Evaluation and Management of Massive Endotracheal Hemorrhage in Pediatric Patients: A Case Report and Review of Literature

doi:10.4236/ijohns.2013.26049

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International Journal of Otolaryngology and Head & Neck Surgery, 2013, 2, 236-239

Published Online November 2013 (http://www.scirp.org/journal/ijohns)

http://dx.doi.org/10.4236/ijohns.2013.26049

Open Access IJOHNS

Evaluation and Management of Massive Endotracheal

Hemorrhage in Pediatric Patients: A Case Report and

Review of Literature

Cory Vaughn, Mona Shete, Rose Mary Stocks, Jerome Thompson

University of Tennessee Health Science Center, Memphis, USA

Email: [email protected]

Received August 5, 2013; revised September 2, 2013; accepted October 1, 2013

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

ABSTRACT

Massive hemoptysis is a frightening and life-threatening event in children. Prompt, aggressive evaluation and manage-

ment are necessary. The most common cause of hemoptysis in a pediatric patient is infectious, but other various etiolo-

gies including tracheotomy related problems, cystic fibrosis, bronchiectasis, congenital an omalies of the cardiopulmon-

ary vasculature and suction trauma must be considered as well. Presented is a report of a case of acute, massive en-

dotracheal hemorrhage with multiple methods of management includ ing balloon tamponade, highly selective emboliza-

tion, and mainstem occlusion. This case is an addition to our previously reported case series of nine pediatric patients

with massive pulmonary hemorrhage. Various diagnostic and management techniques of hemoptyis in pediatric patients

are discussed with an extensive review of the literature.

Keywords: Pediatric; Massive; Hemoptysis; Endotracheal Tube; Management

1. Introduction

Hemoptysis, a relatively common event in the adult

population, is a rare occurrence in the pediatric setting.

The most common cause of hemoptysis in the pediatric

patients is infectious, but a multitude of etiologies must

be considered [1]. In massive pulmonary hemorrhage, the

threat of asphyxia from airway obstruction is greater than

the threat of dying from exsanguination. Successful air-

way management is paramount not only to prevent im-

mediate respiratory failure, but also to the swift determi-

nation of the location of bleeding through clear visualiza-

tion and unobstructed instrumentation. Here a case of

massive hemoptysis is discussed along with new tech-

niques for its management. This case is an addition to the

previously published nine case experiences of large pul-

monary hemorrhage in the pediatric population.

2. Case Report

A 14-year-old male pedestrian was admitted to LeBon-

heur Children’s Medical Center in Memphis, TN with a

diagnosis of a closed head injury and associated intracra-

nial bleed after being struck by a vehicle. The patient was

intubated for a period of 2 weeks, whereupon he devel-

oped brisk bleeding from the endotracheal tube (ETT) as

a sequela of a coughing spell during central line place-

ment. The patient’s past medical history was insignifi-

cant. The patient’s family history was significant for an

unexplained gastrointestinal hemorrhage resulting in his

father’s demise.

Subsequently, the patient was noted to require pro-

gressively higher ventilator settings to achieve appropri-

ate oxygenation. Suction yielded a moderate amount of

bright red blood. A flexible fiberoptic bronchoscopy

demonstrated a significant amount of bright red blood in

tracheobronchial tree bu t no specific site of bleeding was

identified. In the following hours, the rate of bleeding

intensified and clots began to partially obstruct the en-

dotracheal tube. Multiple attempts at clot removal using

suction catheters through the endotrach eal tube failed. At

that point ventilation became progressively more difficult,

then impossible which resulted in rapid desaturation.

Direct suction to the endotracheal tube was applied with

concurrent extubation yielding a coagulated cast ofthe

tracheo-bronchial tree. Subsequently, the patient’s venti-

lation dramatically improved and oxygenation was per-

formed via face mask. The patient was then re-intubated

due to the instability of the airway. This process was re-

C. VAUGHN ET AL. 237

peated sev eral times.

Repeat flexible fiberop tic bronchoscopy failed to iden-

tify the site of lesion. Rigid bronchoscopy was then per-

formed in the operating room, allowing a more accurate

assessment of the airway. The lesion was localized to an

exposed vessel on the left antero-lateral tracheal wall

proximal to the origin of the left main stem bronchus.

The brisk bleeding was initially controlled with direct

bronchoscopic pressure. A cuffed endotracheal tube was

placed deep into the trachearesulting in partial tampo-

nade of the vessel. Hemodynamic status stabilized status

post four units of packed red blood cells, two units of

platelets, and four units of fresh frozen plasma. Interven-

tional Radiology was consulted for embolization of four

branch es of the in ferior thyroid artery supplying the area.

