PICU Articles

7/28/2019 PICU Articles

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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

[email protected]

Kundan MittalTreasurer

[email protected]

Anil SachdevEditor

[email protected]

Santosh T SoanChairman Elect

[email protected]

Rajiv UttamChairman Elect

[email protected]

Kamlesh SrivastavaSecretary

[email protected]

Intensive Care Chapter Indian Academy of Pediatrics 2012

Office BearersOffice Bearers

DP [email protected]

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.


11/32

11

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


13/32

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


15/32

15

inection had procalcitonin levels


16/32

16

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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17

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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19

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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20

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

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