil ailed
to provoke two important protective responses o the
airway-glottis closure and coughing, and by-passed
mucociliary transport mechanism (6).
Epidemiology
Based on the presentation, exogenous lipoid pneumoniacan be classied as acute or chronic. Acute exogenous
lipoid pneumonia is due to acute ingestion o large
quantities o petroleum based products (7,8). Acute
pneumonitis in children is seen due to accidental
ingestion o petroleum-based products.
Chronic exogenous lipoid pneumonia usually results rom
repeated episodes o aspiration or inhalation o animal
at or mineral or vegetable oils over an extended period.
It is usually seen in children with anatomic or unctional
deects, including mental retardation and clet palate, as
well as in inants when mineral oil is used as a lubricant
to acilitate eeding (2). Chronic lipoid pneumonia hasalso been reported in patients without a predisposing
anatomic or unctional abnormality in swallowing, with a
history o chronic use o mineral oil or petroleum-based
lubricants and decongestants such as Vaseline (Unilever),
Vicks VapoRub, and lip gloss (2,9). Several reports o lipoid
pneumonia, especially in inants and small children,
have originated rom traditional olk remedies. In India,
sesame seed was used to fush secretions out through
the nose (10). In Saudi Arabia animal ats, such as ghee,
are oten ed orcibly to establish regular bowel habits
or administered intranasally to treat coughs and colds
(11,12). In Brazil mineral oil used to relieve partial small-bowel obstruction due to Ascaris lumbricoides (13). An
Oriental practice is to instill medicated oil into the nose
and then sni it (14). In children, chronic exogenous
lipoid pneumonia has been reported as a result o
embolization ater rectal or subcutaneous administration
o mineral oils (15).
Pathogenesis
The development o parenchymal abnormalities in
lipoid pneumonia is dependent on the type, amount,
requency, and length o time o aspirated or inhaled
oils or ats. Mineral oil, being bland and nonirritating,can enter the tracheobronchial tree without stimulating
glottic closure or the cough refex, and, once there,
is expelled with diculty because it impairs the
mucociliary transport system (5,16). Mineral and
vegetable oils like sesame seed, poppy seed, and olive
oil provoke minimal to mild infammatory reaction
and are largely removed rom the lung by expectoration
(17). The aspirated oil is emulsied and phagocytosed
by alveolar macrophages. These oil lled macrophages
reach the interlobular septum through the lymphatic
channels and cause thickening o the alveolar walls and
destruction o some alveoli. Later, brotic prolieration
results in decreased lung volume (18). Most o the oil
coalesces, orming large at drops surrounded by brous
tissue and giant cells, creating a tumor mass known as
paranoma (19). Repeated massive aspiration results in
diuse parenchymal consolidation. Animal ats, however,
are hydrolyzed by lung lipases into ree atty acids, which
trigger a severe infammatory reaction that maniests as
ocal edema and intraalveolar hemorrhage (9). Fatty acids
remain either in the alveolar spaces or are phagocytosed
by macrophages, which then migrate to the interlobular
septa. Regardless o location, the infammatory response
can destroy the alveolar walls and the interstitium, and
the resultant brosis can occasionally progress to end-
stage lung disease.
Clinical maniestations
Acute exogenous lipoid pneumonia typically presents
as cough, dyspnea, and low-grade ever that usually
resolves with supportive therapy (2). Patients with
chronic exogenous lipoid pneumonia are requentlyasymptomatic on presentation and are usually identied
because o an incidentally detected abnormality on
radiologic imaging.
Crackles, wheezes, or rhonchi may be heard on
auscultation o the chest. Laboratory investigations
reveal hypoxemia, leukocytosis and an increased
erythrocyte sedimentation rate may occur, especially
when the lipoid pneumonia or a complicating inection
causes ever (16).
In a study done by Balakrishnan (10) rom India in 1973
on 15 children, acute onset o dyspnoea, cough, and
ever mostly mild or moderate, sometimes severe werethe most common presenting symptoms (present in
80%). Recurring lower respiratory inections were ound
at presentation in approximately 17% o the patients and
one out o the 15 patients presented with diarrhea and
ailure to thrive. All cases had history o oil bath at home.