Immediate cessation of bleeding resulted. Status post

arterial embolization, the patient had cumulatively lost

2000 cc of blood. The endotracheal tube was reposi-

tioned to mid-trachea after 48 hours hemodynamic sta-

bility; during this time tracheobronchial cultures showed

no growth and no abnormalities were evident on hema-

tologic testing.

The patient suffered a second episode of extensive,

2500 cc pulmonary hemorrhage 96 hours after arterial

embolization. Repeat rigid bronchoscopy revealed un-

controlled bleeding from the distal left lower lobe (Fig-

ures 1 and 2). Subsequently, selective intubation of the

right main stem bronchus occurred with the cuff inflated

at the carina allowing for full ventilation of the right lung

with complete obstruction the left mainstem (Figure 3).

Arterial embolization was performed on the offending

internal mammary artery.

The cuff was deflated after 7 days without pulmonary

hemorrhage. A tracheotomy was performed for pulmo-

nary toilet and the left lung was re-expanded. Two weeks

later, the patient was successfully de-cannulated after a

final rigid bronchoscopy revealed only linear suction

marks at both previous bleeding sites. A total of 9 units

of packed red blood cells were required to achieve he-

mostasis from a cumulative blood loss greater than 4500

cc. Repeat hematologic studies revealed no abnormalities.

We can only assume the patient was susceptible to trau-

matic suctioning injury due to the Murphy’s eye tip of

the plastic suction catheters.

3. Discussion

In this review, massive hemoptysis will be defined as

greater than 1000 cc blood loss within 24 hours. In all

patients suffering from massive pulmonary hemorrhage,

initial priorities are to maintain the airway, optimize

oxygenation, and obtain hemodynamic stability. It has

been shown that greater morbidity is due to asphyxia

than exsanguinations [2]. A thorough history and physi-

cal exam are essential early steps necessary for proper

Figure 1. ETT through vocal cords with diffuse blood noted

on the true vocal cords.

Figure 2. Left bronchus with active bleeding during second

hemorrhage.

Figure 3. Complete whiteout of left lung from blood/col-

lapse after intentional right main bronchus intubation for

ventilation.

assessment and treatment of suffering patients.

Massive hemoptysis is the result of multiple etiologies

Open Access IJOHNS

C. VAUGHN ET AL.

238

which can be associated with various patient risk factors.

Infection is widely known as the most common cause of

massive hemoptysis in the pediatric population. While

the majority of infectious hemorrhagic episodes are the

result of S. aureus, all varieties of infection have been

reported [3]. Interestingly, there is no correlation be-

tween the severity of infection and rate or volume of

bleeding. Further etiologic consid erations should includ e,

but not be limited to: bleeding disorders, congenital vas-

cular abnormalities, tracheobronchial papillomatosis,

foreign body, tracheostomy tube related, diabetes, and

cystic fibrosis (a 1% yearly incidence) [1,3,4]. In the

previously published series from our institution, we en-

countered infection as the most frequent cause of

hemoptysis, followed by laryngotracheal papillomatosis,

trauma and one case of unknown etiology [1]. In a re-

cently published retrospective review of 15 patients, in-

fection was also found to be the leading cause followed

by tracheotomy related problems [5]. These risk factors

and etiologies can differ greatly from those seen in the

adult population where the incidence of massive pulmo-

nary hemorrhage is much greater. Many reported cases of

massive hempotysis are without known etiology or loca-

tion of lesion .

Endoscopic evaluation frequently allows for both

identification of the lesion site and initial therapy simul-

taneously, especially in cases of tracheal or bronchial

injury. Flexible laryngoscopy and bronchoscopy provides

the ability to examine the distal bronchial tree, to per-

form tracheobronchial washings, and to obtain small bi-

opsies. As in the case presented, flexible endoscopy car-

ries an increased risk of missing view of the lesion. In

general, caution should be exercised using flexible fi-

beroptic bronchoscopy in small children because of the

inability to simultaneously ventilate effectively against

airway resistance and the difficulty of removing large

clots through the small suction lumens or small endotra-

cheal tubes as used in infants. Rigid bronchoscopy with a

ventilating bronchoscope and telescopic capabilities has

been shown to offer the best chance massive hemorrhage

localization in a pediatric patient [2].

