Annals of
Burns and Fire Disasters - vol. XII - n° 4 - December 1999
PERICARDIAL EFFUSION: A RARE COMPLICATION
OF THERMAL BURN
Barr J., Sagi A., Glesinger R., Rosenberg
L.
Department of Plastic Surgery, Assaf
Harofeh Medical Centre, Tel-Aviv University, Sackler School of Medicine, Zerifin, Israel
SUMMARY. The
heart is rarely affected by thermal injury, but here such a case is presented. Following
severe burns a 28-yr-old woman suffered from pericardial effusion together with ARDS and
sepsis. She had sustained 30% TBSA second- and third-degree burns in the face, neck,
chest, arms, hands, abdomen, and thighs. Two days after admission the patient underwent
tangential excision and skin grafting in the hand. The patient eventually developed ARDS,
and in the second week post-burn her blood cultures were positive for Acinetobacter and
enterococei. The patient was treated with intravenous imipenem, which according to
sensitivity was later replaced by ampicillin and Garamycin. It was decided not to drain
the pericardium but rather to continue conservative treatment with aspirin, antibiotics,
and respiratory support. The patient's condition gradually improved and two months after
admission she was discharged with all wounds closed. At follow-up several months later,
she was free of respiratory complaints.
Introduction
Sepsis in the early period
following a major burn is a very common and almost inevitable complication. Losing the
protective skin barrier and immunological defence mechanisms opens the gate for bacteria
to enter the blood stream and infect various organs and systems in the body.
The heart is among the less frequently injured organs following a thermal injury (2.1%).'
We present the case of a woman who developed a post-burn pericardial effusion and several
other complications, including ARDS and sepsis.
Case history
A young woman aged 28 yr
tried to adjust the flame of the petroleum heater in her apartment. While she was doing
so, her dress caught fire. An hour passed before she was found. She was brought to the
emergency room with 30% T13SA second- and third-degree burns in the face, neck, chest,
arms, hands, abdomen, and thighs.
Since the accident took place in a closed space, smoke inhalation was also suspected.
There were signs of charing around the ala nasi. She was highly excited on admission,
pale, and tachypnoeic (40 breaths per min), with shallow breathing and shivering. The
vital signs were stable: blood pressure, 140/90; pulse, 11 0/min; respiration 35/min. The
blood count showed a haemoglobin level of 9. Blood gases and electrolytes were within
normal levels. There was no sign of burn or oedema in the nasopharynx. Chest x-ray and
electrocardiogram were normal. After nasotracheal intubation, mechanical ventilation was
started. A nasogastric tube was inserted and intravenous Tagamet 200 mg x 5/day was
initiated. Intravenous fluid administration with Ringer's lactate solution (4 cc/kg/h) was
also initiated. The burn wounds were cleaned and covered with saline dressing. The patient
was then transferred to the intensive respiratory care unit (IRCU) for continuation of
treatment and monitoring. During the following days she developed ARDS and mechanical
ventilation was therefore continued. Two days after admission the patient underwent
tangential excision and skin grafting in the hand.
In the second week blood cultures were positive for Acinetobacter and enterococci.
Intravenous imipenem 3 gr/d was initiated, which according to sensitivity was later
replaced by ampicillin 12 gr/d and Garamycin 80 mg x 3/d. The patient also gradually
developed respiratory distress. The blood gases deteriorated and a chest x-ray revealed
disseminated pulmonary infiltrates and cardiomegaly. Central venous pressure levels rose
to nearly 30 cin H20 and a paradoxical pulse appeared. The fluid balance was 10 litres
positive, and the patient was oliguric and needed furosemide intravenously a few times to
maintain adequate urine output. The clinical picture was compatible with tamponade and the
next step was to perform echocardiography. A large amount of pericardial fluid and a mild
collapse of the left atrial walls were found. After a joint consultation with the
cardiologists, the IRCU, and plastic surgeons, it was decided not to drain the pericardium
but rather to continue conservative treatment with aspirin 2 gr/d, antibiotic treatment,
and respiratory support. A slow but continuous improvement followed in the next few days.
Central venous pressure levels dropped gradually, urine output increased, blood gases
improved, and the respiratory distress subsided. Mechanical ventilation was terminated and
the patient received a high calorie diet and vigorous physiotherapy. Repeated
echocardiography showed only a residual amount of pericardial fluid. A second skin
grafting operation was performed and two months after admission the patient was discharged
with all wounds closed. At follow-up several months later, she was free of respiratory
complaints.