A case report rom Mexico (20) retrospectively reviewed
the medical records o 16 patients who had presented
rom 1991 to 1996 with lipoid pneumonia. A history o
ingestion o dierent kinds o vegetable oil was positive
in 12 (75%). Ingestion o olive oil was present in 10
children (75%), most receiving it more than once. The
clinical presentation ranged rom mild symptoms todeath. Cough was ound to be present in 100% cases
(16 children). Dyspnea or respiratory distress was seen
in 93.7%. 68.7% (9 children) had recurrent pneumonia
as a presenting complaint. Cyanosis was ound in 9
children (53.2%). Unlike the other case series, ever, was
an uncommon presentation in this case series (10,21).
Less common presentations include chest pain,
hemoptysis, weight loss, and intermittent evers, perhaps
due to the infammatory reaction to oil or to secondary
inection related to bronchiectasis or pneumonia (22).
Radiological evidence o acute exogenous lipoid
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pneumonia can be seen within 30 minutes o the episode
o aspiration or inhalation, and pulmonary opacities
can be seen in most patients within 24 hours (23). The
opacities are typically ground glass or consolidative,
bilateral, and segmental or lobar in distribution and
predominantly involve the middle and lower lobes (24).
Other ndings include poorly marginated nodules,
pneumatoceles, pneumomediastinum, pneumothorax,and pleural eusions (23,24). Pneumatoceles are seen
in regions o ground-glass or consolidative opacities
and typically maniest radiologically within 230 days
ater aspiration or inhalation, and are more common
in patients who have aspirated or inhaled a large
amount o mineral oils or petroleum-based products
(25). Pneumothorax and pneumomediastinum are rare
and have been reported to occur within 4 days ater
hydrocarbon aspiration and are associated with a poor
prognosis.
Computed tomography (CT) scan o chest shows alveolar
consolidations o low attenuation values, ground glassopacities with thickening o intralobular septa (crazy
paving pattern), or alveolar nodules (26,27). Magnetic
resonance imaging (MRI) may reveal high signal intensity
on T1-weighted imaging consistent with lipid content
(28). The radiologic maniestations o acute exogenous
lipoid pneumonia typically improve or resolve over time.
Resolution o opacities usually occurs within 2 weeks to
8 months (7). The imaging eatures o acute and chronic
lipoid pneumonia overlap (2).
Chronic exogenous lipoid pneumonia maniests as
ground glass or consolidative opacities involving one
or more segments, typically with a peribronchovasculardistribution with predominant involvement o the lower
lobes. Chronic exogenous lipoid pneumonia may present
as single or multiple nodules or masses that may or may
not contain at (2,3). These radiologic maniestations can
improve slowly over time but typically remain stable even
i the exposure to vegetable or mineral oils or animal ats
is discontinued (2). Cor pulmonale results due to brosis
and destruction o normal lung architecture.
Diagnosis o lipoid pneumonia is established in a patient
with history o mineral oil ingestion with presence o
lipid-laden macrophages in BAL fuid and oci o at
attenuation within areas o consolidation on high-resolution CT (25,29-31). Lipid-laden macrophages in
BAL fuid (Fig 5) are considered to be the most important
nding or the diagnosis o lipoid pneumonia (25,29,32).
Figure 5: Lipid Laden Macrophages
Endogenous lipoid pneumonia
Cholesterol pneumonia or golden pneumonia is an
obstructive pneumonitis. The diagnosis o endogenous
lipoid pneumonia is made by the characteristic
histopathological ndings. Macroscopically, the
parenchyma has a characteristic yellowish discoloration
due to the accumulation o lipid in the alveoli (33).
Histologically, there is an accumulation o lipid-lledmacrophages and eosinophilic proteinaceous material
derived rom degenerating cells, including suractant
rom type II pneumocytes, in the alveoli distal to the
bronchial obstruction. Endogenous lipoid pneumonia
typically maniests radiologically as consolidative
opacities distal to a central obstructing lesion (35). Unlike
exogenous lipoid pneumonia, the accumulation o lipid-
rich cellular debris does not maniest radiologically
as lipid-containing opacities, and the diagnosis is
histopathologic.
The spectrum o endogenous lipoid pneumonia includes
pulmonary inections, lipid storage diseases, andpulmonary alveolar proteinosis (3).