Once the site of bleeding is localized, method of in-

tervention can be determined. In patien ts with a high rate

of bleeding or diagnosed tuberculosis, surgical interven-

tion has been shown to improve mortality compared to

medical intervention [6]. During rigid bronchoscopy,

options of endo-bronchial treatment become a considera-

tion. Bleeding may be controlled with topical lavage

therapy (i.e. epipherine), rigid bronchoscopic pressure, or

endobronchialtamponade. Topical therapy is unfortu-

nately associated with hemodynamic consequences of

concentrated epinephrine. Valipour et al. reported bron-

choscopy guided topical hemostatic tamponade with oxi-

dized regenerated cellulose mesh is arrests hemoptysis in

98% of 57 patients for the first 48 hours with only 10.5%

of patients experiencing a recurrence of hemoptysis and

to a lesser degree 6 [7]. In a report of seventy-six con-

secutive patients with massive hemoptysis unresponsive

to the bronchoscopic wedging technique, cold saline so-

lution lavage or instillation of regional vasoconstrictors

[7]. Electrical current coagulation still has a role if tech-

nically feasible.

Laser coagulation therapy also is a consideration in

specific circumstances. Use of laser coagulation is a suit-

able option for patients with vascular lesions, tracheo-

bronchial papillomatosis, or other tumor-like growths. In

our previously reported series, a potassium titanyl phos-

phate (KTP) laser was used. It, however, cannot be used

during active bleeding [1]. In a retrospective review of

14 cases of children with life-threatening pulmonary

hemorrhage, both CO2 and Nd-Yag laser use were per-

formed on patients suffering from hemoptysis due to

vascular lesions or tumor-like growths. In all patients

who underwent Nd-Yag laser therapy, disappointing re-

sults revealed only temporary control on discrete bleed-

ing areas and thus required further management for per-

manent hemostasis [8].

If bleeding continues or cannot be localized, emergent

arteriography and embolization is indicated. Bronchial

artery embolization (BAE) is an established treatment for

massive and seriou s hemoptysis with good results and an

acceptable rate of complications and morbidity [9-11].

Occlusion of the bleeding bronchial vessels should be

considered for both short term and long term definitive

therapy as we proved in the presented case report. Remy

et al. treated 49 patients with arterial embolization during

active hemoptysis, 41 of whom had an initial arrest of

bleeding [12]. 6 of those 41 patients suffered a reoccur-

rence of hemorrhage between 2 and 7 months of initial

therapy, 83.3% of which w ere of a lesser severity. In a 20

year retrospective review of patients with cystic fibrosis,

massive pulmonary hemorrhage was more likely to be

treated with BAE [4]. While BAE was highly effective

(98% success rate) at controlling symptoms temporarily,

re-embolization was required in 46% of these patients. In

another review, 22 patients underwent BAE with a reoc-

currence rate of 50%. Reported absolute contraindica-

tions to bronchial arterial embolization include the spinal

artery arising from a variant position, relative contrain-

dications include sepsis, coagulopathy, and renal-insuf-

ficiency [13]. All reported episodes of re-bleeding occur

within 3 years of initial embolization.

Emergency open surgical interv ention for this problem

should be considered when embolization has failed or is

not feasible. Various techniques have been utilized to

treat persistent, severe hemoptysis. An option for tracheal

bleeding is to skeletonize the tracheal wall surgically

when embolization has failed. Methods have included

Open Access IJOHNS

C. VAUGHN ET AL.

Open Access IJOHNS

239

pneumonectomy in an adult, reported by Mehta et al.

[14]. Taguchi reported pneumonectomy and embolec-

tomy in a 10-year-old child [15]. A staged extra-anat-

omic conduit to deliver low-pressure blood to the lung,

and interruption of the high-pressure vessels were re-

ported in a 14-year-old child by Rankin [16]. Kirkpatrick

reported success with a complete anatomic repair of the

congenital heart abnormality in the treatment of a

hemoptysis in a symptomatic 2-month-old in high-output

cardiac failure [17].

4. Conclusion

Hemorrhage into the child’s airway is a frightening and

potentially lethal event. The differential diagnosis in

children is broad and a systematic approach to diagnosis

and management is essential. We add another case report

and two new alternative techniques to our series and to

the armamentarium for the management of massive

hemoptysis in children.

REFERENCES

[1] J. W. Thompson, C. D. Nguyen, R. H. Lazar, R. M.

Stocks, R. A. Schoumacher, F. Hamdan and K. V.

Nguyen, “Evaluation and Management of Hemoptysis in

Infants and Children,” The Annals of Otology, Rhinology,

and Laryngology, Vol. 105, No. 7, 1996, pp. 516-520

[2] L. Tom, R. A. Weisman and S. D. Handler, “Hemoptysis

in Children,” The Annals of Otology, Rhinology, and

Laryngology, Vol. 89, No. 5, 1980, pp. 419-424.