Discussion
The systemic response to a
major thermal burn injury is characterized by a rapid and massive loss of fluids. The loss
of capillary integrity leads to the shift of fluids and plasma proteins from the vascular
bed into the interstitial compartment.' Hypovolaernic shock results. The cardiovascular
response exhibits an ebb-and-flow pattern. The ebb phase represents a 1-3 day period of
decrease in cardiac output, which is mainly the reflection of hypovolaemic shock.' The
following flow phase represents the highly increased metabolic demand, which lasts for
several weeks and is characterized by a marked increase in cardiac output and peripheral
blood flow. Cardiovascular complications become prominent when the partial- to
full-thickness burn area exceeds 20-25% TBSA.' These complications are mainly attributed
to infection and a decrease in body defence mechanisms.
In a large series of 3640 burn patients reviewed by Munster et al., 64 cases of infection
involving the heart were identified.' There were only three survivors among them,
equivalent to a mortality of 95.3%. The injured sites involved the myocardium in 34
patients, the valves in 18, multiple sites in 7, the pericardium in 4, and coronary artery
in one. Pericarditis occurred in three patients owing to extension of myocardial infection
through the epicardium, and in one patient resulted from mediastinitis secondary to
infection spreading from a tracheotomy site. The pathogens responsible for the infection
reflected the predominant organisms in the infected burn wound or cannulated vein. A
diagnosis of purulent pericarditis should be suspected with the development of a heart
murmur, cardiomegaly, pericardial friction rub, high fever with chills, night sweats,
acute heart failure, hypotension, tachycardia, and elevation of central venous
pressure.',' In the case we present here, the elevation of central venous pressure,
cardiomegaly, the development of tachypnoea, the appearance of disseminated pulmonary
infiltrates, a positive fluid balance of nearly 10 litres, and acute heart failure led us
to hypothesize three possible causes: 1. superhydration-induced heart failure; 2.
respiratory failure due to ARDS and septicaemia; 3. heart failure as a result of
pericardial effusion, in view of the high central venous pressure levels. The subsequent
echocardiography showed that indeed there was pericardial involvement. The decision not to
drain the pericardium was based on the assumption that bacteria from the infected burned
chest surface might contaminate the otherwise uninfected reactive pericardial effusion and
complicate the patient's condition. Conservative treatment with antibiotics, aspirin, and
respiratory support proved to be beneficial. Our conclusion is that conservative treatment
should be considered in thermally injured patients complicated by pericardial effusion
before pericardial drainage is carried out.
RESUME. Les
Auteurs décrivent un cas peu commun où le coeur a été atteint par une lésion
thermique. A la suite de brûlures graves une femme âgée de 28 ans souffrait d'effusion
péricardiaque associée au SDRA et à la sepsis. Elle présentait des brûlures de 2ème
et 3ème degré en 30% de la surface corporelle totale dans le visage, le cou, le thorax,
les bras, l'abdomen et les cuisses. Deux jours après l'hospitalisation la patiente a subi
l'excision tangentielle et la greffe cutanée à la main. La patiente à la fin
présentait le SRDA, et dans la deuxième semaine après la brûlure les cultures du sang
étaient positives pour l'Acinetobacter et les entérocoques. La patiente a été traitée
avec l'imipenern intraveineux que selon la sensibilité a été remplacé par
l'ampicilline et le Garamycin. Il a été décidé de ne pas drainer le péricarde et de
continuer plutôt le traitement conservateur avec l'aspirine, les antibiotiques et le
support respiratoire. Les conditions de la patiente ont amélioré graduellement et deux
mois après l'hospitalisation elle a été renvoyée guérie quand toutes les lésions
étaient guéries. Le contrôle effectué après divers mois a montré qu'elle ne
souffrait plus de problèmes respiratoires.
BIBLIOGRAPHY
Munster A.M. et al.: Cardiac infections in burns. American J. Surgery, 122: 524-7, 1971.
Carleton S.C. et al.: Cardiac problems associated with burns. Cardiology Clinics, 13:
257-60, 1995.
Nakamura K. et a].: Survival of an extensively burned infant following purulent
pericarditis. Burns, 11: 202-6, 1985.
Srivastava R.K. et al.: Cardiac infection in acute burn patients. Burns, 6: 48-54.
This paper was received on
18 October 1999.
Address correspondence to:
Dr Jacob Barr
8 Yassour St., POB 2292, Lehavim 85338, Israel
Tel.: 972-7-6512628; fax: 972-7-6519076/8; mobile: 972-50-214850
E-mail: gbarr@isdn.net.il |
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