Treatment
There is no consensus on the right treatment modality
or lipoid pneumonia. Avoiding exposure, treating any
underlying inection and supportive care are the most
important in management o lipoid pneumonia (1,16).
Steroid therapy is a modality that has been tried in the
treatment o lipoid pneumonia (35-38). They help by
limiting the infammatory response and ongoing brosis
(35).
Indumati et al rom India reported the case o a two and
a hal year old child with history o ingestion o machine
oil. Ater 8 weeks o steroid therapy the tachypnea
and oxygen requirements decreased and the steroids
were tapered o by 10 weeks with almost complete
radiological clearance in 5 months (35). Similarly, Annobil
et al reported a series o ve children aged between our
months to our years with lipoid pneumonia ollowing
nasal instillation o olive oil, where prednisolone was
used or a varying periods o two months to ve months
resulting in complete clinical and radiological recovery
(36). Similarly steroids were used in adults with lipoid
pneumonia leading to a complete recovery (37,38).
Others however have reported no benets with steroids
(10).
BAL is a successul strategy recommended in the
treatment o pulmonary alveolar proteinosis but only
ew reports have shown good response o whole lung
lavage in the treatment o adults with lipoid pneumonia
and just one case-report in a child with exogenous lipoid
pneumonia (39 -42).
A case series rom Brazil, evaluated 10 children with
mineral oil aspiration leading to lipoid pneumonia.
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They perormed therapeutic BAL weekly until BAL fuid
was nearly transparent and the cell count returned
to normal range values and concluded that multiple
therapeutic BAL o children with lipoid pneumonia
results in signicant improvement o CT ndings, oxygen
saturation, restoration o BAL fuid cellularity and clinical
recover without any evidence o respiratory distress at
the end o treatment and 6 months ater the last BAL (43).
Lung lavage with emulsiying liquids have been used
successully with good outcomes in severe cases
o lipoid pneumonia (41,44). Russo et al, rom Italy,
reported the use o 0.05% polysorbate-80 in Ringers
lactate (at 20 l/lung) as an emulsier o lipid or repeated
bronchoalveolar lavage. However several other reports
have not shown any benet o bronchoalveolar lavage
(10,45).
Azathioprine has been used in treatment o idiopathic
pulmonary brosis, primarily in patients ailing
response or those with adverse eects rom the use o
corticosteroids (46). Anectdotal responses have beennoted in uncontrolled trials (47). Azathioprine has been
used in 2mg/kg/day (upto maximum o 150mg/day) or
3-6 weeks. The combination o azathioprine and steroids
has shown more benets with enhanced survival in
patients (48).
Immunoglobulins have also been used or successul
treatment o lipoid pneumonia (49). Surgical resection
o nodules and masses has been tried or treatment o
lipoid pneumonia (50). However it should be reserved in
cases with high suspicion o carcinoma (50).
Reerences
1. Simmons A, Rou E, Whittle J. Not Your Typical
Pneumonia: A Case o Exogenous Lipoid Pneumonia.
J Gen Intern Med. 2007; 22: 16131616.
2. Baron SE, Haramati LB, Rivera VT. Radiological and
clinical ndings in acute and chronic exogenous
lipoid pneumonia. J Thorac Imaging 2003; 18:217
224.
3. Betancourt SL, Martinez-Jimenez S, Rossi SE, et
al. Lipoid pneumonia: spectrum o clinical and
radiologic maniestations. Am J Roentgenol. 2010;
194: 103-109.4. Woodhead M, Parkes WR. Disorders caused by other
organic agents. In: Parkes WR, ed. Occupational
lung disorders, 3rd ed. Oxord, United Kingdom:
Butterworth-Heinemann, 1994, Pg778793.
5. Laughlen GG. Studies on pneumonia ollowing
nasopharyngeal injections o oil. Am J Pathol. 1925;
1:407-414.
6. Quinn LH, Meye OO. The relationship o sinusitis and
bronchiectasis. Arch Otolaryngol. 1929; 10: 152-165.
7. Kitchen JM, OBrien DE, McLaughlin AM. Perils o re
eating: an acute orm o lipoid pneumonia or re
eaters lung. Thorax 2008; 63:401- 439.
8. Lishitz M, Soer S, Gorodischer R. Hydrocarbon
poisoning in