[3] P. A. Flume, J. R. Yankaskis, M. Ebeling, T. Hulsey and

L. L. Clark, “Massive Hemoptysis in Cystic Fibrosis,”

Chest, Vol. 128, No. 2, 2005, pp. 729-738.

http://dx.doi.org/10.1378/chest.128.2.729

[4] J. U. Barben, M. Ditchfield, J. B. Carlin, et al., “Major

Hemoptysis in Children with Cystic Fibrosis: A 20-Year

Retrospective Study,” Journal of Cystic Fibrosis, Vol. 2,

No. 3, 2003, pp. 105-111.

http://dx.doi.org/10.1016/S1569-1993(03)00066-3

[5] P. S. Batra and L. D. Holinger, “Etiology and Manage-

ment of Pediatrichemoptysis,” Archives of Otolaryngol-

ogy—Head and Neck Surgery, Vol. 127, No. 4, 2001, pp.

377-382. http://dx.doi.org/10.1001/archotol.127.4.377

[6] R. Corey and K. M. Hla, “Major and Massive Hemoptysis:

Reassessment of Conservative Management,” American

Journal of Medicine, Vol. 294, No. 5, 1987, pp. 301-309.

http://dx.doi.org/10.1097/00000441-198711000-00003

[7] A. Valipour, A. Kreuzer, H. Koller, W. Koessler and O. C.

Burghuber, “Bronchoscopy-Guided Topical Hemostatic

Tamponade Therapy for the Management of Life Threat-

ening Hemoptysis,” Chest, Vol. 127, No. 6, 2005, pp.

1888-1889. http://dx.doi.org/10.1378/chest.127.6.2113

[8] J. D. Sidman, W. B. Wheeler, A. K. Cabalka, B. Sou me k h ,

C. A. Brown and J. B. Wright, “Management of Acute

Pulmonary Hemorrhage in Children,” Laryngoscope, Vol.

111, No. 1, 2001, pp. 33-35.

http://dx.doi.org/10.1097/00005537-200101000-00006

[9] S. Osaki, Y. Nakanishi, H. Wataya, K. Takayama, K.

Inoue, Y. Takaki, S. Murayama and N. Hara, “Prognosis

of Bronchial Artery Embolisation in the Management of

Hemoptysis,” Respiration, Vol. 67, No. 4, 2000, pp. 412-

416. http://dx.doi.org/10.1159/000029540

[10] L. E. Lampmann and T. G. Tjan, “Embolization Therapy

in Hemoptysis,” European Journal of Radiology, Vol. 18,

1994, pp. 15-19.

http://dx.doi.org/10.1016/0720-048X(94)90356-5

[11] M. E. Hansen and S. Kadir, “Elective and Emergency

Embolization Therapy in Children and Adolescents, Effi-

cacy and Safet y, ” Radiology, Vol. 30, 1990, pp. 331-336.

[12] J. Remy, A. Arnaud, H. Fardou, R. Giraud and C. Voisin,

“Treatment of Hemoptysis by Embolization of Bronchial

Arteries,” Diagnostic Radiology, Vol. 122, No. 1, 1997,

pp. 33-37.

[13] J. F. Angle, N. H. Siddiqi, M. J. Wallace, et al., “Quality

Improvement Guidelines for Percutaneous Transcatheter

Embolization Society of Interventional Radiology Stan-

dards of Practice Committee,” Journal of Vascular and

Interventional Radiology, Vol. 21, No. 10, 2010, pp. 1479-

1486. http://dx.doi.org/10.1016/j.jvir.2010.06.014

[14] A. C. Mehta, D. R. Livingston, W. Kawalek, J. A. Golish

and J. K. O’Donnell, “Pulmonary Artery Agenesis Pre-

senting as Massive Hemopty sis,” Angiology, Vol. 38, No.

1, 1987, pp. 67-71.

http://dx.doi.org/10.1177/000331978703800110

[15] T. Taguchi, K. Ikeda, K. Kume, et al., “Isolated Unilat-

eral Absence of Left Pulmonary Artery with Peribron-

chialarteriovenous Malformation Showing Recurrent He-

moptysis,” Pediatric Radiology, Vol. 17, 1987, pp. 316-

318. http://dx.doi.org/10.1007/BF02388246

[16] J. S. Rankin, R. J. Sterba, J. H. Karis and H. N. Oldham

Jr., “Staged Correction of Pulmonary Atresia and Absent

Right Pulmonry Artery,” Archives of Surgery, Vol. 118,

1983, pp. 974-978.

http://dx.doi.org/10.1001/archsurg.1983.01390080076019

[17] S. E. Kirkpatrik, D. A. Girod and H. King, “Aortic Origin

of the Right Pulmonary Artery. Surgical Repair without a

Graft,” Circulation, Vol. 36, No. 5, 1967, pp. 777-782.

http://dx.doi.org/10.1161/01.CIR.36.5.777